Key result
In rabbits, plasma angiotensin I converting enzyme activity remained unchanged during experimental renal hypertension and was independent of sodium intake or depletion.
Why the study?
Does experimental renal hypertension or altered sodium balance affect plasma angiotensin I converting enzyme activity in rabbits?
Does experimental renal hypertension or altered sodium balance affect plasma angiotensin I converting enzyme activity in rabbits?
Answers are grounded in this paper and cite their sources.
Plasma ACE stability in rabbit renal hypertension independent of sodium; leaves open relevance to human pathophysiology.
Plasma angiotension I converting enzyme activity (PCEA), plasma renin activity (PRA) and plasma renin substrate (PRS) were measured in rabbits with experimental renal hypertension and under various sodium intakes. Hypertension was produced by constriction of one renal artery, with or without contralateral nephrectomy. PCEA remained unchanged up to 6 to 7 weeks after clipping. High PRA and hematocrit were observed in rabbits with a clipped renal artery and an intact contralateral kidney, but not in those with a clipped renal artery and contralateral kidney removed. PCEA was independent of the sodium intake or depletion. From these results, it seems that there is no significant role of PCEA in the pathogenesis of experimental renal hypertension in rabbits, and PCEA does not appear to be affected by the same stimuli which are known for the control of PRA.
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Kurihara et al. (1973) studied Experimental renal hypertension (n=50). Experimental renal hypertension (renal artery clipping) and varying sodium intake vs. Sham operation or normal sodium intake was evaluated on Plasma angiotensin I converting enzyme activity (PCEA). In rabbits, plasma angiotensin I converting enzyme activity remained unchanged during experimental renal hypertension and was independent of sodium intake or depletion.
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