Why the study?
Does active immunization against angiotensin I and II prevent renal clip hypertension in rats subjected to unilateral renal artery constriction?
Does active immunization against angiotensin I and II prevent renal clip hypertension in rats subjected to unilateral renal artery constriction?
Combined immunization against angiotensin I and II does not prevent renal clip hypertension in rats, suggesting circulating AI or AII do not have a direct pressor function in this model.
Answers are grounded in this paper and cite their sources.
Does not support targeting circulating angiotensin in renovascular hypertension; leaves open local RAS contributions in this rat model.
Rats, actively immunized against angiotensin I (AI) and angiotensin II (AII), were subjected to unilateral renal artery constriction to determine whether the resulting hypertension, which may still ensue in the animal immunized against AII, could be prevented by such combined immunity. Sustained immunity to both AI and AII neither changed preoperative blood pressures of the rats from those of control mock-immunized rats nor altered the incidence or severity of renal dip hypertension. Vascular hyperresponsiveness to small quantities of free angiotensin could not be invoked to explain the hypertension, for there was no significant difference between mock-immunized hypertensive animals, and those remaining normotensive, regarding pressor sensitivity to intravenous AI, AII, renin, and norepinephrine. (AI + AII)-immunized hypertensive rats required AI doses averaging 260 times greater than nonimmune hypertensives to elicit equipressor responses, and were refractory to renin, but not to norepinephrine. Thus, while previous studies have not excluded direct participation of endogenous AI in renal clip hypertension in rats, evidence from our experiments makes it extremely difficult to sustain any pressor function therein for circulating AI or AII. Our results also preclude involvement of AII produced from circulating AI by conversion within arteriolar walls, close to receptor sites, since AI immunity would block this mechanism of action.
No takes yet. Share an insight, caveat, or question.
Oates et al. (1974) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: