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TRPA1, but not TRPV1, is involved in the increase of the non-adrenergic non-cholinergic outflow induced by hydrogen sulfide in pithed rats. | LitMetric

TRPA1, but not TRPV1, is involved in the increase of the non-adrenergic non-cholinergic outflow induced by hydrogen sulfide in pithed rats.

Peptides

Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Del. Tlalpan, C.P. 14330 México D.F., Mexico. Electronic address:

Published: November 2022

AI Article Synopsis

  • * The study involved 72 male rats to investigate how HS influences non-adrenergic/non-cholinergic (NANC) outflow and its underlying mechanisms through various experimental setups, including electrical stimulation and intravenous bolus injections.
  • * Results indicated that HS infusion enhanced vasodepressor responses from electrical stimulation, suggesting it activates TRPA1 channels, while TRPV1 channels were not involved, indicating a specific mechanism for HS in NANC neurotransmission.

Article Abstract

Hydrogen sulfide (HS) is a gasotransmitter that modulates the peripheral transmission regulating the vascular tone. In vitro studies have suggested that HS induces vasodilation by stimulating capsaicin-sensitive sensory neurons. This study was designed to determine the effects of HS on the non-adrenergic/non-cholinergic (NANC) outflow in the pithed rat, and the underlying mechanisms. For that purpose, 72 male Wistar rats were anesthetized, pithed and the carotid, femoral and jugular veins were cannulated and then divided into two main sets. The first set of animals (n = 48) was used to determine the effect of NaHS (HS donor) on the vasodepressor responses induced by: 1) NANC outflow electrical stimulation (n = 24); and 2) i.v. bolus of α-CGRP (n = 24) and subdivided into 4 groups (n = 6 each): 1) control group (without infusion); continuous infusion of: 2) PBS (vehicle; 0.02 ml/kg·min); 3) NaHS 10 μg/kg·min; and 4) NaHS 18 μg/kg·min. The second set of animals (n = 24) received an i.v. bolus of either (1) HC 030031 (TRPA1 channel antagonist; 18 μg/kg; n = 12) or (2) capsazepine (TRPV1 channel antagonist; 100 μg/kg; n = 12) in presence and absence of 18 µg/kg·min NaHS i.v. continuous infusion to determine the underlying mechanism of the NaHS effect on the NANC outflow. Our results show that NaHS infusion increased the vasodepressor responses induced by electrical stimulation, but not by α-CGRP, effect that was abolished by HC030031 and remained unaffected after capsazepine. These data suggest that activation of TRPA1 channels, but no TRPV1, is responsible for the NaHS-induced NANC neurotransmission stimulation.

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Source
http://dx.doi.org/10.1016/j.peptides.2022.170861DOI Listing

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