ANGIOTENSIN-I- AND ANGIOTENSIN-III-MEDIATED CARDIOVASCULAR-RESPONSES IN THE FRESH-WATER NORTH-AMERICAN EEL, ANGUILLA-ROSTRATA - EFFECT OF PHE(8) DELETION

Cardiovascular responses to synthetic eel [Asn(1), Va1(5), Gly(9)]-ANG-I, ANG-III (2-8), and ANG-I (1-7) were measured in conscious and resting freshwater North American eels. Indwelling Doppler flow probes were placed on the ventral and dorsal aortas, a pressure catheter in the lienomesenteric artery, and a peptide delivery catheter in the caudal vein. Twenty-five and 150 ng.kg(-1) ANG-III increased baseline cardiac output (CO) (15.23 +/- 0.31 ml.min(-1).kg(-1); n = 5) by 23 and 47%, respectively, by increasing stroke volume (SV) but not heart rate (HR). ANG-I(ISO ng.kg(-1)) also elevated CO (62%) by increasing both SV (44%) and HR (14%). Estimated branchial shunting (BS) was increased by 150 ng.kg(-1) ANG-I and -III suggesting that more blood perfused the arteriovenous pathway in the gills. Dorsal aortic blood pressure (P-DA) (3.08 +/- 0.12 kPa) was elevated by 150 ng.kg(-1) ANG-I (67%) and -III (52%). Presser responses temporally preceded the blood flow increases and there was a significant increase in systemic vascular resistance (R(SYS)) at the peak presser responses. At the peak flow responses, increased CO was solely responsible for the increase in P-DA; R(SYS) had returned to baseline values. Presser responses to ANG-III decayed more rapidly (18.6 min) compared with those of ANG-I and -II (36 min). ANG-I (1-7) had no measurable effect on cardiovascular function indicating that the carboxylterminal 8-phenylalanine is an absolute requirement for the hormonal activity of angiotensin in fishes. (C) 1995 Academic Press. Inc.