R-(−)-α-methyl-histamine has nitric oxide-mediated vasodilator activity in the mesenteric vascular bed of the cat

Champion, Hunter C.; Kadowitz, Philip J.

doi:10.1016/s0014-2999(97)01525-2

Cited by 8 publications

(8 citation statements)

References 28 publications

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“…1,3,30) Histamine H 3 receptor-mediated vasodilation has also been reported in the endothelium-dependent rabbit mid- dle cerebral artery, 19,20) the hindlimb vascular bed 22) and the mesenteric vascular bed of the cat. 23) Taken together, the present findings suggest that a-methylhistamine induces endothelium-dependent vasodilation, which is mediated by histamine H 3 receptors located on the endothelium of the rat mesenteric resistance artery. However, since the histamine H 1 receptor antagonist significantly inhibited the response to the highest concentration of a-methylhistamine, a-methylhistamine at higher concentrations of more than 100 mM has histamine H 1 receptor-agonistic activity.…”

Section: Discussionsupporting

confidence: 67%

“…These findings are in line with the observations of other reports. 20,23) Additionally, the present study showed that indomethacin caused partial inhibition of vasodilator responses to a-methylhistamine, which was smaller than that of L-NAME, implicating that a-methylhistamine induces the release of relaxing factors, probably PGI 2 , a metabolite of arachidonic acid, via cyclooxygenase in the endothelium of the rat mesenteric resistance artery. A similar finding has been reported by Ea Kim et al 19,20) In their reports, the H 3 receptors have been shown to relax rabbit middle cerebral artery via an endothelium-dependent mechanism involving both nitric oxide and prostanoid release.…”

Section: )mentioning

confidence: 45%

“…To remove the vascular endothelium, preparations with resting tone were perfused with a 1.80 mg/ml solution of sodium deoxycholate (Sigma Aldrich Japan Co., Tokyo, Japan) in saline for 30 s. This caused a transient increase (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) in perfusion pressure. Then, the preparations were rinsed with sodium deoxycholate-free Krebs solution for 40 min.…”

Section: Chemical Removal Of Vascular Endotheliummentioning

confidence: 99%

“…Evidence has accumulated that NO, PGI 2 and/or EDHFs play a prominent role in the tone control of the endothelium contact arteries. [19][20][21][22][23] Therefore, the purpose of the present study was to investigate the vascular responses mediated by histamine H 3 receptors using a-methylhistamine and the underlying mechanisms in the mesenteric vascular bed of the rat. …”

mentioning

confidence: 99%

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R-(-)-.ALPHA.-Methylhistamine, a Histamine H3 Receptor Agonist, Induces Endothelium-Dependent Vasodilation in Rat Mesenteric Resistance Arteries

Sun

Jin

Koyama

et al. 2010

Biological & Pharmaceutical Bulletin

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The histamine H 3 receptor, a novel histamine receptor subtype, has been identified in rat brain cortical slices and shown to inhibit histamine release 1,2) in the brain and several peripheral tissues.3,4) Inhibitory presynaptic histamine H 3 receptors have also been found on non-histaminergic nerves including cholinergic, 5) adrenergic 6,7) and non-adrenergic noncholinergic nerves. 8) Characterization of histamine H 3 receptor-mediated responses has been greatly facilitated by the development of selective histamine H 3 receptor agonists such as R-(Ϫ)-a methylhistamine (a-methylhistamine), 2,9,10) and antagonists such as thioperamide 2,9) and clobenpropit. 11,12) Various physiological responses to a-methylhistamine, a potent and selective histamine H 3 receptor agonist, have been shown to be reduced by the histamine H 3 receptor antagonists thioperamide and clobenpropit, but not by histamine H 1 or H 2 receptor antagonists. 3,[5][6][7]13) It also has been reported that intravenous administration of a-methylhistamine causes a decrease in systemic blood pressure in the rat and that responses are blocked by histamine H 1 receptor antagonists, but not by histamine H 2 or H 3 receptor antagonists.14) However, the mechanisms of histamine H 3 receptor-mediated vascular relaxant effects induced by a-methylhistamine remain unclear.It is widely accepted that the endothelium at the luminal surface of blood vessels is an important regulator of vascular tone via release of various endothelium-derived endogenous substances, such as relaxing factors (EDRFs) and contracting factors (EDCFs). [15][16][17][18] EDRFs and EDCFs include nitric oxide (NO), prostaglandin I 2 (PGI 2 ), endothelium-derived hyperpolarizing factors (EDHFs) and endothelin, prostaglandin F 2a , thromboxane A 2 , respectively. Evidence has accumulated that NO, PGI 2 and/or EDHFs play a prominent role in the tone control of the endothelium contact arteries. [19][20][21][22][23] Therefore, the purpose of the present study was to investigate the vascular responses mediated by histamine H 3 receptors using a-methylhistamine and the underlying mechanisms in the mesenteric vascular bed of the rat. MATERIALS AND METHODS AnimalsMale Wistar rats weighing 220-350 g were used in the present study. The animals were given food and water ad libitum. They were housed in the Animal Research Center of Okayama University at a controlled ambient temperature of 22Ϯ2°C with 50Ϯ10% relative humidity and with a 12-h light/12-h dark cycle (lights on at 8:00 a.m.). This study was carried out in accordance with the Guidelines for Animal Experiments at Okayama University Advanced Science Research Center, Japanese Government Animal Protection and Management Law (No. 105), and Japanese Government Notification on Feeding and Safekeeping of Animals (No. 6). Every effort was made to minimize the number of animals used and their suffering. Perfusion of Mesenteric Vascular BedsThe animals were anesthetized with pentobarbital-Na (50 mg/kg, intraperitoneally) and mesenteric vascular beds were i...

