Display options
Cite
Sundin L, Axelsson M, Davison W, et al. Cardiovascular responses to adenosine in the antarctic fish pagothenia borchgrevinki. J Exp Biol. 1999;202:2259-67
Sundin, L., Axelsson, M., Davison, W., & Forster, M. E. (1999). Cardiovascular responses to adenosine in the antarctic fish pagothenia borchgrevinki. The Journal of experimental biology, 2022259-67.
Sundin, et al. "Cardiovascular responses to adenosine in the antarctic fish pagothenia borchgrevinki." The Journal of experimental biology vol. 202 (1999): 2259-67.
Sundin L, Axelsson M, Davison W, Forster ME. Cardiovascular responses to adenosine in the antarctic fish pagothenia borchgrevinki. J Exp Biol. 1999 Sep;202:2259-67. PMID: 10441079.
Copy Download .nbib Format: NLM
Share it on

J Exp Biol. 1999 Sep;202:2259-67.

Cardiovascular responses to adenosine in the antarctic fish pagothenia borchgrevinki.

The Journal of experimental biology

Sundin, Axelsson, Davison, Forster

Affiliations

  1. Department of Zoophysiology, University of Goteborg, Box 463, Sweden and Department of Zoology, University of Canterbury, Private Bag 4800, Christchurch, New Zealand. [email protected].

PMID: 10441079

Abstract

We have investigated the effects of adenosine on the cardiovascular system of the Antarctic fish Pagothenia borchgrevinki. Continuous measurements of ventral and dorsal aortic blood pressures, heart rate (fh) and ventral aortic blood flow (cardiac output, q_dot ) were made using standard cannulation techniques and a single-crystal Doppler flowmeter. On line measurements of arterial P(O2) were made using an oxygen electrode connected to an extracorporeal loop. Adenosine (10 nmol kg(-)(1)) and the specific A(1)-receptor agonist N(6)-cyclopentyladenosine (CPA) elicited biphasic changes in the branchial and systemic resistances. While there was an initial decrease in the branchial resistance followed by an increase, the opposite was true for the systemic response. The resistance changes were significantly attenuated by aminophylline (a P(1)-receptor antagonist) and 8-cyclopentyltheophylline (CPT; an A(1)-receptor antagonist). In addition, adenosine induced an aminophylline-sensitive decrease in the arterial P(O2). The reduction was attenuated when pre-injection arterial P(O2) was low. Adenosine and CPA also caused a marked reduction in fh, with CPA being more potent. The bradycardia was blocked by aminophylline and CPT, demonstrating an involvement of A(1) receptors in this response.

Publication Types