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Vascular effects of long-term propranolol administration after chronic nitric oxide blockade.
Eur J Pharmacol. 2007 Oct 01; 571(2-3):189-96.EJ

Abstract

Long-term propranolol treatment reduces arterial blood pressure in hypertensive individuals mainly by reducing peripheral vascular resistance, but mechanisms underlying their vasodilatory effect remain poorly investigated. This study aimed to investigate whether long-term propranolol administration ameliorates the impairment of relaxing responses of aorta and mesenteric artery from rats made hypertensive by chronic nitric oxide (NO) deficiency, and underlying mechanisms mediating this phenomenon. Male Wistar rats were treated with N(omega)-Nitro-L-arginine methyl ester (L-NAME; 20 mg/rat/day) for four weeks. DL-Propranolol (30 mg/rat/day) was given concomitantly to L-NAME in the drinking water. Treatment with L-NAME markedly increased blood pressure, an effect largely attenuated by DL-propranolol. In phenylephrine-precontracted aortic rings, the reduction of relaxing responses for acetylcholine (0.001-10 microM) in L-NAME group was not modified by DL-propranolol, whereas in mesenteric rings the impairment of acetylcholine-induced relaxation by L-NAME was significantly attenuated by DL-propranolol. In mesenteric rings precontracted with KCl (80 mM), DL-propranolol failed to attenuate the impairment of acetylcholine-induced relaxation by L-NAME. The contractile responses to extracellular CaCl2 (1-10 mM) were increased in L-NAME group, and co-treatment with DL-propranolol reduced this response in both preparations in most Ca2+ concentrations used. The NO2/NO3 plasma levels and superoxide dismutase (SOD) activity were reduced in L-NAME-treated rats, both of which were significantly prevented by DL-propranolol. In conclusion, propranolol-induced amplification of the relaxation to acetylcholine in mesenteric arteries from L-NAME-treated rats is sensitive to depolarization. Additional mechanisms involving blockade of Ca2+ entry in the vascular smooth muscle and increase in NO bioavailability contributes to beneficial effects of long-term propranolol treatment.

Authors+Show Affiliations

Department of Pharmacology, Faculty of Medical Sciences, State University of Campinas, P.O. Box 6111, 13084-971, Campinas, São Paulo, Brazil.No 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

17610863

Citation

Priviero, Fernanda B M., et al. "Vascular Effects of Long-term Propranolol Administration After Chronic Nitric Oxide Blockade." European Journal of Pharmacology, vol. 571, no. 2-3, 2007, pp. 189-96.
Priviero FB, Teixeira CE, Claudino MA, et al. Vascular effects of long-term propranolol administration after chronic nitric oxide blockade. Eur J Pharmacol. 2007;571(2-3):189-96.
Priviero, F. B., Teixeira, C. E., Claudino, M. A., De Nucci, G., Zanesco, A., & Antunes, E. (2007). Vascular effects of long-term propranolol administration after chronic nitric oxide blockade. European Journal of Pharmacology, 571(2-3), 189-96.
Priviero FB, et al. Vascular Effects of Long-term Propranolol Administration After Chronic Nitric Oxide Blockade. Eur J Pharmacol. 2007 Oct 1;571(2-3):189-96. PubMed PMID: 17610863.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vascular effects of long-term propranolol administration after chronic nitric oxide blockade. AU - Priviero,Fernanda B M, AU - Teixeira,Cleber E, AU - Claudino,Mário A, AU - De Nucci,Gilberto, AU - Zanesco,Angelina, AU - Antunes,Edson, Y1 - 2007/06/13/ PY - 2006/12/14/received PY - 2007/05/22/revised PY - 2007/05/24/accepted PY - 2007/7/6/pubmed PY - 2007/10/27/medline PY - 2007/7/6/entrez SP - 189 EP - 96 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 571 IS - 2-3 N2 - Long-term propranolol treatment reduces arterial blood pressure in hypertensive individuals mainly by reducing peripheral vascular resistance, but mechanisms underlying their vasodilatory effect remain poorly investigated. This study aimed to investigate whether long-term propranolol administration ameliorates the impairment of relaxing responses of aorta and mesenteric artery from rats made hypertensive by chronic nitric oxide (NO) deficiency, and underlying mechanisms mediating this phenomenon. Male Wistar rats were treated with N(omega)-Nitro-L-arginine methyl ester (L-NAME; 20 mg/rat/day) for four weeks. DL-Propranolol (30 mg/rat/day) was given concomitantly to L-NAME in the drinking water. Treatment with L-NAME markedly increased blood pressure, an effect largely attenuated by DL-propranolol. In phenylephrine-precontracted aortic rings, the reduction of relaxing responses for acetylcholine (0.001-10 microM) in L-NAME group was not modified by DL-propranolol, whereas in mesenteric rings the impairment of acetylcholine-induced relaxation by L-NAME was significantly attenuated by DL-propranolol. In mesenteric rings precontracted with KCl (80 mM), DL-propranolol failed to attenuate the impairment of acetylcholine-induced relaxation by L-NAME. The contractile responses to extracellular CaCl2 (1-10 mM) were increased in L-NAME group, and co-treatment with DL-propranolol reduced this response in both preparations in most Ca2+ concentrations used. The NO2/NO3 plasma levels and superoxide dismutase (SOD) activity were reduced in L-NAME-treated rats, both of which were significantly prevented by DL-propranolol. In conclusion, propranolol-induced amplification of the relaxation to acetylcholine in mesenteric arteries from L-NAME-treated rats is sensitive to depolarization. Additional mechanisms involving blockade of Ca2+ entry in the vascular smooth muscle and increase in NO bioavailability contributes to beneficial effects of long-term propranolol treatment. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/17610863/Vascular_effects_of_long_term_propranolol_administration_after_chronic_nitric_oxide_blockade_ DB - PRIME DP - Unbound Medicine ER -