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This Article Full Text Full Text (PDF) All Versions of this Article: 288/2/R456    most recent 00417.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Galli, G. L. J. Articles by Wang, T. Search for Related Content PubMed PubMed Citation Articles by Galli, G. L. J. Articles by Wang, T.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Cardiovascular actions of rattlesnake bradykinin ([Val¹,Thr⁶]bradykinin) in the anesthetized South American rattlesnake Crotalus durissus terrificus

¹Department of Zoophysiology, Aarhus University, Aarhus, Denmark; ²School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom; ³ Departamento de Zoologia, Centro de Aquicultura, Universidad Estadual Paulista, Rio Claro, SÂo Paulo, Brazil; and ⁴Department of Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates

Submitted 22 June 2004 ; accepted in final form 13 October 2004

Incubation of heat-denatured plasma from the rattlesnake Crotalus atrox with trypsin generated a bradykinin (BK) that contained two amino acid substitutions (Arg¹ Val and Ser⁶ Thr) compared with mammalian BK. Bolus intra-arterial injections of synthetic rattlesnake BK (0.01–10 nmol/kg) 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 an 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). Pretreatment with N^G-nitro-L-arginine methyl ester 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 pretreatment, indicating that the responses are caused, at least in part, by release of cathecholamines and subsequent stimulation of -adrenergic receptors. In contrast, the pulmonary circulation was relatively unresponsive to BK.

reptile; vasoactive kinin; catecholamines; nitric oxide; adrenergic receptor

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