Roles of endogenous angiotensin II or kinin in the mechanism of altered renal vascular responsiveness to angiotensin II following acute blood volume expansion in the dog.

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To examine the role of endogenous angiotensin II or kinins in the mechanism of the increased renal vascular reactivity to exogenous angiotensin II following acute blood volume expansion, we examined whether captopril, a converting enzyme inhibitor, can prevent the increase in renal vascular response in anesthetized dogs. Pretreatment of dogs with captopril increased plasma renin activity, but it did not affect systemic blood pressure, renal blood flow and renal vascular resistance. Acute blood volume expansion with saline suppressed plasma renin activity in dogs with or without pretreatment with captopril. Basal level of renal vascular reactivity to angiotensin II was increased by pretreatment with captopril. In the control animals, acute blood volume expansion enhanced renal vascular reactivity to angiotensin II but not norepinephrine. The enhanced renal vascular reactivity to angiotensin II, however, was not prevented by the captopril treatment. The failure of captopril to prevent an increase in renal vascular reactivity to angiotensin II following acute blood volume expansion was associated with an increase in urinary excretion of bradykinin. These data suggest that endogenous angiotensin II level is not necessarily a determinant for vascular reactivity to exogenous angiotensin II, especially in the case of acute blood volume expansion.
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