Renal trauma and hypertension: the role of renin

Three patients developed hypertension following renal trauma. Trauma produced perinephric hematoma in two and renal artery thrombosis in one. Renal vein plasma renin activity (PRA) from the traumatized kidney was three to eight times greater than renal vein PRA from the untraumatized (contralateral) kidney. Peripheral PRA was elevated in all. A surgical operation lowered peripheral PRA to normal in all, but corrected hypertension in only two of three. Preoperative medical treatment with renin-suppressing pharmacologic agents correctly predicted this response to surgery. Postoperative renal vein PRA in the remaining hypertensive patient demonstrated that surgery successfully alleviated the abnormality in renin secretion. These studies suggest that excessive renin secretion initiate but other unidentified factors may contribute to the hypertension observed after renal trauma.     

Effect of caffeine treatment on plasma renin activity and angiotensin I concentrations in rats on a low sodium diet

Animals treated acutely with an adenosine receptor antagonist have elevated plasma renin activity. This observation suggests that endogenous adenosine plays a physiologically significant role in restraining renin release. However, it is unclear whether chronic blockade of adenosine receptors would cause a rise of renin activity since tolerance to adenosine blockade is known to develop quickly. An earlier study partially addressed this question by showing that chronic blockade of adenosine receptors with caffeine exacerbated both the rise of plasma renin activity and the decline of renal function in 2-kidney-1-clip (2K1C) renovascular hypertensive rats. However, that study did not determine whether the difference in renin activity occurred solely as a secondary result of the difference in renal function. The purpose of this study was to reexamine the effect of chronic caffeine consumption on plasma renin activity and angiotensin I levels in animals in another high-renin model, i.e., the low sodium diet. The low sodium diet is devoid of the potential confounding effect of deteriorating renal function associated with the 2K1C renovascular hypertension model. In this study, animals received normal rat chow and drank either 0.1% caffeine water or vehicle for ten days. After ten days, all rats were switched to a low sodium diet for three weeks. Plasma renin activity and plasma angiotensin I levels were measured before, and at 1 and 3 weeks after initiating the low sodium diet. The results of this study show that chronic blockade of adenosine receptors with 0.1% caffeine water increases plasma renin activity and angiotensin I concentration before and throughout the three weeks when animals were on the low sodium diet. The results of this study suggest that the inhibitory role of adenosine on renin release is a general physiological process, rather than a special situation applicable only to the 2K1C model.     

Incidence and pathophysiological changes in chronic two-kidney hypertension in the dog

Unilateral renal artery plication in dogs reduced renal blood flow by 80% and produced a sustained elevation in arterial pressure whereas plasma renin activity increased for only 4 days. Sodium was retained for 3 days after plication, but this response is similar to that after a sham operation. Of seven dogs studied chronically, elevated arterial pressure was sustained for 27 days or longer in six animals. In three dogs hypertension continued for 2 mo before collateral vessels developed and arterial pressure fell; ligation of these collaterals restored hypertension. Arterial pressure was unaffected by an infusion of [1-sarcosine, 8-alanine] angiotensin II in chronic hypertensive dogs on a normal sodium intake. This angiotensin antagonist lowered arterial pressure after sodium depletion, but became ineffective following rapid sodium repletion. Chronic hypertensive dogs showed normal responses to deoxycorticosterone acetate. These findings suggest that the renin-angiotensin system is not critically involved in maintenace of chronic two-kidney renovascular hypertension in the dog. The data also show that the homeostatic role played by the renin-angiotensin system in the maintenance of arterial pressure remained intact in chronic hypertension.     

