Studies on Experimental Hypertension Using Blockers of Renin, Converting Enzyme, and Angiotensin II
Since the time of Tigerstedt and Bergman it has been known that nephrectomized animals respond to renin with a greater blood pressure rise that is longer lasting than in normal animals. Also, many investigators have observed that the plasma from nephrectomized animals generated angiotensin faster than that from normal animals and have speculated that this is due either to changes in renin substrate or to other unknown factors in the plasma. In our attempts to study this phenomenon, a search for the possibility of an inhibitory substance to renin was initiated. This led to the isolation of a phospholipid substance from the kidney, which proved to be an inhibitor of renin (1). The phospholipid as isolated from the kidney was found to give very little inhibition during the first hour of a 4-h incubation period, and when the lipid was reisolated from the assay mixture after incubation, a new phospholipid was obtained (2). Treatment of the lipid isolated from the kidney with phospholipase A from snake venom, which cleaved saturated fatty acids from the molecule, yielded a lipophospholipid that was shown to have the renin-inhibitory action. This lysophospholipid formed by incubation with phospholipase A or with plasma itself was shown to inhibit renin but to have no effect on the response to angiotensin itself.
KeywordsAngiotensin Renin Ethanolamine
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