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 anesthetized rabbits, the femoral vein just below the Poupart’s ligand was clamped for 20 sec., followed by a release. In controls, after clamping, an immediate slight constriction was monitored by an echo-tracking device. This constriction became more prominent after releasing the clamping, then returned to the pre-clamping value. In another group of animals, 4 mg/kg pyrilamine, a specific H1-histamine receptor blocker was injected into the marginal ear vein. This induced an initial dilation of the femoral vein, which then returned to the control value. When clamping, the femoral vein was not constricted, but dilated and this venodilation became pronounced after the release of the clamp (Fig. 8).
Affiliation: Department of Surgery, Institute of Vascular Surgery, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.