Surgical treatment of renovascular hypertension

Two hundred sixty-four patients exhibiting renal artery occlusive disease underwent operation for renovascular hypertension between 1961 and 1977. Included were 27 pediatric patients. Fibrodysplastic disease affected 132 adults. Atherosclerotic lesions affected 51 patients with and 54 patients without clinically overt extrarenal arteriosclerotic cardiovascular disease. Ischemic kidney renin hypersecretion (renal: systemic index greater than 0.48), associated with suppressed contralateral kidney renin secretion (renal: systemic index approaching 0.0) predicted curability most reliably. Three hundred forty-eight operations were performed, of which 297 were primary and 51 were secondary procedures. Nephrectomy was initial therapy in 15 cases. Three operative deaths occurred among 51 patients manifesting overt extrarenal arteriosclerotic disease. No operative mortality was encountered among the other 213 patients. Surgical benefits were afforded 96% of pediatric patients and adults with fibrodysplastic disease, 91% of patients with focal renal arteriosclerosis, and 73% of those exhibiting overt extrarenal arteriosclerosis.     

Renovascular hypertension. Radionuclide renography for detection and prediction of clinical response to revascularization

The most frequently used non invasive tests in the diagnosis of renovascular hypertension are the measurement of peripheral blood renin before and after captopril administration, intravenous pyelogram, renal Doppler examination and radionuclide renography without and with angiotensin converting enzyme inhibitor administration. Measurement of renal vein renin levels and renal angiography are invasive tests commonly used. The latter allows an anatomical diagnosis of renal vein stenosis but does not give information about the functional consequences of such lesion and thus, does not predict the response of blood pressure to revascularization. Radionuclide renography has become the most useful non invasive diagnostic test, with a sensitivity and specificity of 83-94 and 85-97% respectively. It also predicts clinical response to revascularization and is useful for follow up after surgery or angioplasty. It also has good results in patients with renal failure, bilateral stenosis or stenosis in a solitary kidney and in transplanted patients.     

Nocturnal blood pressure and relation to vasoactive hormones and renal function in hypertension and chronic renal failure

The purpose of this study was to assess the blood pressure profile and to measure vasoactive hormones in patients with essential hypertension (n=61), secondary hypertension (n=32) and chronic renal failure (n=32) matched with healthy control subjects (n=35), and to study the relationship between circadian changes in blood pressure and baseline levels of vasoactive hormones and renal function. Non-invasive, automatic blood pressure measurement was performed for 24 or 48 h. Venous plasma concentrations of renin, angiotensin II, aldosterone, arginine vasopressin, atrial natriuretic peptide and endothelin were measured. The mean 24-h blood pressure was higher in all groups of hypertensive patients than in control subjects. The nocturnal blood pressure fall was preserved in essential hypertension, in contrast to secondary hypertension in which it was attenuated. In the patients with chronic renal failure the 24-h mean blood pressure was the same as in the controls. Night-time blood pressure was higher among the chronic renal failure patients than in the control group, and the nightly blood pressure fall in both diastolic and systolic blood pressure was reduced. Plasma concentrations of renin activity, arginine vasopressin, atrial natriuretic peptide, aldosterone and endothelin were significantly increased in secondary hypertension and chronic renal failure, compared to essential hypertension and control subjects. Plasma angiotensin II was increased in chronic renal failure compared to essential hypertension and controls. Estimated creatinine clearance and nightly blood pressure dips were inversely correlated in essential and secondary hypertension, i.e. with a decreasing renal function both systolic and diastolic nightly blood pressure dips were gradually attenuated. In the whole group of patients the nightly systolic and diastolic blood pressure dips were negatively correlated to basal plasma renin activity, plasma aldosterone and atrial natriuretic peptide levels, i.e. the higher the basal plasma hormone level the lower the blood pressure dip. In conclusion, patients with essential hypertension have elevated but normally configured 24-h blood pressure profiles, and patients with different kinds of secondary hypertension have elevated 24-h blood pressure profiles and attenuated nightly systolic and diastolic blood pressure falls. The more the renal function is reduced and the more the plasma levels of renin and aldosterone are increased, the more the nocturnal fall in blood pressure is reduced. It is suggested that the attenuated or absent decrease in nocturnal blood pressure in secondary renal hypertension is caused by an abnormally increased secretion of vasoactive hormones and/or by so far unknown factors released from the diseased kidney.     

