Physiological inactivation of vasoactive hormones in rainbow trout

Hormone titers are affected by interplay between secretion and inactivation processes. While secretion is a focal process, inactivation mechanisms 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 1/4 ) for recovery of dorsal and ventral aortic and central venous pressure, cardiac output, heart rate, and systemic and branchial vascular resistance following infusion or injection of hormones into conscious rainbow trout, Oncorhynchus mykiss. When possible, these were compared to recovery t 1/4 of isolated vessel rings in vitro. The t 1/4 for epinephrine or norepinephrine recovery in vivo was 3-4 min, approximately twice as long as recovery t 1/4 for isolated celiacomesenteric and epibranchial artery rings in vitro. Thus, the rate-limiting step in vascular relaxation is the concentration of circulating catecholamine concentrations, and not metabolic or mechanical events within the vascular wall. The in vivo recovery t 1/4 following angiotensin II (ANG II) infusion was 6-7 min, nearly twice that of catecholamines, but also greater than the t 1/4 following bolus ANG II injection, inhibition of angiotensin converting enzyme with captopril or injection of trout bradykinin. Arginine vasotocin (AVT) recovery t 1/4 in vivo, was considerably longer (20-30 min) than either catecholamine or ANG II t 1/4 and longer than AVT recovery t 1/4 of isolated vessels in vitro (5-6 min). The inactivation kinetics of catecholamines are consistent with circulatory convection-limited processes and do not appear to be limited by either tissue uptake or enzymatic degradation. This is probably the fastest type of 'on-off' endocline regulation in fish. Inactivation of ANG II and bradykinin are also convection limited, but ANG II metabolism may become saturated with high doses of exogenous ANG II. AVT inactivation is not convection limited and may compensate for a quantitatively lower capacity of the pituitary for peptide secretion, or less emphasis on AVT as an on/off effector of vascular resistance.