RENAL VASCULAR-RESPONSES TO ANGIOTENSIN-II IN CONSCIOUS SPONTANEOUSLYHYPERTENSIVE AND NORMOTENSIVE RATS

It has been postulated that exaggerated renal sensitivity to angiotens in II may be involved in the development and maintenance of hypertensi on in the spontaneously hypertensive rat (SHR). The purpose of this st udy was to compare the renal vascular responses to short-term angioten sin II infusions (50 ng/kg/min, i.v.) in conscious SHRs and Wistar-Kyo to (WKY) rats. Renal cortical blood flow was measured in conscious rat s by using quantitative renal perfusion imaging by magnetic resonance, and blood pressure was measured by an indwelling carotid catheter att ached to a digital blood pressure analyzer. Renal vascular responses t o angiotensin II were similar in control SHRs and WKY rats. Pretreatme nt with captopril to block endogenous production of angiotensin II sig nificantly augmented the renal vascular response to exogenous angioten sin II in the SHRs but not in the WKY rats. The renal vascular respons es to angiotensin II were significantly greater in captopril-pretreate d SHRs than in WKY mts (cortical blood flow decreased by 1.66 +/- 0.13 ml/min/g cortex in WKY rats compared with 2.15 +/- 0.14 ml/min/g cort ex in SHR; cortical vascular resistance increased by 10.5 +/- 1.4 mm H g/ml/min/g cortex in WKY rats compared with 15.6 +/- 1.7 mm Hg/ml/min/ g cortex in SHRs). Responses to angiotensin II were completely blocked in both strains by pretreatment with the angiotensin II AT(1)-recepto r antagonist losartan. Results from this study in conscious rats confi rm previous findings in anesthetized rats that (a) the short-term pres ser and renal vascular responses to angiotensin IT are mediated by the ATI receptor in both SHRs and WKY rats, and (b) the renal vascular re sponses to angiotensin II are enhanced in SHRs compared with WKY rats when endogenous production of angiotensin II is inhibited by captopril pretreatment.