Renal responses of Australian lungfish to vasotocin, angiotensin II, and NaCl infusion

The Australian lungfish (Neoceratodus forsteri) responds to intravenous injections of 0.63 ng/kg or more of arginine vasotocin with increased dorsal aortic blood pressure, inulin clearance, urine flow, and tubular rejection of Na+. Single injections of 1 ng/kg or more of angiotensin II or norepinephrine also increase dorsal aortic pressure but do not cause consistent diuresis and natriuresis, Continuous infusions of angiotensin II or repeated injections of norepinephrine produce sustained hypertension and more modest diuresis and natriuresis than are seen after injections of arginine vasotocin that cause less hypertension. Infusions of isosmolar or hyposmolar NaCl solutions increase blood pressure, inulin clearance, urine flow, and tubular Na+ rejection in a manner resembling the response to argininge vasotocoin injections. These data are consistent with the hypothesis that arginine vasotocin is released in response to volume expansion in lungfishes and that it may act on the kidney as a diuretic and natriuretic hormone. They do not rule out a more direct action of expansion on renal functions.     

Arbitration agreements and your malpractice coverage

With new legislation and favorable case law developments, many providers of health care services are turning to binding arbitration agreements as a partial solution to the medical malpractice crisis. Existing data indicate tremendous advantages can be gained from the use of such agreements, if they are carefully drawn to comply with new law, tailored to the particular situation in which they will be used and coupled with appropriate procedures to secure the intended benefits. Arbitration is not a substitute for insurance, but if a provider has taken the calculated risk of forgoing insurance he should not be without a carefully drawn binding arbitration agreement.     

Pig prothrombin: purification and properties

A procedure for the preparation of highly purified pig prothrombin is described. Compared to the initial clotting activity of the starting plasma, this protein was purified 776 times with a final yield of 8 per cent. The purified zymogen showed a specific activity of 1,460 NH units/mg of protein , a molecular weight of 65,000 as determined by SDS-polyacrylamide disc gel electroesis, E 1.0 mg/ml 1.0 cm, 280 nm = 1.45 at pH 7.0 and the following amino acid composition: Asx 51, Thr 38, Glx 62, Pro 23, Gly44, Ala 25, Half-Cys 30, Val 35, Met 3, Ile 30, Leu 32, Tyr 19, Phe 22, Lys 36, His 8, Arg 28, and Trp 13, which accounts for a minimum molecular weight of 59,370 (carbohydrates not computed). Alanine was found as the only N-terminal residue. Carboxypeptidases A and B failed to release any C-terminal residue. By hydrazinolysis however 0.4 mole of serine was released per mole of prothrombin. The activation of crude and chromatographed pig prothrombin was investigated.     

Mental capability of children exposed to lead pollution

'Eleven-plus' school examination scores were obtained for 851 Birmingham children residing since birth in a lead-polluted area and 1642 children residing in two similar but unpolluted areas. It was found that the children in the lead-polluted area actually scored higher on the average than children in the control areas. Within the area of lead contamination, children living closest to the source of pollution did not have significantly lower scores than children living further away. The results indicate that lead pollution of the magnitude reported in this investigation did not have a demonstrable effect on the mental capabilities of children in the affected community.     

Amplified migration inhibition effect

Upon exposure to specific antigen in tissue culture, sensitive lymphocytes released macrophage migration inhibition factor and other lymphokines into the supernatant culture medium. Migration of peritoneal macrophages from nonsensitive animals was inhibited in the presence of such supernatants. However, with previous techniques it was found that an inhibitory effect was present at only low low titers (less than 10(2)). It is therfore of great interest that by increasing cellular density, the total number of cells being kept constant, inhibitory activity can be amplified by a factor as great as 10(10). This amplification was observed only when lymphocytes and macrophages were loosely packed, as by spontaneous sedimentation in a conical test tube. The effect was abolished by dispersing the cell suspension in a flat-bottomed flask or, alternatively, by shaking the test tube so that intimate prolonged intercellular contact was prevented.     

