This preclinical study demonstrates that the canine kidney can convert angiotensin I to active angiotensin II, a process that is modulated by salt and DOCA administration.
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Should not change clinical practice; leaves open whether renal angiotensin conversion is similarly modulated in humans.
Experiments were carried out on perfused canine kidneys in situ to determine if renal conversion of angiotensin I occurs. Various concentrations of decapeptide produced an immediate increase in renal vascular resistance when injected directly into the renal artery. Since the decapeptide is biologically inactive, the increased resistance was interpreted as indicating generation of angiotensin II. The extent of renal conversion of angiotensin I to angiotensin II was estimated to be approximately 19% in the normal dog. This percent conversion was reduced to about 10% in dogs maintained on high salt and DOCA for 7 to 10 days.
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FRANKLIN et al. (1970) studied this question.
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