Intralymphocyte free magnesium in a group of subjects with essential hypertension

Despite the importance of magnesium in essential hypertension, few data are available on the ionized intracellular concentration of this ion. We therefore studied intralymphocyte free intracellular magnesium (Mgi) in 32 untreated essential hypertensive subjects and 27 normotensive control subjects by means of a fluorimetric technique based on the use of the new magnesium-sensitive dye furaptra. We also measured intralymphocyte ionized calcium (Cai) with fura 2. No statistically significant differences were found in Mgi in hypertensive compared with normotensive subjects (essential hypertensive, 0.291 +/- 0.053 mmol/L; normotensive, 0.293 +/- 0.043 [mean +/- SD]). A statistically significant inverse correlation was established between Mgi and plasma triglycerides in essential hypertensive subjects (r = -.521, P = .002). The hypertensive group was arbitrarily divided into two subgroups according to plasma triglyceride levels (> 2 [n = 10] or < 2 mmol/L [n = 22]), and Mgi proved to be significantly lower in the subgroup with high plasma triglyceride levels compared with either the subgroup with normal triglycerides (P = .009; 95% confidence interval, 0.013-0.088) or the normotensive control group as a whole (P = .03; 95% confidence interval, 0.003-0.069) (high-triglyceride hypertensive subgroup, Mgi = 0.256 +/- 0.045 mmol/L; normal-triglyceride hypertensive subgroup, Mgi = 0.307 +/- 0.049). No statistically significant differences were found in Cai in hypertensive compared with normotensive subjects (hypertensive, 53 +/- 12 nmol/L; normotensive, 54 +/- 14). We did not find statistically significant correlations between Cai and plasma triglycerides, nor did we find any differences in Cai between the subgroup of hypertensive subjects with high plasma triglyceride levels and either the subgroup of hypertensive subjects with normal triglycerides or the normotensive control group as a whole. The discrepancies between our results in lymphocytes and data relating to either erythrocytes or platelets emphasize the need for caution before the results are extrapolated from one tissue to the other. The decreased Mgi levels in the subgroup of high-triglyceride hypertensive subjects may suggest a role for magnesium in plurimetabolic syndrome.     

Altered permeability of the erythrocyte membrane for sodium and potassium ions in spontaneously hypertensive rats

Permeability of the erythrocyte membrane for sodium and potassium ions was studied in 8-10-week old spontaneously hypertensive rats (SHR, Kyoto Wistar strain), normotensive Wistar and Sprague-Dawley rats. The rate constnat of Na/Na exchange was considerably greater in the SHR than in the normotensive Wistar and Sprague-Dawley rats. This difference remained the same in the rats adrenalectomized 7 days prior to the experiment. The maximum difference in the constants was found when the sodium pump was blocked by ouabain. The accumulation of 42K in the erythrocytes of the SHR (the sodium pump being blocked) took place at a considerably slower rate, and the K+ washout into a potassium-free medium was faster than in the normotensive Wistar and Sprague-Dawley rats. These results seem to indicate a higher permeability of the SHR's erythrocyte membrane for Na+ and K+ ions, as compared to normotensive Wistar and Sprague-Dawley strains. It is suggested that the increased permeability of the erythrocyte membrane for Na+ and K+ in the SHR may reflect a more widespread cell membrane defect, which could serve as a general cause for activating the mechanisms maintaing high blood pressure.     

Relationship between erythrocyte membrane permeability and the concentration in it of total cholesterol and its fractions and possible seasonal influences on these indices

A correlation between the content of labilly connected cholesterol fraction in erythrocytes and their penetration for urea was demonstrated. The dependence of erythrocyte membrane penetration on general cholesterol content and cholesterol fractions in the membrane was found to be season-influenced. A biochemical mechanism responsible for the changes in the labilly connected cholesterol fraction in erythrocyte membrane is discussed.     

