4.4 Article

Ventromedial prefrontal cortex CRF1 receptors modulate the tachycardic activity of baroreflex

Journal

PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
Volume 473, Issue 4, Pages 697-709

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s00424-020-02512-z

Keywords

Baroreflex; Ventral medial prefrontal cortex; CRF1 receptors; CRF2 receptors

Categories

Funding

  1. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
  2. Fundacao de Apoio ao Ensino, Pesquisa e Assistencia do Hospital das Clinicas da FMRP-USP (FAEPA)
  3. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)

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The glutamatergic neurotransmission in the ventral medial prefrontal cortex plays a facilitatory role in cardiac baroreflex activity mediated by NMDA receptors activation. The CRF1 and CRF2 receptors in this area are involved in modulating baroreflex bradycardic and tachycardic responses, with CRF1 having an inhibitory effect on tachycardia and CRF2 having no significant impact.
Ventral medial prefrontal cortex (vMPFC) glutamatergic neurotransmission has a facilitatory role on cardiac baroreflex activity which is mediated by NMDA receptors activation. Corticotrophin releasing factor receptors type1 and 2 (CRF1 and CRF2), present in the vMPFC, are colocalized in neurons containing glutamate vesicles, suggesting that such receptors may be involved in glutamate release in this cortical area. Therefore, our hypothesis is that the CRF1 and CRF2 receptors can modulate the baroreflex bradycardic and tachycardic responses. In order to prove this assumption, male Wistar rats had bilateral stainless steel guide cannula implanted into the vMPFC, and baroreflex was activated by intravenous infusion of phenylephrine or sodium nitroprusside through a vein catheter. A second catheter was implanted into the femoral artery for cardiovascular measurements. The CRF1 receptor antagonist administration in either infralimbic cortex (IL) or prelimbic cortex (PL), vMPFC regions, was unable to change the bradycardic responses but increased the slope of the baroreflex tachycardic activity. Microinjection of the CRF2 receptor antagonist into the IL and PL did not alter ether bradycardic nor tachycardic baroreflex responses. The administration of the non-selective CRF receptors agonist, urocortin in these areas, did not modify bradycardic responses but decreased tachycardia slope of the baroreflex. CRF1 receptor antagonist administration prior to non-selective CRF agonist in vMPFC prevented the tachycardic responses reduction. However, CRF2 receptor antagonism could not prevent the effect of CRF receptors agonist. These results suggest that IL and PL CRF1 but not CRF2 receptors have an inhibitory role on the baroreflex tachycardic activity. Furthermore, they have no influence on baroreflex bradycardic activity.

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