Effects of sodium nitroprusside on blood circulation and acid–base and ionic balance in rainbow trout: indications for nitric oxide induced vasodilation

Abstract

The effects of the nitric oxide (NO) releasing antihypertensive agent sodium nitroprusside (SNP) on rainbow trout (Oncorhynchus mykiss) were investigated using either waterborne exposures of up to 1.3 mM SNP over 60 and 90 min or injections via the dorsal aorta, and cardiovascular responses were compared. Doses of up to 40 μg∙kg−1into the blood stream resulted within 5 min in significantly reduced blood pressure and pulse pressure with tachycardia. Waterborne SNP below 0.53 mM had no effect, but concentrations above this level (to 1.3 mM) after 30–60 min produced significant tachycardia and vasodilation, resulting in dose- and time-dependent reductions in dorsal aorta pulse pressure, with maximum decreases of 50–57%. At and above 0.4 mM SNP waterborne exposure, blood [Formula: see text] was significantly increased, plasma Na+, K+, and Cl−values were unchanged, and there was a mild alkalosis. The cardiovascular effects of waterborne isosorbide dinitrate at 40 μM were similar to those of SNP. Exposure of fish to waterborne potassium ferricyanide (0.67 mM), which is structurally similar to SNP but does not release NO, produced only minor cardiovascular effects compared with those of SNP. Pretreatment of fish with propranolol (1.9 mg∙kg−1via the dorsal aorta) followed by exposure to 1 mM waterborne SNP showed that adrenergic responses were unlikely to be involved in the vasodilation. The results of pretreatment with methylene blue (1.5 mg∙kg−1via the dorsal aorta) followed by 1 mM waterborne SNP suggested that the vasodilation was induced by NO activation of soluble guanylyl cyclase. This study demonstrates that NO-releasing compounds cause vasodilation in rainbow trout in vivo and provides a novel way of studying the effects of altered vascular resistance in fish.