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Am J Physiol Regul Integr Comp Physiol (October 21, 2004). doi:10.1152/ajpregu.00417.2004
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Submitted on June 22, 2004
Accepted on October 13, 2004

Cardiovascular actions of rattlesnake bradykinin ([Val1Thr6]bradykinin) in the anesthetized South American rattlesnake Crotalus durissus terrificus

Gina L. J Galli1*, Nini Skovgaard2, Augusto S Abe3, Edwin W Taylor4, J. Michael Conlon5, and Tobias Wang2

1 Department of Zoophysiology, University of Aarhus, Aarhus, Denmark; School of Biosciences, The University of Birmingham, Birmingham, United Kingdom; Department of Zoology, UNESP, Rio Claro, Brazil
2 Department of Zoophysiology, University of Aarhus, Aarhus, Denmark; Department of Zoology, UNESP, Rio Claro, Brazil
3 Department of Zoology, UNESP, Rio Claro, Brazil
4 School of Biosciences, The University of Birmingham, Birmingham, United Kingdom; Department of Zoology, UNESP, Rio Claro, Brazil
5 Deaprtment of Biochemistry, United Arab Emirates University, Al-Ain, United Arab Emirates

* To whom correspondence should be addressed. E-mail: ginaljgalli{at}hotmail.com.

Incubation of heat-denatured plasma from the rattlesnake Crotalus atrox with trypsin generated a bradykinin (BK) that contained two amino acid substitutions (Arg1 {Rightarrow} Val and Ser6 {Rightarrow} Thr) compared with mammalian BK. Bolus intra-arterial injections of synthetic rattlesnake BK (0.01 to 10 nmol kg-1) into the anesthetized rattlesnake, Crotalus durissus terrificus, produced a pronounced and concentration-dependent increase in systemic vascular conductance (Gsys). This caused a fall in systemic arterial blood pressure (Psys) and increase in blood flow. Heart rate and stroke volume also increased. This primary response was followed by a significant rise in Psys and pronounced tachycardia (secondary response). Pre-treatment with L-NAME reduced the NK-induced systemic vasodilatation indicating that the effect is mediated through increased NO synthesis. The tachycardia associated with the late primary and secondary response to BK was abolished with propranolol and the systemic vasodilatation produced in the primary phase was also significantly attenuated by pre-treatment, indicating that the responses are caused, at least in part, by release of cathecholamines and subsequent stimulation {beta}-adrenergic receptors. In contrast, the pulmonary circulation was relatively unresponsive to BK.




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N. Skovgaard, A. S. Abe, D. V. Andrade, and T. Wang
Hypoxic pulmonary vasoconstriction in reptiles: a comparative study of four species with different lung structures and pulmonary blood pressures
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2005; 289(5): R1280 - R1288.
[Abstract] [Full Text] [PDF]


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