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Ethanol dilates coronary arteries and increases coronary flow via transient receptor potential vanilloid 1 and calcitonin gene-related peptide.
Cardiovasc Res. 2006 Jun 01; 70(3):589-99.CR

Abstract

OBJECTIVES

Consumption of alcoholic beverages reduces the risk of coronary artery disease (CAD), and epidemiological studies have shown that ethanol per se is protective. However, the mechanism by which ethanol exerts protection is not fully known. Ethanol can stimulate neuropeptide-containing primary sensory neurons via the activation of transient receptor potential vanilloid 1 (TRPV1). Here, we have studied whether ethanol-mediated TRPV1 activation causes the release of calcitonin gene-related peptide (CGRP) that, via dilatation of coronary arteries and other mechanisms, may protect the heart from CAD.

METHODS AND RESULTS

Ethanol caused a marked relaxation of small-sized porcine isolated coronary (0.008-2.37%, w/v) and human isolated gastro-epiploic (0.0008-2.37%, w/v) arteries in vitro, an effect that was abolished by capsaicin-desensitization, the TRPV1 antagonist capsazepine, and the CGRP receptor antagonist, CGRP(8-37). In guinea-pig isolated and perfused hearts, ethanol (0.079-0.79%, w/v) increased baseline coronary flow in a concentration-dependent manner: 0.237% ethanol doubled baseline coronary flow. This effect was also abolished by capsaicin-desensitization, capsazepine, and CGRP((8-37)). Finally, the ethanol-induced increase in CGRP release from guinea-pig isolated and perfused hearts and from slices of porcine coronary arteries was abolished by capsaicin-desensitization and by capsazepine. Similar functional and neurochemical results were obtained in all preparations with capsaicin.

CONCLUSIONS

Ethanol, at low concentrations not dissimilar from those found in blood following low to moderate consumption of alcoholic beverages, releases CGRP within coronary arteries via stimulation of TRPV1 on perivascular sensory nerve terminals. Ethanol-induced release of CGRP may contribute to the reduction in the risk of CAD associated with alcohol consumption by various mechanisms, including the increase in coronary flow and arterial dilatation.

Authors+Show Affiliations

Center of Excellence for the Study of Inflammation, University of Ferrara, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16579978

Citation

Gazzieri, David, et al. "Ethanol Dilates Coronary Arteries and Increases Coronary Flow Via Transient Receptor Potential Vanilloid 1 and Calcitonin Gene-related Peptide." Cardiovascular Research, vol. 70, no. 3, 2006, pp. 589-99.
Gazzieri D, Trevisani M, Tarantini F, et al. Ethanol dilates coronary arteries and increases coronary flow via transient receptor potential vanilloid 1 and calcitonin gene-related peptide. Cardiovasc Res. 2006;70(3):589-99.
Gazzieri, D., Trevisani, M., Tarantini, F., Bechi, P., Masotti, G., Gensini, G. F., Castellani, S., Marchionni, N., Geppetti, P., & Harrison, S. (2006). Ethanol dilates coronary arteries and increases coronary flow via transient receptor potential vanilloid 1 and calcitonin gene-related peptide. Cardiovascular Research, 70(3), 589-99.
Gazzieri D, et al. Ethanol Dilates Coronary Arteries and Increases Coronary Flow Via Transient Receptor Potential Vanilloid 1 and Calcitonin Gene-related Peptide. Cardiovasc Res. 2006 Jun 1;70(3):589-99. PubMed PMID: 16579978.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ethanol dilates coronary arteries and increases coronary flow via transient receptor potential vanilloid 1 and calcitonin gene-related peptide. AU - Gazzieri,David, AU - Trevisani,Marcello, AU - Tarantini,Francesca, AU - Bechi,Paolo, AU - Masotti,Giulio, AU - Gensini,Gian Franco, AU - Castellani,Sergio, AU - Marchionni,Niccolo', AU - Geppetti,Pierangelo, AU - Harrison,Selena, Y1 - 2006/03/03/ PY - 2005/11/23/received PY - 2006/02/01/revised PY - 2006/02/21/accepted PY - 2006/4/4/pubmed PY - 2007/4/3/medline PY - 2006/4/4/entrez SP - 589 EP - 99 JF - Cardiovascular research JO - Cardiovasc Res VL - 70 IS - 3 N2 - OBJECTIVES: Consumption of alcoholic beverages reduces the risk of coronary artery disease (CAD), and epidemiological studies have shown that ethanol per se is protective. However, the mechanism by which ethanol exerts protection is not fully known. Ethanol can stimulate neuropeptide-containing primary sensory neurons via the activation of transient receptor potential vanilloid 1 (TRPV1). Here, we have studied whether ethanol-mediated TRPV1 activation causes the release of calcitonin gene-related peptide (CGRP) that, via dilatation of coronary arteries and other mechanisms, may protect the heart from CAD. METHODS AND RESULTS: Ethanol caused a marked relaxation of small-sized porcine isolated coronary (0.008-2.37%, w/v) and human isolated gastro-epiploic (0.0008-2.37%, w/v) arteries in vitro, an effect that was abolished by capsaicin-desensitization, the TRPV1 antagonist capsazepine, and the CGRP receptor antagonist, CGRP(8-37). In guinea-pig isolated and perfused hearts, ethanol (0.079-0.79%, w/v) increased baseline coronary flow in a concentration-dependent manner: 0.237% ethanol doubled baseline coronary flow. This effect was also abolished by capsaicin-desensitization, capsazepine, and CGRP((8-37)). Finally, the ethanol-induced increase in CGRP release from guinea-pig isolated and perfused hearts and from slices of porcine coronary arteries was abolished by capsaicin-desensitization and by capsazepine. Similar functional and neurochemical results were obtained in all preparations with capsaicin. CONCLUSIONS: Ethanol, at low concentrations not dissimilar from those found in blood following low to moderate consumption of alcoholic beverages, releases CGRP within coronary arteries via stimulation of TRPV1 on perivascular sensory nerve terminals. Ethanol-induced release of CGRP may contribute to the reduction in the risk of CAD associated with alcohol consumption by various mechanisms, including the increase in coronary flow and arterial dilatation. SN - 0008-6363 UR - https://www.unboundmedicine.com/medline/citation/16579978/Ethanol_dilates_coronary_arteries_and_increases_coronary_flow_via_transient_receptor_potential_vanilloid_1_and_calcitonin_gene_related_peptide_ L2 - https://academic.oup.com/cardiovascres/article-lookup/doi/10.1016/j.cardiores.2006.02.027 DB - PRIME DP - Unbound Medicine ER -