Plasma triglycerides cosegregate with erythrocyte sodium content in F2 rats of HTG x Lewis cross

The possible association of plasma lipids (triglycerides and cholesterol) with erythrocyte Na+ content (Na+i) and/or with alterations in red cell Na+ and K+ (Rb+) transport was studied in a population of F2 hybrids obtained by crossing hypertensive Prague hereditary hypertriglyceridaemic (HTG) rats with normotensive Lewis rats. The obtained data indicated a strong cosegregation (p < 0.001) of plasma triglycerides with erythrocyte Na+ content. This was the cause for the close correlation of plasma triglycerides with the Na(+)-K+ pump activity (measured as ouabain-sensitive Na+ extrusion). On the contrary, there was only marginal association (p < 0.05) of erythrocyte Na+ content with plasma cholesterol which was significantly (p < 0.01) related to burnetanide-sensitive Rb+ uptake mediated by the Na(+)-K+ cotransport system. Na+ leak (bumetanide-resistant net Na+ uptake) correlated positively with blood pressure in female but not in male F2 rats. The close association between plasma triglycerides and erythrocyte Na+ content suggests that ion transport alterations might contribute to mechanisms responsible for the cosegregation of blood pressure with plasma triglycerides in HTG x Lewis F2 hybrids.     

2 clinico-genetic types of primary congenital glaucomas in Slovakia

We studied transketolase activity of red blood cell hemolysates, and Na+, K+, ATPase activity and sialic acid concentration in red blood cell membranes from 52 patients with rheumatoid arthritis and 24 control subjects. Decreased red blood cell membrane Na+, K+, ATPase activity and sialic acid concentration and decreased transketolase in red blood cell hemolysates were observed in rheumatoid arthritis patients compared with control subjects (p < 0.001). Erythrocyte sedimentation rate and C-reactive protein values were increased in rheumatoid arthritis patients compared with control subjects (p < 0.0001). Significant correlations between sialic acid and Na+, K+, ATPase (r = 0.65, p < 0.001) and between sialic acid and transketolase (r = 0.58, p < 0.001) were observed. Erythrocyte sedimentation rate and C-reactive protein levels did not correlate with Na+, K+, ATPase activity or with sialic acid or transketolase in rheumatoid arthritis patients. These data show that decreases in Na+, K+, ATPase, and transketolase activities and sialic acid concentration are present in rheumatoid arthritis patients, and that the decrease in Na+, K+, ATPase and transketolase activities in rheumatoid arthritis might be due to decreased sialic acid.     

Low-density lipoprotein oxidation and vitamins E and C in sustained and white-coat hypertension

Low-density lipoprotein oxidation and antioxidant vitamins E and C were investigated in white-coat hypertension in comparison with sustained hypertension and normotension. We selected 21 sustained hypertensive subjects, 21 white-coat hypertensive subjects, and 21 normotensive subjects matched for gender, age, and body mass index. White-coat hypertension was defined as clinical hypertension and daytime ambulatory blood pressure <139/90 (subjects were also reclassified using 134/90 and 135/85 mm Hg as cutoff points for daytime blood pressure). Blood samples were drawn for lipid profile determination, assessment of fluorescent products of lipid peroxidation in native LDL, evaluation of susceptibility to LDL oxidation in vitro (lag phase and propagation rate), and determination of LDL vitamin E and plasma vitamins E and C contents. Compared with sustained hypertensive subjects, white-coat hypertensives had significantly lower fluorescent products of lipid peroxidation (15.4+/-3.4 versus 10.2+/-3 units of relative fluorescence/mg LDL protein, P<.05), longer lag phase (54+/-10 versus 88+/-10 minutes, P<.05), lower propagation rate (8.2+/-2.5 versus 5.95+/-2.1 nmol diene/min per mg LDL cholesterol, P<.05), higher LDL vitamin E content (8.3+/-1.1 versus 10.1+/-1.8 nmol/mg LDL cholesterol, P<.05), and plasma vitamin C content (40+/-13 versus 57+9 micromol/L, P<. 05). No significant difference was observed between white-coat hypertensive and normotensive subjects. The results did not change after reclassification of subjects. Our data show that white-coat hypertensive subjects do not show an enhanced propensity to LDL oxidation or reduction in antioxidant vitamins. Given the role of LDL oxidation in the development of atherosclerosis and that of vitamin E and C in protecting against it, these findings suggest that white-coat hypertension per se carries a low atherogenic risk.     

