Resistance to blockade by saralasin of effect of ACE inhibitors in conscious sodium-restricted dog

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Abstract
Comparison of the effect of captopril and enalaprilal was made on mean systemic arterial blood pressure (BP), renal blood flow (RBF), and renal vascular resistance (RVR) of conscious sodium-replete and sodium-restricted dogs (plasma renin activity = 6.66 ng angiotensin l .cntdot. ml-1 .cntdot. h-1). BP was decreased by -8 .+-. 2 mmHg and RBF was increased by 34 .+-. 12 ml/min with captopril given intravenously and by -5 .+-. 2 mmHg and 28 .+-. 7 ml/min with enalaprilal in sodium-replete dogs. The respective changes in BP and RBF in sodium-restricted dogs were -29 .+-. 2 mmHg and 62 .+-. 12 ml/min with captopril and -25 .+-. 6 mmHg and 53 .+-. 18 ml/min with enalaprilat. Saralasin infused intra-arterially to the kidney significantly blocked the increase in RBF seen after angiotensin-coverting enzyme (ACE) inhibition in sodium-replete dogs, and reduced the increase in RBF in sodium-restricted dogs, but the latter effect was not statistically significant. A more moderate increase in plasma renin activity was established in another group of sodium-restricted dogs, and saralasin was administered intravenously instead of intra-arterially. Enalaprilal increased RBF in these dogs in the presence of a saralasin blockade (42 .+-. 7 ml/min), and this effect was not significantly changed by prior administration of indomethacin (28 .+-. 6 ml/min). The results suggest that blockade of the influence of the renin-angiotensin system and possibly another vasodilator mechanism, such as kinin potentiation, account for the increase in RBF after ACE inhibition in the low-sodium state.