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Cardiovascular effects of noradrenaline microinjected into the insular cortex of unanesthetized rats
  • Universidade de São Paulo (USP)
  • Universidade Estadual Paulista (UNESP)
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
  • Fundação de Apoio ao Ensino, Pesquisa e Assistência do Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto da USP (FAEPA)
Sponsorship Process Number: 
  • CNPq: 870307/1997-5
  • CNPq: 306381/2003-6
  • CNPq: 505394/2003-0
  • FAPESP: 06/57670-4
The insular cortex (IC) has been reported to be involved in central cardiovascular control. In the present study, we investigated the cardiovascular responses evoked by microinjection of noradrenaline into the IC as well as the central and peripheral mechanisms involved in their mediation. Microinjection of noradrenaline into the IC (3, 7, 10, 15,30 and 45 nmol/100 nL) caused long-lasting dose-related pressor and bradycardiac responses. The cardiovascular responses evoked by 15 nmol of noradrenaline were blocked by IC pretreatment with WB4101 or 5-methyl-urapidil, selective alpha(1)-adrenoceptor antagonists. IC pretreatment with either the selective alpha(2)-adrenoceptor antagonists RX821002 or the beta-adrenoceptor antagonist propranolol did not affect noradrenaline cardiovascular responses. Noradrenaline cardiovascular responses were mimicked by microinjection of the selective alpha(1)-adrenoceptor agonist phenylephrine into the IC, thus reinforcing the idea that alpha(1)-adrenoceptors mediate cardiovascular responses to noradrenaline microinjected into the IC. The pressor response to noradrenaline microinjection was potentiated by i.v. pretreatment with the ganglion blocker pentolinium and inhibited by i.v. pretreatment with the selective V(1)-vasopressin receptor antagonist dTyr(CH(2))(5)(Me)AVP. The bradycardiac response to noradrenaline microinjection into the IC was abolished by pretreatment with either pentolinium or the V(1)-vasopressin receptor antagonist, indicating its reflex origin. In conclusion, our results suggest that pressor response evoked by microinjection of noradrenaline into the IC involve the activation of IC alpha(1)-adrenoceptors to cause the release of vasopressin into the circulation. (C) 2010 Elsevier B.V. All rights reserved.
Issue Date: 
Autonomic Neuroscience-basic & Clinical. Amsterdam: Elsevier B.V., v. 160, n. 1-2, p. 90-98, 2011.
Time Duration: 
Elsevier B.V.
  • Prefrontal cortex
  • Blood pressure
  • Heart rate
  • Noradrenergic neurotransmission
  • Adrenoceptors
  • Vasopressin
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Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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