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The role of nitric oxide in the regulation of the systemic and pulmonary vasculature of the rattlesnake, Crotalus durissus terrificus
Authors:Gina?LJ?Galli  author-information"  >  author-information__contact u-icon-before"  >  mailto:ginaljgalli@hotmail.com"   title="  ginaljgalli@hotmail.com"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author,Nini?Skovgaard,Augusto?S.?Abe,Edwin?W.?Taylor,Tobias?Wang
Affiliation:(1) Departamento de Zoologia, Centro de Aquicultura, UNESP, Caixa Postal, 199, 13506-907 Rio Claro, Brazil;(2) School of Biosciences, University of Birmingham, Edgbaston, Birmingham, B19 2TT, England;(3) Department of Zoophysiology, Aarhus University, Building 131, 8000 Aarhus C, Denmark
Abstract:The functional role of nitric oxide (NO) was investigated in the systemic and pulmonary circulations of the South American rattlesnake, Crotalus durissus terrificus. Bolus, intra-arterial injections of the NO donor, sodium nitroprusside (SNP) caused a significant systemic vasodilatation resulting in a reduction in systemic resistance (Rsys). This response was accompanied by a significant decrease in systemic pressure and a rise in systemic blood flow. Pulmonary resistance (Rpul) remained constant while pulmonary pressure (Ppul) and pulmonary blood flow (Qpul) decreased. Injection of L-Arginine (L-Arg) produced a similar response to SNP in the systemic circulation, inducing an immediate systemic vasodilatation, while Rpul was unaffected. Blockade of NO synthesis via the nitric oxide synthase inhibitor, L-NAME, did not affect haemodynamic variables in the systemic circulation, indicating a small contribution of NO to the basal regulation of systemic vascular resistance. Similarly, Rpul and Qpul remained unchanged, although there was a significant rise in Ppul. Via injection of SNP, this study clearly demonstrates that NO causes a systemic vasodilatation in the rattlesnake, indicating that NO may contribute in the regulation of systemic vascular resistance. In contrast, the pulmonary vasculature seems far less responsive to NO.
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