A computer-based statistical pattern recognition for Doppler spectral waveforms of intracranial blood flow

The effects of 2 months treatment with simvastatin (40 mg, 20 mg p.o. daily) or placebo on erythrocyte membrane cholesterol content and acyl chain composition have been studied in 36 patients with a clinical history of atherosclerosis enrolled in the Oxford Cholesterol Study. All patients received advice corresponding to a standard phase 1 cholesterol-lowering diet. As expected the mean serum total cholesterol fell substantially (-26.5%, 20 mg simvastatin, P < 0.05; -32.7%, 40 mg simvastatin, P < 0.05) compared to placebo (-6.3%, ns). However, mean erythrocyte cholesterol content did not change significantly in any group (2 months therapy: 20 mg simvastatin, -0.62%; 40 mg simvastatin, +2.2%; placebo, -4.2%). Erythrocyte cholesterol was also unaltered after 5 months of therapy. Erythrocyte osmotic fragility was unchanged in the treatment and placebo groups. In the placebo group dietary advice alone was associated with a significant increase in the linoleic acid content of erythrocytes from 9.4 mole% of total acyl chains to 11.8 mole% (P < 0.05). Treatment with simvastatin was associated with an increase in the arachidonic acid content of the erythrocyte membrane from 12.2 to 15.3 mole% (P < 0.05). Treatment with simvastatin does not alter erythrocyte cholesterol content, but does alter acyl chain distribution. These results suggest that the chemical potential of cholesterol in serum is not markedly altered by HMG-CoA reductase inhibition.     

Impaired left ventricular relaxation and hyperinsulinemia in patients with primary hypercholesterolemia

Fifteen non-obese patients with familial hypercholesterolemia and fifteen normocholesterolemic subjects matched for age, body mass index, waist/hip ratio, arterial blood pressure and sedentary life style underwent blood sampling for determination of fasting plasma glucose, insulin, total-, LDL-, HDL-cholesterol, triglycerides, free fatty acids, apolipoprotein A1 and B. In both groups of subjects we determined erythrocyte membrane microviscosity and performed an echocardiographic study. We demonstrated that hypercholesterolemic patients had a significant increase in fasting plasma total cholesterol (8.9 +/- 0.5 vs. 5.5 +/- 0.3 mmol/l, P less than 0.001), insulin (79 +/- 4 vs. 58 +/- 4 pmol/l, P less than 0.05) and apolipoprotein B (2.2 +/- 0.5 vs. 1.3 +/- 0.5 g/l P less than 0.01). In the echocardiographic study we found a significant impairment in left ventricular relaxation (isovolumic relaxation time (IRT) 106 +/- 6 vs. 73 +/- 7 ms, P less than 0.01). Erythrocyte membrane microviscosity (0.253 +/- 0.004 vs. 0.225 +/- 0.003, P less than 0.05) was also increased in hypercholesterolemic patients. Finally we found that erythrocyte membrane microviscosity correlated with fasting plasma insulin levels (r = -0.46, P less than 0.03) and IRT (r = -0.52, P less than 0.01).     

Relationship of red blood cell ion transport alterations and serum lipid abnormalities in Lyon genetically hypertensive rats

Alterations of Na+ and K+ transport in erythrocytes of hypertensive humans or animals are often associated with abnormal lipid metabolism. The aim of the present study was to investigate red blood cell ion transport in Lyon inbred strains selected from Sprague-Dawley rats for different blood pressure levels. Lyon strains are characterized by important metabolic changes, including plasma lipid abnormalities. Serum triglycerides, cholesterol, and uric acid as well as red blood cell Na+ and K+ (Rb+) transport mediated by Na(+)-K+ pump or Na(+)-K+ cotransport and cation leaks were studied in hypertensive (LH), normotensive (LN), and low blood pressure (LL) Lyon rats aged 12 weeks. Increased erythrocyte Na+ content (Nai+) and higher levels of serum triglycerides, cholesterol, and uric acid were demonstrated in LH rats compared with LN animals. Nevertheless, at this age serum triglycerides and erythrocyte Nai+ of LL rats were even higher than those of LH animals. There were no significant differences between Lyon strains in either Na(+)-K+ pump activity or bumetanide-resistant (BR) cation leaks. The activity of bumetanide-sensitive (BS) Na(+)-K+ cotransport mediating inward Na+ movement was highest in LL rats and lowest in LH animals. In Lyon rats, Nai+ was positively related to serum triglycerides, whereas blood pressure correlated positively with BR Na+ leak and negatively with BS net Na+ uptake. A similar association of erythrocyte Nai+ with serum triglycerides was also observed in Prague hereditary hypertriglyceridemic rats (HTG) that were selected from Wistar rats for high plasma triglycerides. The major difference of the two forms of genetic hypertension associated with abnormal lipid metabolism was in BS net Na+ uptake, which was enhanced in HTG but reduced in LH rats. This was probably due to differences in plasma cholesterol, which was elevated in LH but not in HTG animals. Our study in Lyon rats confirmed the positive association of blood pressure with Na+ leak as a characteristic feature of genetic hypertension.     

