Cardiovascular responses of eggs, embryos and alevins of Atlantic salmon and rainbow trout to nitric oxide donors, sodium nitroprusside and isosorbide dinitrate, and inhibitors of nitric oxide synthase, N‐nitro‐l‐arginine methyl ester and aminoguanidine, following short‐ and long‐term exposure

Abstract

Atlantic salmon embryos and alevins Salmo salar that had been exposed to isosorbide dinitrate (ISDN) for 4 weeks, on transfer to fresh water, showed an increase in heart rate. Unexposed embryos and alevins showed a decrease in heart rate following transfer to 100 μmol l−1 ISDN for 4 h. This is in contrast to adult rainbow trout and higher vertebrates where tachycardia occurred in response to nitric oxide (NO) donors. The decreased heart rate in response to ISDN was inhibited by 2 mg 1−1 methylene blue, indicating that NO activates cardiovascular events via guanylyl cyclase and cyclic guanidine monophosphate. Heart rate of rainbow trout alevins Oncorhynchus mykiss exposed to 100 μmol l−1 aminoguanidine responded with a slowly developed but significant bradycardia over 10 min as did those reared in aminoguanidine for 4 weeks then transferred to fresh water. A potentiated increase in heart rate on exposure to the NO donor sodium nitroprusside (SNP), occurred within 1 min in salmon alevins reared in l‐nitro‐arginine methyl ester (l‐NAME) for 4 weeks, indicating up‐regulation of NO receptors. The evidence for down‐regulation of SNP‐reared alevins exposed to l‐NAME was less well defined. The results suggest that both salmonid embryos and alevins have a functional l‐arginine‐NO pathway and that NO has a physiological role in control of cardiovascular events.