HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 291/3/R711    most recent 00893.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Sandblom, E. Articles by Axelsson, M. Search for Related Content PubMed PubMed Citation Articles by Sandblom, E. Articles by Axelsson, M.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

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

Department of Zoology, Göteborg University, Gothenburg, Sweden

Submitted 20 December 2005 ; accepted in final form 26 February 2006

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 P_ven, dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (P_WO₂ = 9 kPa), where P_WO₂ 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 P_ven 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 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, P_ven 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

This article has been cited by other articles:

				E. Sandblom, G. K. Cox, S. F. Perry, and A. P. Farrell The role of venous capacitance, circulating catecholamines, and heart rate in the hemodynamic response to increased temperature and hypoxia in the dogfish Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2009; 296(5): R1547 - R1556. [Abstract] [Full Text] [PDF]

				E. Sandblom and M. Axelsson Venous hemodynamic responses to acute temperature increase in the rainbow trout (Oncorhynchus mykiss) Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2007; 292(6): R2292 - R2298. [Abstract] [Full Text] [PDF]