Trimethoprim resistance and susceptibility genes in Staphylococcus epidermidis

OBJECTIVES: This study was performed to assess the acute effects of the new angiotensin II antagonist, candesartan cilexetil, on systemic and renal haemodynamics in patients with sustained essential hypertension [diastolic blood pressure (DBP) 95-114 mmHg]. METHODS: After 4 weeks of placebo treatment, systemic and renal haemodynamics were investigated in 17 patients with a mean age of 62 years and a mean systolic and diastolic blood pressure of 170/98 mmHg, just before (baseline) and for 4 h after administration of a single oral dose of candesartan cilexetil, 16 mg. Plasma concentrations of candesartan (the active compound formed from the pro-drug candesartan cilexetil), angiotensin II (Ang II), as well as plasma renin activity (PRA), were measured before and after dosing. RESULTS: At 2, 3 h and 4 h after dosing with candesartan cilexetil, systolic blood pressure (SBP) and DBP, as well as mean arterial pressure (MAP), were significantly lower than at baseline. The mean reduction in MAP 4 h after dosing was 8.8 mmHg (-6.5%). This effect was due to a fall in total peripheral resistance (TPR), while heart rate (HR), stroke volume (SV) and cardiac output (CO) were virtually unchanged. After 4 h there was a marked reduction in renal vascular resistance (RVR) of 0.0273 mmHg x ml(-1) x min (-16%), resulting in an increased renal plasma flow of 64.9 ml x min(-1) (14%). The glomerular filtration rate was increased by 7.75 ml x min(-1) (8%), and the filtration fraction (FF) was not significantly changed. There was no apparent relationship between the changes observed in systemic and renal haemodynamic variables and plasma concentrations of candesartan. Plasma renin activity increased over the study period, but in general the patients had low PRA. Changes in plasma concentrations of angiotensin II were inconsistent between patients. CONCLUSION: A single oral tablet of candesartan cilexetil, 16 mg, induced systemic and renal arterial vasodilatation and blood pressure reduction, without compromising renal perfusion or filtration or affecting cardiac performance. Plasma renin activity which was low in general, increased over the study period, but changes in plasma concentrations of angiotensin II were inconsistent.     

Renal tissue angiotensins during converting enzyme inhibition of angiotensin I in spontaneously hypertensive rat

To compare the effects of an angiotensin-converting enzyme inhibitor on circulating and tissue renin-angiotensin system, we measured different renin-angiotensin system parameters during the first day of treatment (Day 1) as well as after two weeks of treatment (Day 14). Ramipril was given orally once daily to adult male spontaneously hypertensive rats. Renin activity, angiotensin-converting enzyme activity and levels of angiotensin I and angiotensin II in the plasma, renal cortex and renal medullar were assessed at Day 1 and Day 14 of the treatment. In the plasma, both renin activity and angiotensin I increased 10 to 15 fold one to four hours after acute as well as at Day 14 of ramipril treatment and then returned to basal values within 24 hours. Plasma angiotensin II levels were not significantly decreased at Day 1 or Day 14. The decrease in the angiotensin II/angiotensin I ratio suggested a sustained inhibition of plasma angiotensin-converting enzyme at Day 14. In the renal cortex and medulla, a clearly different pattern was observed: in ramipril treated rats, renin activity in the renal cortex and medulla did not change at Day 1 but at Day 14 we observed a slight and sustained increase in renin activity. Despite very high basal levels of renin activity, angiotensin I levels in the renal cortex were comparable to those in the plasma. The angiotensin I level increased only one-fold one hour after ramipril intake at Day 1 and Day 14. This suggests that angiotensinogen may have a limiting role in the synthesis of angiotensin I in the kidney. Angiotensin II levels were slightly higher in the renal cortex and medulla than in the plasma suggesting local synthesis of the peptide. In the kidney, angiotensin II levels decreased one and four hours after the acute or prolonged ramipril treatment and the angiotensin II/angiotensin I ratio was reduced at the same time. Our results show that the responses of the plasma and kidney components of the renin-angiotensin system to angiotensin-converting enzyme inhibition are different in the plasma and the kidney suggesting that the circulating and tissue renin-angiotensin system are at least in part independent.     

