ABSTRACT
To determine the contribution of plasma catecholamines to the cardiovascular effects of elevated levels of angiotensin II (Ang II) in trout, this study investigated (1) the stimulatory effects of [Asn1-Val5]-Ang II on plasma catecholamine levels, (2) the cardiovascular effects of Ang II with and without α-adrenoceptor blockade and (3) the relationship between plasma adrenaline concentrations and their cardiovascular effects. Bolus intravascular injections of Ang II (25–1200 pmol kg−1) elicited dose-dependent (between 75 and 1200 pmol kg−1) increases in plasma adrenaline levels; mean plasma noradrenaline levels only increased in response to a dose of 1200 pmol kg−1. Ang-II-elicited increases in plasma adrenaline levels ranged from 3.3±0.3 nmol l−1 for 75 pmol kg−1 Ang II to 125.1±40.0 nmol l−1 for 1200 pmol kg−1 Ang II. Injections of Ang II (25–1200 pmol kg−1) also elicited dose-dependent increases in dorsal aortic pressure (PDA), systemic resistance (RS), cardiac output (Q̇) and stroke volume (VS). In fish first treated with the α-adrenoceptor blocker phenoxybenzamine, Ang II injections elicited a decrease in Q̇ and VS, and the increases in PDA and RS following administration of the 600 and 1200 pmol kg−1 Ang II doses were significantly reduced. Bolus injections of adrenaline (1.8×10−10 to 1.4×10−8 mol kg−1) elicited dose-dependent increases in PDA at a plasma adrenaline concentration of 16.5 nmol l−1 and in RS at a plasma adrenaline concentration of 50.5 nmmol l−1. Adrenaline injections also elicited increases in Q̇ and VS at plasma adrenaline concentrations of 50.5 nmol l−1; however, higher plasma adrenaline concentrations were not associated with further increases in either Q̇ or VS. These results demonstrate that, in vivo, Ang II can act as a potent non-cholinergic secretagogue of humoral adrenaline in trout and that some of the cardiovascular effects of exogenous Ang II can be attributed to increased levels of plasma adrenaline. Our data also indicate that the cardiovascular effects of Ang-II-mediated humoral catecholamines are recruited in a dose-dependent manner and, as such, may require an acute stimulation of the renin–angiotensin system to contribute significantly to the pressor activity of endogenous angiotensins.
