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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION
Department of Zoology, Göteborg University, Gothenburg, Sweden
Submitted 20 December 2005 ; accepted in final form 26 February 2006
Central venous blood pressure (Pven) 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 (PWO2 =
9 kPa), where PWO2 is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80100, 90110, and 100120% 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
-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 80100% blood volume, whereas vascular capacitance decreased significantly at 90110% 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
-adrenergic mechanism with both humoral and neural components.
adrenergic nerves; venous pressure
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