Characterization of Histamine H1 and H2 Receptors in the Rabbit Isolated Ovarian Artery and Vein

Ma, Oriowo; Ja, Bevan

doi:10.1097/00005344-198707000-00011

Cited by 9 publications

(2 citation statements)

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“…However, to the best of our knowledge, there are no convincing experimental data for the role of these substances -with the exception of adrenergic neurotransmitters -in the involvement of physiology and pathophysiology of venous return [2,31]. Vasoactivity of histamine is also well known, and it is described that this autacoid has a prominent action not only in arteries, but in veins as well [32][33][34][35][36][37][38][39][40].…”

Section: Introductionmentioning

confidence: 99%

Histamine and H1-histamine receptors faster venous circulation

Galajda

Balla

Szentmiklósi

et al. 2011

Journal of Cellular and Molecular Medicine

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The study has analysed the action of histamine in the rabbit venous system and evaluated its potential role in contraction during increased venous pressure. We have found that a great variety exists in histamine sensitivity and H1-histamine receptor expression in various types of rabbit veins. Veins of the extremities (saphenous vein, femoral vein, axillary vein) and abdomen (common iliac vein, inferior vena cava) responded to histamine by a prominent, concentration-dependent force generation, whereas great thoracic veins (subclavian vein, superior vena cavas, intrathoracic part of inferior vena cava) and a pelvic vein (external iliac vein) exhibited slight sensitivity to exogenous histamine. The lack of reactivity to histamine was not due to increased activity of nitric oxide synthase (NOS) or heme oxygenase-1. H1-histamine receptor expression of veins correlated well with the histamine-induced contractions. Voltage-dependent calcium channels mediated mainly the histamine-induced force generation of saphenous vein, whereas it did not act in the inferior vena cava. In contrast, the receptor-operated channels were not involved in this response in either vein. Tyrosine phosphorylation occurred markedly in response to histamine in the saphenous vein, but not in the inferior vena cava. Histamine induced a prominent ρ kinase activation in both vessels. Protein kinase C and mitogen-activated protein kinase (MAPK) were not implicated in the histamine-induced intracellular calcium sensitization. Importantly, transient clamping of the femoral vein in animals caused a short-term constriction, which was inhibited by H1-histamine receptor antagonist in vivo. Furthermore, a significantly greater histamine immunopositivity was detected in veins after stretching compared to the resting state. We conclude that histamine receptor density adapts to the actual requirements of the circulation, and histamine liberated by the venous wall during increased venous pressure contributes to the contraction of vessels, providing a force for the venous return.

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Section: Introductionmentioning

confidence: 99%

Histamine and H1-histamine receptors faster venous circulation

Galajda

Balla

Szentmiklósi

et al. 2011

Journal of Cellular and Molecular Medicine

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“…In many in vivo studies, histamine readily causes a vasodilatation mediated by either histamine H 1 or H 2 receptors of peripheral resistance vessels (Levi et al, 1982;Marshall, 1984). On the other hand, in many in vitro investigations, histamine causes a vasoconstriction via histamine H 1 receptors and a vasodilatation via H 2 receptors (Levi et al, 1982;Oriowo & Bevan, 1987). As recently reviewed, histamine H 1 and H 2 receptors on vascular smooth muscle generally cause direct constriction and dilatation, respectively, whereas endothelial histamine H 1 receptors promote a vasorelaxation via a release of endothelium-derived relaxing factors (Levi, Rubin & Gross, 1991).…”

Section: Introductionmentioning

confidence: 99%

Endothelium‐dependent vasodilatation mechanisms by histamine in simian but not in canine femoral arterial branches

Arai

Chiba

1999

Journal of Autonomic Pharmacology

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1. The vascular response of isolated, perfused canine and simian femoral arteries, which distribute blood to deep skeletal muscles, were investigated. 2. The vascular responses to histamine, 2-pyridylethylamine (2-PEA), dimaprit and alpha-methylhistamine were pharmacologically analyzed in canine and simian vessels, using diphenhydramine (DPH, a histamine H1 receptor antagonist), cimetidine (a histamine H2 antagonist) and saponin which readily removed the endothelium. 3. In canine arteries, alpha-methylhistamine showed no vascular response, but in simian preparations, it caused a slight vasoconstriction. 4. In canine arteries, histamine and 2-PEA consistently induced a vasoconstriction in preconstricted and non-preconstricted preparations. However, in simian arteries histamine usually produced a vasodilatation at small doses (less than 10(-7) mol) and a vasoconstriction at large doses in preconstricted preparations. 5. Vasoconstrictor responses to histamine and 2-PEA were significantly inhibited by DPH in both species. In simian vessels, histamine- and dimaprit-induced vasodilatations were significantly inhibited by cimetidine. 6. After removal of the endothelium by intraluminal treatment with saponin in canine femoral arteries, the vascular responses to histamine, 2-PEA and dimaprit were not significantly affected. On the other hand, in simian femoral arteries, the vasodilatation responses to histamine and 2-PEA were significantly depressed by the removal of endothelium. 7. It is concluded that (1) in both simian and canine femoral arterial branches, there are abundant histamine H1 and H2 receptors (2) in simian but not in canine arteries, there exist histamine H3 receptors, although their role is not clear (3) histamine induces a vasoconstriction mediated via histamine H1 receptors and a vasodilatation via H2 receptors which exist in vascular smooth muscle, and (4) in simian but not in canine arteries, there are endothelium-dependent vasodilatation mechanisms.

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A basic molecular model for the H2 histamine receptor. Part 1

Olea‐Azar

Parra-Mouchet

Cassels

et al. 1996

Mol Eng

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A 3D model of the canine H2 receptor was built and analysed. This model was constructed using primary sequence comparisons and three-dimensional homology building with bacteriorhodopsin serving as a template. The energy analysis of the interaction between the N3H+ form and the NlH+ form of histamine with the receptor shows that both have the same binding affinity for the H2 receptor, but only the N3H+ form provokes structural changes. The calculated potential energies are consistent with the published binding data and suggest that Asp 98 is the principal residue for ligand recognition. On the basis of sequence alignment studies we postulate that Glu 270 in helix 7 may be important for activation of the H2 receptor. Docking studies of the N3H+ folded conformation in our model show that an intramolecular hydrogen bond between N3 and the amino group of the histamine molecule is broken, and the histamine then adopts a conformation similar to the N3H+ extended form to interact optimally with the H2 receptor. Mutations were made in the H2 receptor model to mimic published experimental point mutations. The interactions of the mutated receptor models with histamine are consistent with the experimental data.

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Characterization of Histamine H1 and H2 Receptors in the Rabbit Isolated Ovarian Artery and Vein

Cited by 9 publications

References 0 publications

Histamine and H1-histamine receptors faster venous circulation

Histamine and H1-histamine receptors faster venous circulation

Endothelium‐dependent vasodilatation mechanisms by histamine in simian but not in canine femoral arterial branches

A basic molecular model for the H2 histamine receptor. Part 1

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