Frequency of the carrier state for X-linked chronic granulomatous disease among females with lupus erythematosus

Carriers for chronic granulomatous disease (CGD) and patients with lupus erythematosus (LE) share several characteristics: They are mostly females, they reduce nitroblue tetrazolium (NBT) poorly in their neutrophils, and, in some cases, they have similar skin lesions. We thus investigated 19 female LE patients for the presence of laboratory findings characteristic of the carrier state for CGD. None of these patients turned out to have the combined abnormality of neutrophil bactericidal activity and neutrophil NBT-reduction that is diagnostic of CGD carrier state in the X-linked form. An increased frequency of CGD carriers among female LE patients thus appear to be unlikely. Why some CGD carriers develop skin lesions typical of LE remains unexplained.     

Zinc therapy in acrodermatitis enteropathica

Albino Holtzman, albino Wistar and hooded HS rats were injected fortnightly for 14 weeks with human glomerular basement membrane (GBM) emulsified in Freund's complete adjuvant. Half of the rats were pretreated with Freund's complete adjuvant and some were unilaterally nephrectomized. Anti-GBM antibody glomerulonephritis, characterized by proteinuria (greater than 100 mg/16 h) and a diffuse linear deposition of host immunoglobulin along the glomerular basement membrane, was first detected in Holtzman rats 4 weeks after treatment with GBM had begun, and had developed in 69% of these rats by 15 weeks. In contrast, none of the similarly treated Wistar or HS rats became proteinuric at any time, although a few showed weak glomerular fluorescence at the end of the experiment. Thus Holtzman rats are susceptible, and HS and Wistar rats are resistant to experimental anti-GBM antibody glomerulonephritis. Pretreatment with Freund's complete adjuvant apparently shortened the induction period of the experimental disease in the Holtzman rats whereas unilateral nephrectomy appeared to decrease their susceptibility to it.     

Fungal products. Part XVII. Microbiological hydroxylation of gibberellin A9 and its methyl ester

Angiotensin II (A II) and analogues were tested for their ability to restore electrical and mechanical activity to cardiac muscle preparations in which the fast Na+ channels had been inactivated by partial depolarization (22-27 mM K+) or by tetrodotoxin (TTX). The partially depolarized or TTX-blocked preparations were chosen because under these conditions electrical and mechanical responses are primarily Ca2+ -dependent. In depolarized rabbit right atria, A II restored spontaneous mechanical and electrical activity (measured by both intracellular and extracellular recording techniques). The frequency of action potential discharge was concentration-dependent; the threshold concentration of A II was 10(-10) M, the ED50 was 8 X 10(-9) M, and the maximum effect was observed at 5 X 10(-8) M. In contrast, depolarized guinea pig atria were insensitive to A II, Sar1-angiotensin II, and des-Asp1-angiotensin II, even at concentrations as high as 10(-5) M. Rabbit papillary muscle (TTX-blocked), embryonic (18-day) chick heart (partially depolarized) and chick heart reaggregates (TTX-blocked) responded similarly to rabbit atria in that A II (9.6 X 10(-7) M) restored both electrical and mechanical activity. We found that in these preparations the action of A II was unaffected by propranolol (5.0 X 10(-6) M to 5.0 X 10(-5) M) but was blocked by Mn2+ (10(-3) M), D-600 (1 X 10(-7) g/ml) and the specific A II antagonists Sar1-Ala8-angiotensin II (P-113) (5.0 X 10(-5) M) and Sar1-Ile8-angiotensin II (5.28 X 10(-5) M). We conclude that the positive inotropic effect of A II on the myocardium is due to its ability to increase transmembrane ion movements in or through the cell membrane. The ability of Mn2+ and D-600 to block this effect suggests that this ion movement is via the so-called "slow channels."