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Adrenergic control of venous capacitance during moderate hypoxia in the rainbow trout (Oncorhynchus mykiss): role of neural and circulating catecholamines

Journal article
Authors Erik Sandblom
Michael Axelsson
Published in American Journal of Physiology-Regulatory Integrative and Comparative Physiology
Volume 291
Issue 3
Pages R711-R718
ISSN 0363-6119
Publication year 2006
Published at Department of Zoology
Pages R711-R718
Language en
Links dx.doi.org/10.1152/ajpregu.00893.20...
Keywords adrenergic nerves, venous pressure, bass dicentrarchus-labrax, atrial-natriuretic-factor, cod gadus-morhua, blood-pressure, atlantic cod, vascular capacitance, salmo-gairdneri, reflex control, heart-rate, cardiac-performance
Subject categories Biological Sciences

Abstract

Central venous blood pressure (P-ven) increases in response to hypoxia in rainbow trout ( Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including Pven, dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (PwO(2) = similar to 9 kPa), where PwO(2) is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80-100, 90-110, and 100-120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure Pven during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by alpha-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80-100% blood volume, whereas vascular capacitance decreased significantly at 90-110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, Pven always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an alpha-adrenergic mechanism with both humoral and neural components.

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