Anti-oxidant status and lipid peroxidation in patients with essential hypertension

BACKGROUND: Lipid peroxidation and derived oxidized products are being intensively investigated, because of their potential to cause injury and their pathogenetic role in several clinically significant diseases. The view that an excess of lipid peroxidation products is present and relevant in the pathogenesis of human essential hypertension or in hypertension-induced damage has still not received definitive support. OBJECTIVE: To evaluate both the extent of lipoperoxidation in essential hypertensive patients and the status of enzymatic and non-enzymatic antioxidants that potentially are able to modulate it METHODS: We selected 105 newly diagnosed essential hypertensives among those referred to our hypertension outpatient clinic and compared them with 100 normotensive controls matched for age. Plasma malondialdehyde was measured by high-performance liquid chromatography after reaction with thiobarbituric acid, as an end product of lipid peroxidation; serum selenium (Se), plasma copper (Cu) and zinc (Zn), vitamins A and E, erythrocyte superoxide dismutase and glutathione peroxidase levels were evaluated as indices of oxidant balance. Differences between the groups were tested by Student's t test and chi2 test. RESULTS: Compared with controls, essential hypertension patients had higher malondialdehyde and glutathione peroxidase activities (P<0.05 for both) and Zn concentrations (P<0.001) and lower superoxide dismutase activities (P<0.005), vitamin A (P<0.05) and E (P<0.001) levels and Cu concentrations (P<0.005). We found no difference between Se levels of essential hypertensive and control subjects. CONCLUSIONS: Essential hypertension is associated with greater than normal lipoperoxidation and an imbalance in anti-oxidant status, suggesting that oxidative stress is important in the pathogenesis of essential hypertension or in arterial damage related to essential hypertension.     

Percutaneous transluminal coronary angioplasty reverses vasoconstriction of stenotic coronary arteries in hypertensive patients

BACKGROUND: Endothelial dysfunction of coronary arteries with impaired vasodilation has been reported in patients with arterial hypertension. However, the effect of dynamic exercise on coronary vasomotion of a stenotic vessel segment before and after PTCA has not yet been evaluated in these patients. METHODS AND RESULTS:Coronary vasomotion of a normal and a stenotic vessel segment was studied in 39 patients with coronary artery disease during supine bicycle exercise before and 9+/-3 months after PTCA. Luminal area changes were determined by biplane quantitative coronary arteriography. There were 21 normotensive and 18 hypertensive patients who did not differ with regard to clinical characteristics. Percent area stenosis decreased after PTCA from 90% to 39% (P<0.001) in normotensive and from 86% to 33% (P<0.001) in hypertensive patients. Exercise-induced vasomotion of the normal vessel segment was significantly different between normotensives and hypertensives before (+19% versus +1%, P<0.01) and after (+16% versus +3%, P<0.01) PTCA. In contrast, stenotic vessel segments showed vasoconstriction in both normotensive and hypertensive patients (Deltaexercise, -11% versus - 20%, P=NS), which was reversed after PTCA (+3% versus +2%, P=NS). CONCLUSIONS: Normal coronary arteries show reduced vasodilation during exercise in hypertensive patients that may be explained by the presence of endothelial dysfunction. Stenotic vessels demonstrate paradoxical vasoconstriction during exercise in both normotensive and hypertensive patients. PTCA reverses vasoconstriction by elimination of the flow-limiting stenosis and prevention of coronary stenosis narrowing during exercise in normotensive and hypertensive patients.     

