The effects of nitrendipine infusions were evaluated in conscious dogs on measurements of arterial pressure and blood flow in the ascending aorta (cardiac output), left circumflex coronary, and mesenteric, renal, and iliac arteries. Nitrendipine (8 μg/kg/min) reduced mean arterial pressure by 17 ±1.4% from 95 ± 2.2 mm Hg, while increasing cardiac output (85 ± 4.6%), mean coronary blood flow (116 ± 8.1%), mesenteric blood flow (40 ± 4.8%), renal blood flow (4 ± 1.3%), and iliac blood flow (89 ± 13%). The percent increase in mean coronary blood flow was greater (p < 0.01) than that of cardiac output. and the percent increases in mesenteric and renal blood flows were less (p < 0.01) than that of cardiac output. After propranolol (1 mg/kg) and atropine (0.1 mg/kg), nitrendipine still increased coronary blood flow (73 ± 4.7%) significantly more (p < 0.01) than cardiac output (39 ± 11%), while the percent increases in mesenteric and renal blood flows were less (p < 0.01) than cardiac output. Nitrendipine also increased coronary blood flow (98 ± 16%) more (p < 0.01) than cardiac output (44 ± 7.1%) after α2-adrenergic receptor bockade with rauwolscine while in the presence of β-adrenergic and cholinergic blockades. However, after adding α1-adrencrgic receptor blockade with prazosin (1 mg/kg) to the β-adrenergic and cholinergic receptor blockades, nitrendipine no longer increased coronary blood flow (39 ± 3.5%) more than cardiac output (34 ± 3.3%), while still increasing mesenteric and renal blood flow less (p < 0.01) than cardiac output. Thus, in conscious dogs, nitrendipine redistributes cardiac output preferentially to the coronary bed. Since this preferential effect is abolished by prazosin, but not rauwolscine, in the presence of propranolol and atropine, an α1-adrenergic mechanism is implicated.
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