Amino acid composition and biological value of rice proteins]

The study concerns the effect of angiotensin II when infused into the systemic and portal blood flow upon the general and renal haemodynamics in normal dogs and in hypertensive animals, as well as the effect of the operation of porto-caval transposition upon the course of renovascular hypertension. When peptide is infused, at a rate that causes a moderate pressor effect, into the systemic blood flow of normal animals, an antidiuretic and antinatriuretic effect is obtained, in hypertensive animals--an increase of diuresis, natriuresis and a less distinct pressor effect are obtained. When angiotensin II is infused into the portal flow, a less distinct pressor and renal effect is seen in animals with renovascular hypertension. The operation of porto-caval transposition of the vessels results in a hypotensive effect in the animals with renovascular hypertension.     

Effects of varying sodium intake on blood pressure and renin-angiotensin system in subtotally nephrectomized rats

In rats in which the renal mass had been reduced by 70 per cent, the effects of varying sodium intake on blood pressure, serum electrolytes, renin-angiotensin system, and some other parameters that were modified simultaneously were studied. Within 4 weeks, a high sodium diet (750 mEa. per kilogram) resulted in marked hypertension, whereas a standard sodium diet (150 mEq. per kilogram) elevated the blood pressure only slightly. A low sodium diet (less than 0.2 mEq. per kilogram) prevented the rise in blood pressure. In the hypertensive group, the hematocrit values were markedly decreased, indicating the expansion of extracellular and intravascular spaces. The compensatory renal hypertrophy was accelerated by the high sodium diet and retarded during restriction. During low sodium intake, the serum concentration of sodium was diminished and that of potassium elevated. During the high sodium diet, the sodium concentration was unchanged, but the potassium concentration was decreased. Subtotal nephrectomy diminished the plasma angiotensin II concentration, and the renin content of the kidney remnant was lower than that of the kidneys from control animals. Sodium restriction stimulated the renin angiotensin system markedly, whereas high sodium intake suppressed it. After subtotal nephrectomy, elevation of blood pressure, renal hypertrophy, and suppression of the renin-angiotensin system are closely related to sodium intake.     

The investigation of renovascular hypertension in children: the accuracy of radio-isotopes in detecting renovascular disease

Renovascular disease is an important cause of hypertension in children because it is potentially treatable by surgical or angioplasty techniques. The aim of this study was to assess the accuracy of radio-isotopes (DMSA, DTPA and MAG3) combined with the angiotensin converting enzyme inhibitor, captopril, in detecting children with renovascular hypertension. We retrospectively reviewed the ultrasound and pre- and post-captopril radionuclide studies (either DMSA and/or DPTA and/or MAG3) of children with sustained hypertension investigated at our institution. Renal angiography was used as the 'reference technique'. Thirty-nine children, over a period of 10 years, were evaluated: 17 (44%) children had renovascular disease that involved the proximal three divisions of the renal arteries, some of which were amenable to treatment. The overall sensitivity, specificity, positive predictive value and negative predictive value for detecting such renovascular disease, as assessed by changes between pre- and post-captopril radio-isotope studies, were disappointing at 59%, 68%, 59% and 68%, respectively. When considering only abnormalities in post-captopril studies, these indices were 82%, 41%, 52% and 75%, respectively. Three children with potentially treatable renovascular disease were not identified on the captopril studies. We conclude that renal angiography should remain the 'reference technique' in identifying children suspected of renovascular hypertension.     