Age and blood pressure related changes in cholesterol esterase activity and cholesterol content in aortas of stroke prone spontaneously hypertensive rats, spontaneously hypertensive rats and normotensive Wistar Kyoto rats

Changes in aortic lipolytic enzyme activities (cholesterol esterase and lipoprotein lipase) and acid phosphatase activity during aging were investigated in three strains of rats with different blood pressures; stroke prone spontaneously hypertensive rats (SHRSP), spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKR). The blood pressures of male, 7 month old animals, was 234 (SHRSP), 173 (SHR) and 128 (WKR) mmHg. The cholesterol esterase activity markedly decreased with age in the aortas of SHRSP, SHR and normotensive WKR rats, while acid phosphatase activity decreased only slightly, if at all, and lipoprotein lipase activity remained unchanged. This effect was enhanced by increasing blood pressure in SHRSP, SHR and WKR. The total aortic cholesterol content increased significantly with hypertension in a inverse relation with cholesterol esterase activity. These results suggest that cholesterol deposition in aged arteries is, at least partialy, ascribable to an age-related decrease in cholesterol esterase, and that hypertension aggravates the deposition of arterial cholesterol by accelerating the age-related decrease in aortic cholesterol esterase activity.     

International Colloquium on Ebola Virus Research: summary report

Desaturase enzymes are responsible for the conversion of essential fatty acids to the longer-chain eicosanoid precursors. These enzymes require zinc as an essential cofactor, and the following ratios-C20:4/C18:2, C20:5/C18:3, and C22:6/C20:5-are considered indexes of their activity. We analyzed these parameters in plasma and erythrocyte membranes of 105 essential hypertensive patients, 20 white coat hypertensive patients, and 100 age-matched normotensive control subjects. Dietary analysis excluded significant quantitative and qualitative differences in fatty acid dietary intake between essential hypertensive patients and normotensive control subjects. Zinc levels and C20:4/C18:2, C20:5/C18:3, and C22:6/ C20:5 ratios were significantly higher in essential hypertensive patients than control subjects, whereas white coat hypertensive patients showed intermediate values for all these parameters. These data provide evidence for an alteration in fatty acid metabolism of essential hypertensive patients, consistent with increased activity of desaturase enzymes. The consequent greater bioavailability of eicosanoid precursors, and in particular of arachidonic acid, could affect several vascular functions and have a bearing on the pathogenesis or complications of hypertension.     

Lectin histochemistry of fallopian tube epithelial cells. Relation to ovum transport and ovum pickup

BACKGROUND: This study was designed to investigate whether collagen type I degradation is altered in patients with essential hypertension and whether this alteration could be related to disturbances in the serum matrix metalloproteinase pathway of collagen degradation. A second aim of the study was to assess whether some relation exists between serum markers of collagen type I degradation and left ventricular hypertrophy in hypertensive patients. METHODS AND RESULTS: We measured serum concentrations of carboxy-terminal telopeptide of collagen type I (CITP) as a marker of extracellular collagen type I degradation, of total matrix metalloproteinase-1 (MMP-1), or collagenase, of total tissue inhibitor of metalloproteinases 1 (TIMP-1), and of MMP-1/TIMP-1 complex in 37 patients with never-treated essential hypertension and in 23 normotensive control subjects. Serum concentrations of free MMP-1 and free TIMP-1 were calculated by subtracting the values of MMP-1/TIMP-1 complex from the values of total MMP-1 and total TIMP-1, respectively. Measurements were repeated in 26 hypertensive patients after 1 year of treatment with the ACE inhibitor lisinopril. Baseline free MMP-1 was decreased (P<0.001) and baseline free TIMP-1 was increased (P<0.001) in hypertensives compared with normotensives. No significant differences were observed in the baseline values of CITP between the 2 groups of subjects. Hypertensive patients with baseline left ventricular hypertrophy exhibited lower values of free MMP-1 (P<0.01) and CITP (P<0.05) and higher (P<0.001) values of free TIMP-1 than hypertensive patients without baseline left ventricular hypertrophy. Treated patients attained an increase (P<0.001) in free MMP-1 and a decrease (P<0.05) in free TIMP-1. In addition, serum CITP was increased (P<0.05) in treated hypertensives compared with normotensive subjects. CONCLUSIONS: These findings suggest that systemic extracellular degradation of collagen type I is depressed in patients with essential hypertension and can be normalized by treatment with lisinopril. A depressed degradation of collagen type I may facilitate organ fibrosis in hypertensive patients, namely, in those with left ventricular hypertrophy.     

