ANGIOTENSINS STIMULATE CATECHOLAMINE RELEASE FROM THE CHROMAFFIN TISSUE OF THE RAINBOW-TROUT

Immunohistochemical and pharmacological techniques were utilized to in vestigate the relationships between angiotensins and catecholamine rel ease from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss) . Double labeling with [Asp(1),Ile(5)]angiotensin II-fluorescein isoth iocyanate (ANG II-FITC) and anti-dopamine P-hydroxylase revealed speci fic ANG II binding sites on chromaffin cells. Injection (1 nmol/kg bod y wt) of either ANG II-FITC, [Asn(1),Val(5),Asn(9)]ANG I, [Asp(1),Ile( 5),His(9)]ANG I, [Asn(1),Val(5)]ANG II, [Asp(1),Val(5)]ANG II, or [Asp (1),Ile(5)]ANG II elicited catecholamine release from in situ perfusio n preparations of the head kidney. Catecholamine release elicited by [ Asn(1),Val(5)]ANG II (10(-13) to 10(-7) mol/kg body wt) was dose depen dent, and the secretion of epinephrine (Epi) was greater than that of norepinephrine (NE). Relative to the results obtained with the [Asn(1) ,Val(5)]ANG II treatment (1 nmol/kg body wt), Epi release was 72 and 8 2% lower in response to injections (1 nmol/kg body wt) of [Asn(1),Val( 5)]ANG I [amino acid (AA) positions 1-7] and [Asn(1),Val(5)]ANG I(AA 1 -6), respectively. Pretreatment with either losartan (10(-5) M), PD-12 3319 (10(-5) M), or hexamethonium (10(-3) M) had no effect on [Asn(1), Val(5)]ANG II-elicited catecholamine release. Pretreatment with captop ril(10(-4) M) significantly reduced [Asn(1),Val(5),Asn(9)]ANG I-elicit ed Epi and NE release and decreased basal catecholamine release. These results provide direct evidence that angiotensins can elicit catechol amine release from the chromaffin tissue via specific ANG II binding s ites and indicate that the synthesis of ANG II may be either local or systemic.