Induction of proinflammatory cytokine and antioxidant enzyme gene expression following brief myocardial ischaemia

PURPOSE: In a recent study we found an increased resistive index immediately after extracorporeal shock wave lithotripsy (ESWL) in patients older than 60 years, which suggests renovascular disturbance. The present 26-month followup study was undertaken to investigate the relevance of elevated resistive index levels and the incidence of new onset hypertension. MATERIALS AND METHODS: Of the initial 76 patients 57, including 20 of the 23 at risk patients 60 or greater years, group 3), were followed for more than 26 +/- 6 months after ESWL. Followup included 2 resistive index measurements by Doppler ultrasound of the treated and the contralateral kidney, at least 2 blood pressure measurements 1 week apart and excretory urography as well as determination of plasma renin activity in 9 patients. RESULTS: With 1 exception, elevated resistive index levels and hypertension were observed exclusively in patients older than 60 years. In these patients the resistive index ranged between 0.65 and 0.86 (mean plus or minus standard deviation 0.74 +/- 0.05, normal less than 0.7). This increase in resistive index was statistically significant (p < 0.0001). Compared to the levels obtained immediately after ESWL, the resistive index continued to increase in all 9 patients older than 60 years who had hypertension (45%), whereas in the normotensive patients the resistive index was either stable or decreased. There was a strong positive correlation (0.903) between pathological resistive index levels and blood pressure. CONCLUSIONS: Patients older than 60 years are at risk for disturbances of renal perfusion as assessed by the resistive index, and 45% of these patients have new onset hypertension within 26 months of treatment.     

Renin-specific antibody for study of cardiovascular homeostasis

Antiserum specific for purified canine renal renin was used to inhibit this enzyme in trained, conscious dogs. The antiserum did not affect blood pressure in sodium-replete dogs but decreased plasma renin activity and blood pressure in sodium-depleted animals. The antiserum also reduced blood pressure to control levels concomitant with suppression of plasma renin activity in uninephrectomized dogs with acute renovascular hypertension. These observations establish the role of the renin-angiotensin system in the maintenance of blood pressure in the sodium-depleted state as well as in the initiation of renovascular hypertension.     

Renin response and angiotensinogen control during graded hemorrhage and shock in the dog

Hemorrhage and hemorrhagic hypotension have been shown to be potent stimulators of renin release. However, the relationship between angiotensinogen consumption and angiotensinogen production has yet to be completely defined during this type of circulatory stress. Peripheral renin activity increased progressively as the blood pressure was decreased stepwise by hemorrhage to 50 mmHg and remained elevated throughout the shock phase of the experiment. Angiotensinogen did not change from control (809 ng/ml) throughout hemorrhabic hypotension and shock. During hemorrhagic hypotension, with the infusion of the angiotensin antagonist, [1-sarcosine, 8-alanine]angiotensin II, angiotensinogen concentration fell progressively from 693 to 208 ng/ml at 50 mmHg. Intravenous angiotensin II infused continuously after the mean blood pressure reached 50 mmHg significantly elevated plasma angiotensinogen concentration. In conclusion, during hemorrhagic hypotension and shock, the kidney and the liver appeared capable of maintaining elevated plasma renin activity and adequate plasma renin substrate, angiotensinogen, respectively. The mechanism responsible for the maintenance of plasma angiotensinogen is suggested to involve a positive-feedback effect of angiotensin II on the liver.     

Influence of the renal sympathetic nerves on renal renin and angiotensinogen gene expression in spontaneously hypertensive rats during development

