The estimation of plasma renin concentration in the dog.
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Biomedical subjects
Publications and source records attributed to M Tree.
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Hypertension may result from chronic lead exposure. Lead poisoning arising from "moonshine whiskey" drinking has been associated with a rise in plasma renin activity. In the present study, plasma renin concentration following intravenous administration of frusemide was measured in eleven subjects with moderate or severe lead poisoning of industrial origin. The results were compared with those obtained for seven normal, control subjects. There was no significant difference in response obtained in the two groups. Industrial lead poisoning does not appear to affect renin release. The combined insult of lead and alcohol may explain the findings in the previous study.
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Chemical modification of the backbone at the cleavage site in the (6-13)-octapeptide of equine angiotensinogen resulted in greatly increased binding affinity and resistance to cleavage by renin. The D-His6-Tyr13 octapeptide analog containing the reduced bond -CH2-NH-instead of a peptide bond -CO-NH- at the Leu10-Leu11 linkage (H-77) was a powerful in vitro inhibitor of canine renin (IC50 = 24nM). It gave an IC50 of 1 microM against human renin and 0.6 microM against rat renin. In sodium-depleted conscious dogs, infusion of H-77 caused dose-related falls of plasma angiotensin I plasma angiotensin II concentration and mean arterial pressure; the minimum effective dose was 0.1 mg . kg-1 hr-1. Similar infusions of H-77 in chronically catheterized rats have no effect on blood pressure or plasma angiotensin II concentration. Thus, the in vitro effect of H-77 as an inhibitor of renin in dog, human, and rat plasma was paralleled by its action in the whole animal.