Medial prefrontal cortex TRPV1 and CB1 receptors modulate cardiac baroreflex activity by regulating the NMDA receptor/nitric oxide pathway
| Autor: | Leonardo B.M. Resstel, Davi Campos Lagatta, Nilson C. Ferreira-Junior, Luciana B. Kuntze |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Agonist Male Physiology medicine.drug_class Clinical Biochemistry TRPV1 Prefrontal Cortex TRPV Cation Channels Nitric Oxide Synthase Type I Baroreflex Pharmacology Nitric Oxide Receptors N-Methyl-D-Aspartate 03 medical and health sciences 0302 clinical medicine Receptor Cannabinoid CB1 Heart Rate Physiology (medical) Cannabinoid receptor type 1 medicine Animals Enzyme Inhibitors Rats Wistar Receptor Cannabinoid Receptor Antagonists Chemistry musculoskeletal neural and ocular physiology Glutamate receptor Heart CÓRTEX PRÉ-FRONTAL Rats 030104 developmental biology nervous system Guanylate Cyclase Nitric Oxide Pathway cardiovascular system NMDA receptor lipids (amino acids peptides and proteins) Excitatory Amino Acid Antagonists 030217 neurology & neurosurgery |
| Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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