LOCALIZATION OF ANGIOTENSIN-II RESPONSES IN THE TROUT CARDIOVASCULAR-SYSTEM

The renin/angiotensin system (RAS) is a tonic anti-drop regulator of a rterial blood pressure in many teleosts. In trout, angiotensin II (ANG II) has no direct constrictor effect on large arteries or veins and t he identity of specific cardiovascular presser effecters is unknown. P otential targets of angiotensin activation were examined in the presen t experiments using perfused organs and isolated tissues from the rain bow trout Oncorhynchus mykiss. Perfused gill (arches 2 and 3), perfuse d skeletal muscle-kidney (via the dorsal aorta; PDA) and perfused spla nchnic (via the celiacomesenteric; PCM) circulations vasoconstrict in response to salmonid ANG II in a dose-dependent manner. ANG II was sig nificantly (P less than or equal to 0.05) more potent in the PCM than in the PDA, and both preparations were more responsive than the gills: pD(2)=8.0+/-0.20 (10) for PCM; pD(2)=7.5+/-0.07 (13) for PDA; pD(2)=6 .9+/-0.21 (8) for gill arch 3; pD(2)=6.7+/-0.23 (8) for gill arch 2; m ean +/- S.E.M. (N), respectively. Salmonid angiotensin I (ANG I) also produced a dose-dependent constriction of the PDA and PCM. Angiotensin converting enzyme (ACE) activated nearly 100% of ANG I to ANG II in a single pass through the PDA, whereas PCM conversion was estimated to be less than 10%. Inhibitors of adrenergic constriction partially prev ented ANG II responses in the PDA but did not affect PCM responses. AN G II did not affect paced rings of ventricular muscle in the presence of high or low [Ca2+] or epinephrine concentrations, nor did it have a ny inotropic or chronotropic effects in the in situ perfused heart. Re d blood cell swelling was unaffected by ANG II. Similarly, the effects of ANG II on gut, urinary bladder and gall bladder smooth muscle were negligible or non-existent; thus, an increase in splanchnic resistanc e due to extravascular compression can be discounted.