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 (Asn(1), Val(5)) 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 alpha-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 alpha-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.