Correction of erythrocyte shape abnormalities in familial hypercholesterolemia after LDL-apheresis: does it influence cerebral hemodynamics?

It is well known that red blood cells incubated in low-density lipoprotein (LDL)-rich medium show shape abnormalities that revert to normal after reincubation in normal plasma. Patients with homozygous familial hypercholesterolemia (HFH) have an increased percentage of abnormally-shaped erythrocytes (mostly stomatocytes, knisocytes, and crenated cells) compared to normocholesterolemic controls: 7.73+/-0.96 versus 3.52+/-0.52 (mean+/-SEM; P = 0.001). To confirm the role of high LDL concentration in inducing red cell shape abnormalities we determined the percentage of abnormally shaped erythrocytes in seven HFH patients 1 day after the procedure of LDL-apheresis with a 40% cholesterol decrease. A reduction in kniscocytes, stomatocytes, and crenated cells was observed in the patients treated by LDL-apheresis (P < 0.01). To investigate the possible benefit of a reduction in erythrocyte shape abnormality on cerebral hemodynamics, cerebral flow velocity, as evaluated by transcranial Doppler, was evaluated concomitantly and found to be remarkably increased after apheresis (P < 0.01). No significant change in hematocrit, plasma viscosity, blood viscosity, mean pressure, or cardiac output was detected, 1 day after apheresis. An inverse correlation was demonstrated (r = 0.55; P = 0.04) between changes in the percentage of knisocytes+stomatocytes +crenated cells and percent changes in middle cerebral artery peak systolic velocity. The correction of erythrocyte shape abnormalities after LDL-apheresis might be related to dramatic changes in plasma phospholipid concentration and proportion occurring after this procedure in HFH patients. The reduction of erythrocyte shape abnormalities could contribute, together with other hemorheological factors, to the improvement of cerebral hemodynamics after LDL-apheresis.     

Insulin resistance and essential hypertension in Vietnamese subjects

Several epidemiological and experimental studies suggest that essential arterial hypertension is associated with hyperinsulinism and insulin resistance in obese subjects and also in subjects with normal body weight. Undernutrition remains frequent in adult Vietnamese people and mean body mass index is around 18.5 kg/m2 in Vietnam. The aim of this study was to look for insulin resistance in hypertensive Vietnamese subjects, despite a markedly lower BMI in Vietnam than in occidental countries. One hundred and eight hypertensive patients (51 men and 57 women) over 40 years (mean = 65.4 years) were compared with 36 healthy subjects (23 men and 13 women) over 40 years (mean = 63.8 years). Hypertensive patients had significantly higher BMI (20.5 +/- 0.3 (SEM) kg/m2 vs 18.4 +/- 0.4 kg/m2; p < 0.01), thicker triceps skinfold (1.26 +/- 0.07 cm vs 0.71 +/- 0.07 cm; p < 0.001) and not significantly different waist/hip ratio (0.88 +/- 0.01 vs 0.85 +/- 0.01). Blood glucose at fasting and 2 hours after 75 g glucose taken orally were similar in hypertensive and normotensive subjects. Plasma insulin at fasting and 2 hours after glucose were significantly higher in hypertensive patients (44.4 +/- 5.1 pmol/L vs 21.6 +/- 3.2 pmol/L; p < 0.05 and 271.1 +/- 21.6 pmol/L vs 139.1 +/- 15.2 pmol/L; p < 0.001). Thus, despite under-nutrition, hypertensive Vietnamese patients have a moderate but significant increase in BMI and fat mass without predominant abdominal localization, and a state of insulin-resistance, compared with normotensive healthy subjects.     

