Role of Nitric Oxide in the Renin and Heart Rate Responses to β-Adrenergic Stimulation

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Abstract

Studies in vitro and in vivo have implicated nitric oxide in the control of renin secretion. In the present study, the effect of inhibition of nitric oxide synthesis with NG-nitro- L-arginine methyl ester hydrochloride (L-NAME) on the renin secretory response to β-adrenergic stimulation was investigated in conscious, chronically prepared rabbits. Intravenous infusion of isoproterenol at 0.02 μg · kg−1 · min−1 for 30 minutes increased mean arterial pressure by 5 mm Hg (P<.05), heart rate by 51 beats per minute (P<.001), and plasma renin activity by 56% (P<.001). Intravenous infusion of L-NAME at 0.5 mg · kg−1 · min−1 increased mean arterial pressure by 6 mm Hg (P<.01) and decreased heart rate by 15 beats per minute (P<.01) and plasma renin activity by 31% (P<.05). L-NAME reduced the heart rate response to isoproterenol by 50% and inhibited the renin response. Infusion of isoproterenol at 0.05 μg · kg−1 · min−1 did not change blood pressure but increased heart rate by 62 beats per minute (P<.001) and plasma renin activity by 283% (P<.001). Treatment with L-NAME again suppressed the heart rate response to isoproterenol and inhibited the renin response. Intravenous infusion of the nitric oxide donor nitroprusside at 2 μg · kg−1 · min−1 in the presence of L-NAME decreased mean arterial pressure by 7 mm Hg (P<.05), increased heart rate by 14 beats per minute (P<.05), but did not change plasma renin activity. Nitroprusside fully restored the heart rate response to isoproterenol and partially restored the renin response. These results provide evidence that nitric oxide plays an important role in the renin and heart rate responses to β-adrenergic stimulation.

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