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

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.