PHYSIOLOGICAL INACTIVATION OF VASOACTIVE HORMONES IN RAINBOW-TROUT

Hormone titers are affected by interplay between secretion and inactiv ation processes. While secretion is a focal process, inactivation mech anisms are often complex and poorly understood. In the present study, inactivation of cardiovascular regulatory hormones was examined from a physiological perspective by analyzing the half-time (t(1/2)) for rec overy of dorsal and ventral aortic and central venous pressure, cardia c output, heart rate, and systemic and branchial vascular resistance f ollowing infusion or injection of hormones into conscious rainbow trou t, Oncorhynchus mykiss. When possible, these were compared to recovery t(1/2), of isolated vessel rings in vitro. The t(1/2) for epinephrine or norepinephrine recovery in vivo was 3-4 min, approximately twice a s long as recovery t(1/2) for isolated celiacomesenteric and epibranch ial artery rings in vitro. Thus, the rate-limiting step in vascular re laxation is the concentration of circulating catecholamine concentrati ons, and not metabolic or mechanical events within the vascular wall. The in vivo recovery t(1/2) following angiotensin II (ANG II) infusion was 6-7 min, nearly twice that of catecholamines, but also greater th an the t(1/2) following bolus ANG II injection, inhibition of angioten sin converting enzyme with captopril or injection of trout bradykinin. Arginine vasotocin (AVT) recovery t(1/2) in vivo, was considerably lo nger (20-30 min) than either catecholamine or ANG II t(1/2) and longer than AVT recovery t(1/2) of isolated vessels in vitro (5-6 min). The inactivation kinetics of catecholamines are consistent with circulator y convection-limited processes and do not appear to be limited by eith er tissue uptake or enzymatic degradation. This is probably the fastes t type of 'on-off' endocrine regulation in fish. Inactivation of ANG I I and bradykinin are also convection limited, but ANG II metabolism ma y become saturated with high doses of exogenous ANG II. AVT inactivati on is not convection limited and may compensate for a quantitatively l ower capacity of the pituitary for peptide secretion, or less emphasis on AVT as an on/off effector of vascular resistance. (C) 1997 Wiley-L iss, Inc.