Histamine and H1 -histamine receptors faster venous circulation.
Bottom Line: Voltage-dependent calcium channels mediated mainly the histamine-induced force generation of saphenous vein, whereas it did not act in the inferior vena cava.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.
Affiliation: Department of Surgery, Institute of Vascular Surgery, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.Show MeSH
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Mentions: In these experiments, the signalling of two high histamine-sensitive veins (saphenous vein, inferior vena cava) was compared. The possible role of membrane calcium channels (voltage-dependent calcium channels [VOC] and receptor-operated channels [ROC]), intracellular calcium stores and enzymes involved in calcium sensitization (ρ-kinase, tyrosine kinase, MAPK, protein kinase C) were studied. In saphenous vein, experiments with nifedipine and SKF-96365 demonstrated that histamine activates mainly VOC, whereas the role of ROC is negligible. In the inferior vena cava, the roles of both types of calcium channels are minor in mechanical activity induced by histamine (Fig. 5).
Affiliation: Department of Surgery, Institute of Vascular Surgery, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.