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Circulatory function at sub-zero temperature: Venous haemodynamic responses to catecholamines and angiotensin II in the Antarctic fish Pagothenia borchgrevinki

Journal article
Authors Erik Sandblom
Michael Axelsson
W. Davison
Published in Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology
Volume 179
Pages 165-173
ISSN 1432-136X
Publication year 2009
Published at Department of Zoology
Pages 165-173
Language en
Links dx.doi.org/10.1007/s00360-008-0299-...
Keywords Adrenaline, Cardiac output, Central venous blood pressure, Mean circulatory filling pressure, Stroke volume
Subject categories Animal physiology

Abstract

Catecholamines increase arterial pressure by increasing cardiac output (Q) and stroke volume (V s), while angiotensin II (ang II) also increases vascular resistance (R sys) in the Antarctic fish Pagothenia borchgrevinki. Adrenaline, phenylephrine and ang II (Asn1, Val5) were injected into P. borchgrevinki. Cardiovascular variables, including central venous pressure (P cv) and mean circulatory filling pressure (P mcf; an index of venous capacitance), were recorded to investigate if venous vasoconstriction can explain the increased V s and Q and the arterial pressor response in this species. Routine P cv and P mcf were 0.11 ± 0.01 and 0.18 ± 0.02 kPa, respectively. All of the drugs caused moderate increases in P cv and P mcf and the responses were attenuated after α-adrenergic blockade with prazosin. Although dorsal aortic pressure (P da) also increased in response to all agonists, the mechanisms differed. Adrenaline caused sustained increases in V s and Q, while R sys only rose transiently. Ang II had a slower effect than adrenaline and increased both R sys and Q, while phenylephrine only increased R sys. This study demonstrates that P cv is positive and controlled by an α-adrenergic mechanism in P. borchgrevinki. However, given the relatively small venous response to adrenaline it seems more likely that the increases in V s and Q from this agonist are due to direct effects on the heart.

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