Nitric oxide and the control of catecholamine secretion in rainbow trout (Oncorhynchus mykiss)

Abstract

The aim of this thesis was to investigate the effects of nitric oxide (NO) on both basal and stimulus-evoked catecholamine secretion in rainbow trout (Oncorhynchus mykiss). Experiments were performed in vivo and in situ using an electrical field stimulation technique. Catecholamine secretion rates in situ were markedly reduced in response to electrical stimulation in the presence of the NO donor sodium nitroprusside (SNP; 5 X 10-3 M). This reduction was through the activation of soluble guanylyl cyclase (sGC) rather than via an acceleration of catecholamine degradation. Pre-treatment with the NO inhibitors 7-nitroindazole (10-4 M) and L-NAME (5 X 10-3 M) decreased NO production in response to electrical stimulation while increasing catecholamine secretion rates approximately 2-fold. Experimental evidence suggests that nNOS is the main isoform involved in the inhibition of catecholamine secretion. Following the repeated exposure of rainbow trout to hypoxia over 4 days in vivo, in situ preparations derived from these fish showed an approximately 2- and 1.8-fold increase in basal and stimulated NO levels, respectively, while catecholamine secretion rates were reduced by approximately 50%. Expression levels for the nNOS isoform in the head kidney and anterior posterior cardinal vein (PCV) suggests that this isoform is involved in the catecholamine response. In summary, nNOS appears to be the main isoform in producing NO under neuronal stimulation and that this NO decreases stimulus-evoked catecholamine secretion through the activation of sGC.