OBJECTIVE: To investigate the influence of renal sympathetic denervation on renin and angiotensinogen gene expression in the kidney during growth and the development of hypertension in spontaneously hypertensive rats (SHR). Comparative studies were undertaken in age-matched normotensive Wistar rats. DESIGN: Four-week-old SHR and Wistar rats were subjected to either denervation of the left kidney or sham operation. At age 5, 7 or 9 weeks the rats were lightly anaesthetized, carotid blood pressure was measured, a blood sample was taken and both kidneys were removed. METHOD: Plasma renin activity was measured by radioimmunoassay, and renal renin and angiotensinogen messenger RNA (mRNA) levels were measured by Northern blot hybridization followed by densitometric analysis. RESULTS: In 5- and 7-week-old SHR the renin mRNA level in the left kidney was significantly suppressed compared with that in the sham-operated right kidney and with the level in 9-week-old SHR. The renal renin mRNA level in sham-operated SHR decreased significantly with increasing age, whereas in the Wistar rats the renal renin mRNA level did not change at any age and was not affected by renal denervation. The renal angiotensinogen mRNA level gradually increased with age in both rat strains and was not affected by denervation, but much higher levels were attained in the Wistar rats than in the SHR. CONCLUSION: Renal angiotensinogen gene expression was depressed in the SHR, with little evidence of neural regulation at any age in the SHR or the Wistar rats. However, in the SHR the renal sympathetic nerves elevated renal renin gene expression in the prehypertensive stage, but their influence decreased as hypertension developed.     

Renovascular hypertension: anatomic and renal function changes during drug therapy

Serial renal function studies were performed on 41 patients wtih renovascular hypertension (RVH) secondary to atherosclerotic renal artery disease who had been randomly selected for nonoperative management. In 19 patients, serum creatinine levels increased between 25% and 120%. The glomerular filtration rates dropped between 25% and 50% in 12 patients. Fourteen patients (37%) lost more than 10% of renal length. In four patients (12%), a significant stenosis progressed to total occlusion. Seventeen patients (41%) had deterioration of renal function or loss of renal size that led to operation. One patient required removal of a previously reconstructible kidney. Of the 17 patients with deterioration, 15 had acceptable blood pressure (BP) control during the period of nonoperative observation. Progressive deterioration of renal function in nonoperatively treated patients with atherosclerotic renal artery stenosis and RVH is common, and occurs even in the presence of BP control with drugs.     

Renovascular arterial hypertension. From physiopathology to therapy

Understanding the pathophysiology, diagnosis, and management of renovascular hypertension (RVH) is of paramount importance due to the severity of hypertension (HT) and renal insufficiency (RI). Moreover, adequate treatment by surgery and/or endovascular intervention can improve HT and revert RI. The comprehension of the pathophysiology of RVH had its origin on the experiments of Goldblatt which led to the recognition of the renin dependent, volume dependent, and mixed types. A continuum seems to exist, from an acute phase, supported by the endocrine renin angiotensin aldosterone system, evolving towards a chronic phase sustained by the local renin angiotensin system. The involved vasoconstrictor and mitogenic mechanisms may contribute to the arterial remodeling. The most common forms of pathology, i.e. atherosclerosis, fibromuscular dysplasia (FD), and Takayasu's arteritis, and their natural history, are described. The prevalence of RVH, ranging from 0.2% to more than 25%, depending on the clinical situation, is evidenced. Clinical symptoms and signs and the most important diagnostic tests are pointed out: functional tests (captopril test, postcaptopril renography, scintigraphy, and renin determinations) and anatomical tests (intravenous digital angiography and intrarterial angiography). New imaging techniques are also referred. A diagnostic work-up based on the index of clinical suspicion is described. The therapeutic goal is the resolution of the two main problems of RVH: hypertension and ischemic nephropathy. Revascularization is becoming mandatory either by percutaneous transluminal angioplasty mostly for FD and atheromatous non-ostial stenoses, or by surgery, which is preferred for patients with ostial or peripheral stenoses, aneuryms, occlusions and concomitant aortic disease. A better knowledge of RVH allows, not only diagnosis and treatment of one of the most frequent types of secondary hypertension, but also the control of the resulting ischemic nephropathy.     