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Section: Discussionsupporting

confidence: 67%

Section: )mentioning

confidence: 45%

Section: Chemical Removal Of Vascular Endotheliummentioning

confidence: 99%

mentioning

confidence: 99%

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R-(-)-.ALPHA.-Methylhistamine, a Histamine H3 Receptor Agonist, Induces Endothelium-Dependent Vasodilation in Rat Mesenteric Resistance Arteries

Sun

Jin

Koyama

et al. 2010

Biological & Pharmaceutical Bulletin

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“…Vasodilators are the only class of drugs commonly employed in the therapy of heart failure that have been shown to reduce mortality in this syndrome. Hydralazine, minoxidil, sodium nitroprusside, diazoxide and calcium channel blockers are the compounds used for vasodilatation with different modes of actions [1][2][3][4][5]. In the present study, we synthesized a new isoquinolinone derivative, i.e.…”

Section: Introductionmentioning

confidence: 99%

A New Isoquinolinone Derivative with Noble Vasorelaxation Activity

Lin¹,

Lin

Lin³

et al. 2003

Pharmacology

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The pharmacological effects of BDPBI (7-bromo-1,4-dihydro-2-phenyl-4,4-bis(4-pyridinylmethyl)2H-isoquinolin-3-one dihydrochloride) were tested on isolated endothelium-containing or denuded aorta of the guinea pig. BDPBI with the formula C₂₇H₂₄BrCl₂N₃O was synthesized starting with 3-isochromanone. In the endothelium-containing preparations of the aortic rings, phenylephrine (PHE; 10 µmol/l) elicited contracture and acetylcholine (ACh; 10 µmol/l) or BDPBI (0.01–10 µmol/l) elicited relaxation effects on the PHE-precontracted preparations. The BDPBI-elicited effect on the PHE-precontracted aortic rings was not altered in the presence of adrenergic blockers (propranolol or yohimbine; 1 µmol/l) or pretreated preparations with aspirin, indomethacin (10 µmol/l) or L-NAME (1 mmol/l). However, the relaxation effects of BDPBI were blocked if the preparations were pretreated with diphenhydramine (10 µmol/l) or chloropheniramine maleate (10 µmol/l). In contrast to lower concentrations of atropine (1 µmol/l), higher concentrations of atropine (30 µmol/l) did block the effects of BDPBI on the PHE-precontracted aortic rings. HTMT dimaleate (0.01–10 µmol/l), a histamine H₁ receptor agonist, also elicited relaxation effects on the PHE-precontracted preparation, and the effects were blocked if the preparations were pretreated with diphenhydramine or chloropheniramine maleate. On isolated denuded aorta of the guinea pig, BDPBI did not elicit relaxation effects on the PHE-precontracted aortic rings. These results demonstrated that the vasorelaxation effect of BDPBI on PHE-precontracted aortic rings is partly dependent on the activation of a histaminergic receptor from the vascular endothelium. We suggested that BDPBI would be an effective vasorelaxant for cardiovascular systems.

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Regulation of the Cardiovascular System by Histamine

Hattori

Matsuda

2016

Handbook of Experimental Pharmacology

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Histamine mediates a wide range of cellular responses, including allergic and inflammatory reactions, gastric acid secretion, and neurotransmission in the central nervous system. Histamine also exerts a series of actions upon the cardiovascular system but may not normally play a significant role in regulating cardiovascular function. During tissue injury, inflammation, and allergic responses, mast cells (or non-mast cells) within the tissues can release large amounts of histamine that leads to noticeable cardiovascular effects. Owing to intensive research during several decades, the distribution, function, and pathophysiological role of cardiovascular H- and H-receptors has become recognized adequately. Besides the recognized H- and H-receptor-mediated cardiovascular responses, novel roles of H- and H-receptors in cardiovascular physiology and pathophysiology have been identified over the last decade. In this review, we describe recent advances in our understanding of cardiovascular function and dysfunction mediated by histamine receptors, including H- and H-receptors, their potential mechanisms of action, and their pathological significance.

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R-(−)-α-methyl-histamine has nitric oxide-mediated vasodilator activity in the mesenteric vascular bed of the cat

Cited by 8 publications

References 28 publications

R-(-)-.ALPHA.-Methylhistamine, a Histamine H3 Receptor Agonist, Induces Endothelium-Dependent Vasodilation in Rat Mesenteric Resistance Arteries

R-(-)-.ALPHA.-Methylhistamine, a Histamine H3 Receptor Agonist, Induces Endothelium-Dependent Vasodilation in Rat Mesenteric Resistance Arteries

A New Isoquinolinone Derivative with Noble Vasorelaxation Activity

Regulation of the Cardiovascular System by Histamine

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