Vascular responses of the perfused intestine to vasoactive agents during the development of two-kidney, one-clip Goldblatt hypertension in dogs.

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Abstract
The potential role of altered vascular reactivity in the pathogenesis of 2-kidney, 1-clip Goldblatt hypertension (2-KGH) was studied in dogs, in the mesenteric vasculature preparation perfused, in situ, with autologous blood at constant flow. Changes in segmental vascular resistance in response to vasoactive agents were studied 1, 4 and 32 days after unilateral renal artery constriction (URAC) or sham occlusion of the renal artery (SHAM). On day 1 post-URAC, prior to any increase in arterial pressure or resistance, the pressor responses to serotonin (5-HT), angiotensin II (AII) and 9.alpha.,11.alpha.-epoxymethanoprostaglandin H2 (EMP) were enhanced from pre-URAC values. The major change occurred in small arteries, arterioles and veins, but not in larger arteries. Mesenteric vascular responses to 5-HT, AII and EMP were enhanced 4 and 32 days post-URAC. At this time, large artery vascular reactivity was enhanced. Mesenteric vascular responses to NE [norepinephrine] did not differ from pre-URAC values on day 1 post-URAC; 4 and 32 days post-URAC, mesenteric arterial and venous pressor responses to NE were enhanced. Intestinal smooth muscle responses to 5-HT, EMP and AII were enhanced within day 1 post-URAC. Changes in vascular reactivity precede the increased arterial resistance of 2-KGH in dogs and occur first in the smaller arteries, arterioles and venules and in non-vascular smooth muscle of the intestine. Within days 4-32 post-URAC, changes are apparent in the larger arteries. At this time decreases in compliance contribute to the increase in flow resistance of 2-KGH.