Captopril renal scintigraphy in renovascular hypertension

Renovascular disease is a common cause of secondary hypertension. Renal artery stenosis is present in up to one third of patients with clinical markers suggestive of renovascular hypertension, such as hypertension refractory to medical management, severe hypertension in a young patient and worsening of renal function after the use of an angiotensin-converting enzyme inhibitor. Early discovery of renal artery stenosis may allow amelioration or cure of the hypertension and halt progressive loss of renal function. Although renal arteriography remains the gold-standard aid to diagnosis and to planning surgical intervention, it is an invasive procedure that may cause deterioration of renal function. In the presence of renal artery stenosis, glomerular filtration is maintained by angiotensin. Administration of captopril in renal scintigraphy removes this compensatory mechanism and causes a temporary impairment of renal function in the affected kidney. Nuclear tracers can visualize this impairment, thus allowing assessment of the physiologic significance of a renal artery stenosis. The test can be done as a outpatient procedure.     

Industrial hygiene and occupational health studies in Australian (New South Wales) shipyards

Twenty one subjects with sistemic arterial hypertension and arteriographic signs of obstructive lesion of the renal artery were studied and classified in 3 groups: group A, 13 cases with bilateral renovascular lesions; group B, 4 patients with unilateral renovascular stenosis and group C, formed by 4 subjects with a segmental branch stenosis of a renal artery. In all cases an special protocol was followed to measure plasma renin activity (PRA) in blood taken from a peripheral vein, inferior vena cava and both renal veins and also to determine 24 hrs. urinary excretion of aldosterone (UEA). PRA and UEA were clasified as high, normal and low by comparing the results with those of normal subjects in a nomogram estimated in the same laboratory in which PRA and UEA values were correlated with 24 hrs. urinari sodium excretion. Besides, R greater than /R less than index (highest PRA of renal vein blood/PRA of contralateral renal vein) and V-A A index (V = PRA of renal vein blood; A = PRA of inferior vena cava) were calculated. Forty eight and thirty eight percentage of the cases had either high renin in peripheral venous blood or high UEA. Similar data in patients with essential hypertension previously studied in the same laboratory were 12 and 10% respectively. V-A A index was incongruent with the arteriographic image in 3 cases of group B; 4 cases of group A and 2 of group B had a pattern of bilateral stenosis, and one case in each group A and C had a unilateral stenosis pattern. In the other patients the samples were "non representative" due to a high level of PRA in the inferior vena cava blood comparable to PRA of the renal veins. Six cases of group A had a R greater than /R less than index superior to 1.5, which suggested a predominant vascular lesion in one side not always congruent with the arteriographic findings. In 3 cases of group B this index was higher than 1.5 in favor of the ipsilateral lesion. Three cases of group C had a normal R greater than /R less than index and one with a total oclussion of a segmental artery presented an index superior to 1.5, ipsilateral to the lesion. The latter index was of value in the diagnosis of renovascular arterial hypertension.     

Increased plasma endothelin concentration in atherosclerotic renovascular hypertension

The aim was to investigate circulating levels of immunoreactive endothelin (ir-ET) in atherosclerotic renovascular hypertension (RVH), and to assess the role of the kidneys in its overall plasma concentration. We studied 16 hypertensive patients with renal artery stenosis evidenced by angiography and admitted to hospital for the diagnostic evaluation of RVH by renal vein plasma renin activity (PRA) determinations. The right femoral vein was catheterized to simultaneously measure PRA and ir-ET in both renal veins and inferior vena cava below the origin of the renal veins. RVH was present in 9 patients as indicated by diagnostic PRA renal vein ratios and the remaining 7 patients were considered to have essential hypertension (EH). Patients with RVH showed a marked increase in systemic plasma ir-ET concentration (10.3 +/- 0.9 pg/ml). Despite a significant increase of PRA in the vein of the ischemic (IK) versus the contralateral (CK) kidney in patients with RVH, no significant differences in ir-ET concentration were observed between both kidneys. These results indicate that patients with RVH have increased circulating levels of ir-ET. However, the higher systemic plasma ir-ET do not arise from the renal circulation, since plasma ir-ET is significantly higher in systemic circulation than in renal veins.