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Nitric oxide mechanisms of nebivolol.
Ther Adv Cardiovasc Dis. 2009 Aug; 3(4):317-27.TA

Abstract

beta-blockers are among the most widely used drugs in the prevention and treatment of cardiovascular disease, although they are associated with increased peripheral resistance. Third-generation beta-blockers avoid this adverse effect by inducing vasodilation through different mechanisms. In particular, nebivolol, a highly selective blocker of beta(1)-adrenergic receptors, is the only beta-blocker known to induce vascular production of nitric oxide, the main endothelial vasodilator. The specific mechanism of nebivolol is particularly relevant in hypertension, where nitric oxide dysfunction occurs. Indeed, nebivolol is able to reverse endothelial dysfunction. Nebivolol induces nitric oxide production via activation of beta(3)-adrenergic receptors, which can explain the good metabolic profile observed after treatment with this drug. Moreover, nebivolol can also stimulate the beta(3)-adrenergic receptor-mediated production of nitric oxide in the heart, and this stimulation can result in a greater protection against heart failure. In conclusion, nebivolol has a unique profile among antihypertensive drugs, adding to a very high selectivity against beta(1) adrenergic receptors, and an agonist action on beta(3) receptors and nitric oxide (NO), which has led to clinically significant improvements in hypertensive patients.

Authors+Show Affiliations

Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli (IS), Italy.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

19443516

Citation

Maffei, Angelo, and Giuseppe Lembo. "Nitric Oxide Mechanisms of Nebivolol." Therapeutic Advances in Cardiovascular Disease, vol. 3, no. 4, 2009, pp. 317-27.
Maffei A, Lembo G. Nitric oxide mechanisms of nebivolol. Ther Adv Cardiovasc Dis. 2009;3(4):317-27.
Maffei, A., & Lembo, G. (2009). Nitric oxide mechanisms of nebivolol. Therapeutic Advances in Cardiovascular Disease, 3(4), 317-27. https://doi.org/10.1177/1753944709104496
Maffei A, Lembo G. Nitric Oxide Mechanisms of Nebivolol. Ther Adv Cardiovasc Dis. 2009;3(4):317-27. PubMed PMID: 19443516.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitric oxide mechanisms of nebivolol. AU - Maffei,Angelo, AU - Lembo,Giuseppe, Y1 - 2009/05/14/ PY - 2009/5/16/entrez PY - 2009/5/16/pubmed PY - 2009/10/7/medline SP - 317 EP - 27 JF - Therapeutic advances in cardiovascular disease JO - Ther Adv Cardiovasc Dis VL - 3 IS - 4 N2 - beta-blockers are among the most widely used drugs in the prevention and treatment of cardiovascular disease, although they are associated with increased peripheral resistance. Third-generation beta-blockers avoid this adverse effect by inducing vasodilation through different mechanisms. In particular, nebivolol, a highly selective blocker of beta(1)-adrenergic receptors, is the only beta-blocker known to induce vascular production of nitric oxide, the main endothelial vasodilator. The specific mechanism of nebivolol is particularly relevant in hypertension, where nitric oxide dysfunction occurs. Indeed, nebivolol is able to reverse endothelial dysfunction. Nebivolol induces nitric oxide production via activation of beta(3)-adrenergic receptors, which can explain the good metabolic profile observed after treatment with this drug. Moreover, nebivolol can also stimulate the beta(3)-adrenergic receptor-mediated production of nitric oxide in the heart, and this stimulation can result in a greater protection against heart failure. In conclusion, nebivolol has a unique profile among antihypertensive drugs, adding to a very high selectivity against beta(1) adrenergic receptors, and an agonist action on beta(3) receptors and nitric oxide (NO), which has led to clinically significant improvements in hypertensive patients. SN - 1753-9447 UR - https://www.unboundmedicine.com/medline/citation/19443516/Nitric_oxide_mechanisms_of_nebivolol_ L2 - https://journals.sagepub.com/doi/10.1177/1753944709104496?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -