Aglomerular toadfish, Opsanus tau, release renin in response to hemorrhage or vasodilator drugs, presumably by stimulating a renal arterial baroreceptor. We aimed to determine whether the adrenergic nervous system and prostaglandins play a role in the control of renin release in unanesthetized toadfish kept in 50% seawater. Isoproterenol (1 microgram/kg) increased plasma renin activity (PRA) fourfold and decreased blood pressure (BP); both effects were abolished by a concomitant infusion of propranolol. Propranolol itself slightly decreased the basal level of heart rate and BP, but not that of PRA. Norepinephrine (1 microgram/kg) increased BP, but did not change PRA. Repeated injection of 6-hydroxydopamine did not alter resting levels of either PRA or BP. Monoamine-specific nerve fluorescence activity could not be demonstrated in association with arterioles of kidneys from intact toadfish or from those treated with monoamine oxidase inhibitor and norepinephrine (5 mg/kg). Furthermore, treatment of toadfish with indomethacin (10 or 20 mg/kg) prevented neither the increase in PRA nor the reduction in BP after a massive hemorrhage. These results indicate that renin release in toadfish primarily occurs in response to a reduction in renal arterial pressure, whereas it appears unlikely that the adrenergic nervous system or prostaglandins have a significant role in the control of renin release.