Cardiovascular responses in vivo to angiotensin II and the peptide antagonist saralasin in rainbow trout Oncorhynchus mykiss

Department of Biological Sciences, University of Dundee, Dundee DD1 4HN, Scotland, UK.
Journal of Experimental Biology (Impact Factor: 2.9). 02/1998; 201(Pt 2):267-72.
Source: PubMed


The effects of [Asn1,Val5]-angiotensin II (AngII) and [Sar1,Val5, Ala8]-angiotensin II (saralasin) on dorsal aortic blood pressure, pulse pressure and heart rate were examined in rainbow trout in vivo. AngII when administered as a single dose of 25 microg kg-1 induced a biphasic response in blood pressure, with a significant hypertensive response during the initial 10 min, followed by a significant hypotension of 70-75 % compared with the initial blood pressure after 50 min and continuing until approximately 80 min post-injection. The co-administration of AngII (25 microg kg-1) and saralasin (50 microg kg-1) resulted in the same hypertensive response during the initial phase, but abolished the hypotensive effect of AngII. Heart rate was significantly increased in response to AngII, but the administration of AngII and saralasin together attenuated the increase by approximately 44 %. Stimulation of the endogenous renin-angiotensin system using a vasodilator, sodium nitroprusside, significantly increased drinking rate in rainbow trout fry, a response inhibited by saralasin, indicating a role for AngII-induced hypotension in drinking. For the first time, a decrease in blood pressure in response to AngII in vivo has been demonstrated in fish, and this is discussed in relation to homeostasis of blood pressure and a possible role in the control of drinking.

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    • "The physiological significance of an interaction between Ang II and catecholamine release stems from the importance of the renin–angiotensin system and the adrenergic system in the homeostatic regulation of blood pressure in teleosts (Olson, 1992; Nilsson, 1994; Bernier and Perry, 1999). In O. mykiss and A. rostrata both Ang II and catecholamines are potent vasopressors (Nishimura et al., 1978; Gamperl et al., 1994; Oudit and Butler, 1995a,b; Fuentes and Eddy, 1998; Bernier and Perry, 1999) and thereby key effectors of cardiovascular control. During hypotensive stress in trout, the renin–angiotensin system and humoral catecholamines are both recruited and play significant roles in the compensatory response to hypotension (Bernier et al., 1999b). "
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    ABSTRACT: The stimulatory effects of angiotensin II (Ang II) on catecholamine release and the contributions of the renin-angiotensin system, humoral catecholamines and adrenergic nerves to blood pressure regulation were investigated in rainbow trout (Oncorhynchus mykiss) and American eel (Anguilla rostrata). In trout, bolus injections of homologous [Asn1,Val5]-Ang II (100 or 500 pmol kg-1) increased catecholamine secretion rates and plasma catecholamine concentrations from in situ posterior cardinal vein preparations and chronically cannulated fish, respectively. In contrast, in situ or in vivo injections of similar doses of Ang II in eel did not affect catecholamine release. &agr; -Adrenoceptor blockade (prazosin; 1 mg kg-1) reduced the pressor effect of exogenous Ang II (500 pmol kg-1) in both species. In eel, intravenous injection of the smooth muscle relaxant papaverine (10 mg kg-1) elicited a rapid decrease in dorsal aortic pressure (PDA; 58 %) followed by a gradual recovery back to the baseline value 85 min after the treatment. In trout, papaverine elicited a similar decrease in blood pressure (62 %); however, PDA recovered fully 20 min after treatment. Blockade of either &agr; -adrenoceptors with prazosin or adrenergic nerves with bretylium (10 mg kg-1) prior to papaverine treatment did not alter PDA recovery in eel. In trout, &agr; -adrenoceptor and adrenergic nerve blockade prior to the papaverine treatment prevented and attenuated PDA recovery, respectively. In both species, papaverine treatment elicited significant increases in plasma catecholamine and Ang II concentrations. However, the increases in plasma catecholamine concentrations were markedly greater in trout than in eel. Similarly, the papaverine-elicited increase in plasma Ang II levels occurred earlier and was greater in trout than in eel. Thus, while Ang II stimulates humoral catecholamine release in trout, there is no evidence for a similar interaction in eel. Moreover, during hypotensive stress, although the renin-angiotensin system is recruited in both species, an essential involvement of adrenergic nerves and humoral catecholamines in the restoration of blood pressure is only apparent in trout.
    Journal of Experimental Biology 06/1999; 202 (Pt 12)(12):1677-90. · 2.90 Impact Factor
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    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 alpha-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 (Q) and stroke volume (Vs). In fish first treated with the alpha -adrenoceptor blocker phenoxybenzamine, Ang II injections elicited a decrease in q_dot 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 (1.8x10(-10) to 1.4x10(-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 nmol l-1. Adrenaline injections also elicited increases in Q 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 Q 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.
    Journal of Experimental Biology 02/1999; 202(Pt 1):55-66. · 2.90 Impact Factor
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