Effects of a calcium channel blocker on cardiac output distribution in conscious hypertensive dogs.

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Abstract
The effects of nitrendipine, 8 .mu.g/kg per min were evaluated in 6 conscious dogs through measurements of arterial pressure and blood flow in the ascending aorta (cardiac output), mesenteric, renal and iliac arteries before and after induction of chronic perinephritic hypertension. Before hypertension was induced, nitrendipine reduced mean arterial pressure 19 .+-. 2.3% (from 95 .+-. 3.2 mm Hg), decreased total peripheral resistance (60 .+-. 2.6%), and increased cardiac output (108 .+-. 10.5%). These values returned to baseline within 15-30 min. Nitrendipine caused the greatest increase in blood flow in the iliac bed (98 .+-. 9.9%), an intermediate increase in the mesenteric bed (37 .+-. 3.7%), and the least increase in the renal bed (7 .+-. 2.2%). Two to 6 wk after induction of hypertension, administration of nitrendipine elicited significant (P < 0.01) decreases in mean arterial pressure (32 .+-. 2.5% from 151 .+-. 4.8 mm Hg) and total peripheral resistance (67 .+-. 1.3%) compared with its administration in nonmotensive dogs, while the increase in cardiac output was not significantly changed (11 .+-. 10.9%). These changes in arterial pressure and vascular resistances also were prolonged (i.e., hemodynamics returned to baseline after 75-90 min). The increase in iliac (99 .+-. 16.8%) and renal (9 .+-. 6.1%) blood flows after nitrendipine administration in hypertensive dogs was similar to that found in the normotensive dogs, but mesenteric blood flow doubled (84 .+-. 8.4%). In conscious hypertensive dogs, nitrendipine administration appears to markedly decrease arterial pressure and total peripheral and regional resistances, which also require more time to return to baseline, but appears to increase blood flow by a greater amount only in the mesenteric bed.