The role of angiotensin II in regulating catecholamine secretion during hypoxia in rainbow troutOncorhynchus mykiss

Abstract

SUMMARYExperiments were performed in vivo on chronically cannulated adult rainbow trout (Oncorhynchus mykiss) to assess the involvement of serotonergic or muscarinic receptor stimulation or activation of the renin–angiotensin system in eliciting catecholamine release during acute hypoxia during periods of nicotinic receptor desensitisation.Despite nicotinic receptor desensitisation induced by intravenous infusion of nicotine (1.3×10–5 mol kg–1 h–1), plasma catecholamine levels were increased to levels (adrenaline plus noradrenaline 125–200 nmol l–1) similar to those in control fish during severe hypoxia (40–45 mmHg; 5.3–6.0 kPa). Blockade of serotonergic receptors using methysergide or of muscarinic receptors using atropine did not affect the ability of fish to elevate circulating catecholamine levels during hypoxia. However, selective blockade of the renin–angiotensin system, using lisinopril to inhibit angiotensin-converting enzyme, prevented the elevation of both angiotensin II and circulating catecholamine levels in acutely hypoxic fish experiencing nicotinic receptor desensitisation. In fish possessing functional nicotinic receptors, angiotensin-converting enzyme blockade attenuated but did not prevent the elevation of plasma catecholamine levels during hypoxia. The results of this study indicate that the renin–angiotensin system is activated during hypoxia and plays a role in eliciting catecholamine release that is secondary to activation of nicotinic receptors. However, under conditions of nicotinic receptor desensitisation, activation of the renin–angiotensin system during hypoxia is a prerequisite for catecholamine release.