THE EFFECTS OF ARGININE VASOTOCIN AND CATECHOLAMINES ON NITROGEN-EXCRETION AND THE CARDIORESPIRATORY PHYSIOLOGY OF THE GULF TOADFISH, OPSANUS-BETA

Citation
Sf. Perry et al., THE EFFECTS OF ARGININE VASOTOCIN AND CATECHOLAMINES ON NITROGEN-EXCRETION AND THE CARDIORESPIRATORY PHYSIOLOGY OF THE GULF TOADFISH, OPSANUS-BETA, Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology, 168(6), 1998, pp. 461-472
Citations number
59
Categorie Soggetti
Zoology,Physiology
ISSN journal
01741578
Volume
168
Issue
6
Year of publication
1998
Pages
461 - 472
Database
ISI
SICI code
0174-1578(1998)168:6<461:TEOAVA>2.0.ZU;2-1
Abstract
Simultaneous measurements of cardio-respiratory variables, oxygen upta ke and whole body urea/ ammonia/tritiated water effluxes were performe d on cannulated gulf toadfish, Opsanus beta, before and after intra-ar terial injection of the vasoactive agents, adrenaline, isoproterenol a nd arginine vasotocin. These experiments were conducted to test the hy pothesis that the phenomenon of pulsatile urea excretion might reflect sudden changes in the general diffusive properties of the gill for so lute transfer. Injection of isoproterenol (final nominal circulating l evel = 10(-6) mol l(-1)), was used as a tool to maximise the diffusive and perfusive conditions for branchial solute transfer. This protocol caused a pronounced reduction in arterial blood pressure, an elevatio n of cardiac frequency and associated increases in whole body urea and tritiated water effluxes; ammonia excretion and oxygen uptake were un affected. Injection of adrenaline (final nominal circulating level = 1 0(-6) mol l(-1)), caused a significant increase in arterial blood pres sure and a tachycardia, yet nitrogen excretion and oxygen uptake were unaffected. Injection of arginine vasotocin, caused a dose-dependent ( final nominal circulating levels = 10(-11)-10(-9) mol l(-1)) increase in arterial blood pressure without affecting cardiac or ventilation fr equency. At the two higher concentrations, arginine vasotocin caused l arge and transient increases in urea excretion without significantly a ffecting ammonia, water or oxygen fluxes. These results suggest that i ncreased gill diffusive or perfusive conductance, while capable of aug menting urea efflux, cannot fully explain the sudden and massive incre ases in urea transfer associated with pulsatile urea excretion in toad fish. It is suggested that pulsatile urea excretion in this species ma y reflect a specific enhancement of urea excretion under the control o f the neurohypophyseal hormone, arginine vasotocin.