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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Medial prefrontal cortex TRPV1 and CB1 receptors modulate cardiac baroreflex activity by regulating the NMDA receptor/nitric oxide pathway

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Author(s):
Lagatta, Davi C. [1] ; Kuntze, Luciana B. [1] ; Ferreira-Junior, Nilson C. [1] ; Resstel, Leonardo B. M. [1]
Total Authors: 4
Affiliation:
[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pharmacol, Bandeirantes Ave 3900, BR-14049900 Ribeirao Preto, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY; v. 470, n. 10, p. 1521-1542, OCT 2018.
Web of Science Citations: 2
Abstract

The ventral medial prefrontal cortex (vMPFC) facilitates the cardiac baroreflex response through N-methyl-d-aspartate (NMDA) receptor activation and nitric oxide (NO) formation by neuronal NO synthase (nNOS) and soluble guanylate cyclase (sGC) triggering. Glutamatergic transmission is modulated by the cannabinoid receptor type 1 (CB1) and transient receptor potential vanilloid type 1 (TRPV1) receptors, which may inhibit or stimulate glutamate release in the brain, respectively. Interestingly, vMPFC CB1 receptors decrease cardiac baroreflex responses, while TRPV1 channels facilitate them. Therefore, the hypothesis of the present study is that the vMPFC NMDA/NO pathway is regulated by both CB1 and TRPV1 receptors in the modulation of cardiac baroreflex activity. In order to test this assumption, we used male Wistar rats that had stainless steel guide cannulae bilaterally implanted in the vMPFC. Subsequently, a catheter was inserted into the femoral artery, for cardiovascular recordings, and into the femoral vein for assessing baroreflex activation. The increase in tachycardic and bradycardic responses observed after the microinjection of a CB1 receptors antagonist into the vMPFC was prevented by an NMDA antagonist as well as by the nNOS and sGC inhibition. NO extracellular scavenging also abolished these responses. These same pharmacological manipulations inhibited cardiac reflex enhancement induced by TRPV1 agonist injection into the area. Based on these results, we conclude that vMPFC CB1 and TRPV1 receptors inhibit or facilitate the cardiac baroreflex activity by stimulating or blocking the NMDA activation and NO synthesis. (AU)

FAPESP's process: 11/19494-8 - Involvement of the dorsal hippocampus in the modulation of cardiac baroreflex activity: implication of NMDA, CB1, TRPV1 and muscarinic receptors and of the nitric oxide.
Grantee:Nilson Carlos Ferreira Junior
Support Opportunities: Scholarships in Brazil - Doctorate