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.Importantly, transient clamping of the femoral vein in animals caused a short-term constriction, which was inhibited by H(1) -histamine receptor antagonist in vivo.Furthermore, a significantly greater histamine immunopositivity was detected in veins after stretching compared to the resting state.
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: For investigating the role of the possible implication of Ca2+ sensitization pathways, we studied the action of various protein kinases previously known to be involved in Ca2+ sensitization process. Thus the effects of inhibitors of ρ kinase, protein kinase C, MAPK and tyrosine kinase were investigated. ρ kinase inhibitors (50 μM HA-1077 or Y-27632 10 μM) all virtually completely inhibited the histamine-induced force generation in both saphenous vein and inferior vena cava ring preparations (Figs 6–7). Tyrosine phosphorylation was studied by application of genistein 50 μM. Strong difference was observed between the two types of vessels in the genistein-induced inhibition of histamine contraction. In saphenous veins, genistein induced a 43% inhibition, whereas it was practically ineffective in inferior vena cava indicating the diverse implication of tyrosine phosphorylation in histamine’s actions in the above vessels. The inhibition of protein kinase C by calphostin 0.2 μM or inhibition of MAPK by PD-098059 10 μM did not influence significantly the development of force in both saphenous veins and the inferior vena cava (data not shown).
Affiliation: Department of Surgery, Institute of Vascular Surgery, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.