Adrenergic and adenosinergic regulation of the cardiovascular system in an Antarctic icefish:Insight into central and peripheral determinants of cardiac output

• Published in: Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology
• Main Authors: Joyce, William, Egginton, Stuart, Farrell, Anthony P., Axelsson, Michael
• Format: Article in Journal/Newspaper
• Language: English
• Published: 2019
• Subjects: Adenosine; Adrenaline; Channichthyidae; Conductance; Heart rate; Antarctic; Antarc*; Icefish
• Online Access: https://pure.au.dk/portal/en/publications/cd285c4d-3027-45a0-bebc-5d1ef850bde9; https://doi.org/10.1016/j.cbpa.2018.12.012; http://www.scopus.com/inward/record.url?scp=85059345699&partnerID=8YFLogxK

Icefishes characteristically lack the oxygen-binding protein haemoglobin and therefore are especially reliant on cardiovascular regulation to augment oxygen transport when oxygen demand increases, such as during activity and warming. Using both in vivo and in vitro experiments, we evaluated the roles for adrenaline and adenosine, two well-established cardio- and vasoactive molecules, in regulating the cardiovascular system of the blackfin icefish, Chaenocephalus aceratus. Despite increasing cardiac contractility (increasing twitch force and contraction kinetics in isometric myocardial strip preparations) and accelerating heart rate (ƒ H ), adrenaline (5 nmol kg −1 bolus intra-arterial injection) did not significantly increase cardiac output (Q̇) in vivo because it elicited a large decrease in vascular conductance (G sys ). In contrast, and despite preliminary data suggesting a direct negative inotropic effect of adenosine on isolated atria and little effect on isolated ventricle strips, adenosine (500 nmol kg −1 ) generated a large increase in Q̇ by increasing G sys , a change reminiscent of that previously reported during both acute warming and invoked activity. Our data thus illustrate how Q̇ in C. aceratus may be much more dependent on peripheral control of vasomotor tone than direct regulation of the heart.