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Triphasic vascular responses to bradykinin in the mesenteric resistance artery of the rat.
Eur J Pharmacol. 2001 Dec 14; 433(1):105-13.EJ

Abstract

The vascular effects of bradykinin were studied in rat perfused mesenteric vascular beds with active tone. Bolus injections of bradykinin (1-1000 pmol) but not des-Arg(9)-bradykinin (bradykinin B(1) receptor agonist) induced triphasic vascular responses: the initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. The triphasic vascular responses to bradykinin were abolished by FR 172357 (3-bromo-8-[2,6-dichloro-3-[N-[(E)-4-(N,N-dimethylcarbamoyl) cinnamidoacetyl]-N-methylamino]benzyloxy]-2-metylimidazo[1,2-a]pyridine) (bradykinin B(2) receptor antagonist, 0.1 microM). Endothelium removal with sodium deoxycholate and N(w)-nitro-L-arginine (300 microM) abolished the bradykinin-induced initial sharp vasodilation. Indomethacin (0.5 microM) and seratrodast (thromboxane A(2) receptor antagonist, 0.5 and 5 microM) abolished the bradykinin-induced second vasoconstriction. The bradykinin-induced third vasodilation was abolished by capsaicin (1 microM) and calcitonin gene-related peptide (CGRP)-(8-37) (CGRP receptor antagonist, 0.5 microM). These findings suggest that the bradykinin-induced initial sharp vasodilation is endothelium dependent, that endogenous thromboxane A(2) is involved in the second vasoconstriction, and that the third slow vasodilation is produced by activation of capsaicin-sensitive CGRP-containing nerves.

Authors+Show Affiliations

Department of Clinical Pharmaceutical Science, Graduate School of Natural Science and Technology, Okayama University, 1-1-1 Tsushima-naka, Okayama 700-8530, Japan.No 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

11755140

Citation

Nawa, H, et al. "Triphasic Vascular Responses to Bradykinin in the Mesenteric Resistance Artery of the Rat." European Journal of Pharmacology, vol. 433, no. 1, 2001, pp. 105-13.
Nawa H, Kawasaki H, Nakatsuma A, et al. Triphasic vascular responses to bradykinin in the mesenteric resistance artery of the rat. Eur J Pharmacol. 2001;433(1):105-13.
Nawa, H., Kawasaki, H., Nakatsuma, A., Isobe, S., & Kurosaki, Y. (2001). Triphasic vascular responses to bradykinin in the mesenteric resistance artery of the rat. European Journal of Pharmacology, 433(1), 105-13.
Nawa H, et al. Triphasic Vascular Responses to Bradykinin in the Mesenteric Resistance Artery of the Rat. Eur J Pharmacol. 2001 Dec 14;433(1):105-13. PubMed PMID: 11755140.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Triphasic vascular responses to bradykinin in the mesenteric resistance artery of the rat. AU - Nawa,H, AU - Kawasaki,H, AU - Nakatsuma,A, AU - Isobe,S, AU - Kurosaki,Y, PY - 2002/1/5/pubmed PY - 2002/7/26/medline PY - 2002/1/5/entrez SP - 105 EP - 13 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 433 IS - 1 N2 - The vascular effects of bradykinin were studied in rat perfused mesenteric vascular beds with active tone. Bolus injections of bradykinin (1-1000 pmol) but not des-Arg(9)-bradykinin (bradykinin B(1) receptor agonist) induced triphasic vascular responses: the initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. The triphasic vascular responses to bradykinin were abolished by FR 172357 (3-bromo-8-[2,6-dichloro-3-[N-[(E)-4-(N,N-dimethylcarbamoyl) cinnamidoacetyl]-N-methylamino]benzyloxy]-2-metylimidazo[1,2-a]pyridine) (bradykinin B(2) receptor antagonist, 0.1 microM). Endothelium removal with sodium deoxycholate and N(w)-nitro-L-arginine (300 microM) abolished the bradykinin-induced initial sharp vasodilation. Indomethacin (0.5 microM) and seratrodast (thromboxane A(2) receptor antagonist, 0.5 and 5 microM) abolished the bradykinin-induced second vasoconstriction. The bradykinin-induced third vasodilation was abolished by capsaicin (1 microM) and calcitonin gene-related peptide (CGRP)-(8-37) (CGRP receptor antagonist, 0.5 microM). These findings suggest that the bradykinin-induced initial sharp vasodilation is endothelium dependent, that endogenous thromboxane A(2) is involved in the second vasoconstriction, and that the third slow vasodilation is produced by activation of capsaicin-sensitive CGRP-containing nerves. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/11755140/Triphasic_vascular_responses_to_bradykinin_in_the_mesenteric_resistance_artery_of_the_rat_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(01)01513-8 DB - PRIME DP - Unbound Medicine ER -