Tags

Type your tag names separated by a space and hit enter

Histamine-induced vasodilation and vasoconstriction in the mesenteric resistance artery of the rat.
Eur J Pharmacol. 2006 Jan 04; 529(1-3):136-44.EJ

Abstract

The present study was designed to examine the vascular response to histamine in rat perfused mesenteric vascular beds with active tone. In preparations with intact endothelium, perfusion of histamine (1 nM-100 microM) produced a concentration-dependent vasodilation. Histamine-induced vasodilation was attenuated by L-NAME (nitric oxide (NO) synthase inhibitor, 100 microM) and olopatadine (histamine H(1) receptor antagonist, 1 microM) but not by lafutidine (histamine H(2) receptor antagonist, 1 microM). Cold-storage denervation (4 degrees C for 72 h) of the preparation with intact endothelium attenuated the histamine-induced vasodilation. In preparations without endothelium, histamine at low concentrations (1-100 nM) produced only a small and rapid vasodilation, whereas histamine at concentrations higher than 1 muM produced triphasic vascular responses: initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. Lafutidine abolished only the histamine-induced initial vasodilation. Olopatadine abolished the histamine-induced second vasoconstriction and third vasodilation. Cold-storage denervation of the denuded preparation abolished the histamine-induced second vasoconstriction and third vasodilation. These findings suggest that histamine induced endothelium-dependent vasodilation via endothelium histamine H(1) receptors and endothelium-independent vasodilation via smooth muscle histamine H(2) receptors. It is also suggested that the histamine-induced endothelium-independent vasoconstriction and vasodilation are mediated by histamine H(1) receptors and perivascular nerves.

Authors+Show Affiliations

Department of Clinical Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 1-1-1 Tsushima-naka, Okayama 700-8530, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16337938

Citation

Jin, Honghua, et al. "Histamine-induced Vasodilation and Vasoconstriction in the Mesenteric Resistance Artery of the Rat." European Journal of Pharmacology, vol. 529, no. 1-3, 2006, pp. 136-44.
Jin H, Koyama T, Hatanaka Y, et al. Histamine-induced vasodilation and vasoconstriction in the mesenteric resistance artery of the rat. Eur J Pharmacol. 2006;529(1-3):136-44.
Jin, H., Koyama, T., Hatanaka, Y., Akiyama, S., Takayama, F., & Kawasaki, H. (2006). Histamine-induced vasodilation and vasoconstriction in the mesenteric resistance artery of the rat. European Journal of Pharmacology, 529(1-3), 136-44.
Jin H, et al. Histamine-induced Vasodilation and Vasoconstriction in the Mesenteric Resistance Artery of the Rat. Eur J Pharmacol. 2006 Jan 4;529(1-3):136-44. PubMed PMID: 16337938.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Histamine-induced vasodilation and vasoconstriction in the mesenteric resistance artery of the rat. AU - Jin,Honghua, AU - Koyama,Toshihiro, AU - Hatanaka,Yukako, AU - Akiyama,Shinji, AU - Takayama,Fusako, AU - Kawasaki,Hiromu, Y1 - 2005/12/09/ PY - 2005/06/16/received PY - 2005/10/21/revised PY - 2005/10/28/accepted PY - 2005/12/13/pubmed PY - 2006/3/10/medline PY - 2005/12/13/entrez SP - 136 EP - 44 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 529 IS - 1-3 N2 - The present study was designed to examine the vascular response to histamine in rat perfused mesenteric vascular beds with active tone. In preparations with intact endothelium, perfusion of histamine (1 nM-100 microM) produced a concentration-dependent vasodilation. Histamine-induced vasodilation was attenuated by L-NAME (nitric oxide (NO) synthase inhibitor, 100 microM) and olopatadine (histamine H(1) receptor antagonist, 1 microM) but not by lafutidine (histamine H(2) receptor antagonist, 1 microM). Cold-storage denervation (4 degrees C for 72 h) of the preparation with intact endothelium attenuated the histamine-induced vasodilation. In preparations without endothelium, histamine at low concentrations (1-100 nM) produced only a small and rapid vasodilation, whereas histamine at concentrations higher than 1 muM produced triphasic vascular responses: initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. Lafutidine abolished only the histamine-induced initial vasodilation. Olopatadine abolished the histamine-induced second vasoconstriction and third vasodilation. Cold-storage denervation of the denuded preparation abolished the histamine-induced second vasoconstriction and third vasodilation. These findings suggest that histamine induced endothelium-dependent vasodilation via endothelium histamine H(1) receptors and endothelium-independent vasodilation via smooth muscle histamine H(2) receptors. It is also suggested that the histamine-induced endothelium-independent vasoconstriction and vasodilation are mediated by histamine H(1) receptors and perivascular nerves. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/16337938/Histamine_induced_vasodilation_and_vasoconstriction_in_the_mesenteric_resistance_artery_of_the_rat_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(05)01126-X DB - PRIME DP - Unbound Medicine ER -