The changes in plasma arginine-vasopressin in patients with essential hypertension and the correlation with patient's condition

The levels of plasma arginine-vasopressin (AVP) in 80 patients with essential hypertension were measured, and its impact on the disease and its clinical significance were studied. The results showed that: (1) The levels of plasma AVP in patients with essential hypertension were significantly higher than that in normotensive subjects (P < 0.001). It dropped to normal level after antihypertensive drugs. (2) The concentrations of plasma AVP in both hypertensive subjects and normotensive subjects were not correlated with age and sex (P < 0.05). (3) The concentration of plasma AVP in patients with essential hypertension was the highest in stage III, the lowest in stage I, and middle in stage II. (4) The levels of plasma AVP in patients with malignant hypertension were significantly higher than that in patients with benign hypertension (P < 0.05). A positive correlation was found between the levels of plasma AVP and blood pressure (r = 0.3398, P < 0.01). (5) The concentrations of plasma AVP in hypertensive subjects with ventricular hypertrophy were higher than that in hypertensive subjects with out ventricular hypertrophy (P < 0.05). (6) The concentrations of plasma AVP in hypertensive subjects with heart failure were significantly higher than that in hypertensive subjects with out heart failure (P < 0.001). The results suggest that AVP has a role in the pathogenesis of hypertension, hypertension complicated with ventricular hypertrophy and hypertension complicated with heart failure. The levels of plasma AVP may be viewed as an index of the patient's condition in hypertensive subjects.     

Monoamine responses to acute and chronic aerobic exercise in normotensive and hypertensive subjects

OBJECTIVES: The purpose of the present study was to compare the plasma and serum monoamine levels in sedentary, untrained normotensive and hypertensive men at rest with levels measured after an acute bout of exercise and to compare similar measurements following a 12-week aerobic training program. PLACE OF STUDY: The data obtained for this study was collected from a clinic for the prevention of heart disease and cardiac rehabilitation (FITCOR) and analyzed in the Federal University of S?o Paulo (EPM), Laboratory of Experimental Neurology. SUBJECTS: Two groups of untrained male subjects, i.e., normotensive (N = 16) and hypertensive (N = 19), were submitted to an acute bout of exercise to analyze the acute effect of exercise on the monoamine levels. To study the chronic effect of exercise (physical training program), some individuals of each group were arranged in two other groups; normotensive (N = 11) and hypertensive (N = 8). MEASUREMENT: Plasma catecholamines and serum serotonin levels were determined by high performance liquid chromatography coupled with electrochemical detection. RESULTS: A significant reduction in diastolic blood pressure at rest was observed in the hypertensive group after the physical training program (p < 0.05). Only the mean plasma noradrenaline concentration increased significantly post-exercise in all groups of individuals (acute effect of exercise--p < 0.01 for untrained normotensive and hypertensive; chronic effect of exercise--p < 0.001 for untrained and trained normotensive, p < 0.01 for untrained and trained hypertensive). CONCLUSION: These data show the beneficial effect of physical exercise in reducing the blood pressure in hypertensive patients, which does not seem to be related to changes in circulating monoamines.     

Treatment with enalapril modifies the pain perception pattern in hypertensive patients

The cardiovascular system shares numerous anatomic and functional pathways with the antinociceptive network. The aim of this study was to investigate whether angiotensin-converting enzyme (ACE) inhibitor treatment could affect hypertension-related hypalgesia. Twenty-five untreated hypertensive patients, together with a control group of 14 normotensive subjects, underwent dental pain perception evaluation by means of a pulpar test (graded increase of test current applied to healthy teeth). After the evaluation of the dental pain threshold (occurrence of pulp sensation) and tolerance (time when the subjects asked for the test to be stopped), all the subjects underwent a 24-hour ambulatory blood pressure monitoring. The hypertensive group then was treated with 20 mg/d enalapril, whereas the normotensive subjects remained without any treatment. After a time interval of 6+/-2 months, the dental pain sensitivity was retested in all the subjects, and ambulatory blood pressure was recorded during treatment in the hypertensive patients. At the first assessment, hypertensive patients showed a higher pain threshold than normotensive subjects (P<.001). On retesting of pain sensitivity in hypertensive patients, a significant decrease of both pain threshold and tolerance, leading to their normalization, was observed during treatment (P<.001 and P<.005, respectively), in the presence of reduced 24-hour and office blood pressure values. A slight, though significant, correlation was observed between variations in pain tolerance and baseline blood pressure changes occurring during treatment. During follow-up, the normotensive subjects did not show any significant pain perception or office blood pressure changes. Hypertension-related hypalgesia was confirmed. Mechanisms acting both through lowering of blood pressure and specific pharmacodynamic properties may account for the normalization of pain sensitivity observed in hypertensive patients during treatment with ACE inhibitors.