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: 3). 02/1998; 201(Pt 2):267-72.
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ABSTRACT 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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    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.
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    04/2007, Degree: PhD
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