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 beta-adrenergic stimulation was investigated in conscious, chronically prepared rabbits. Intravenous infusion of isoproterenol at 0.02 microgram.kg-1 x 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 x 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 microgram.kg-1 x 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 micrograms.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.(ABSTRACT TRUNCATED AT 250 WORDS)