(Vladimir V. Matchkov, Ph.D, DMSc, Associate Professor, Department of Biomedicine, Aarhus University)
(Mechanisms behind the modulatory role of ?2-Na,K-ATPase in the wall of small arteries).
Лекция состоится в ауд. 343, начало в 11-00 (язык – русский).
Annotation. The Na,K-ATPase is essential for maintaining the transmembrane ion gradients required for normal cell function. Previous studies clearly indicate that a specific Na,K-ATPase inhibitor, ouabain can initiate Src kinase signaling independently of the effects on Na,K-ATPase mediated ion translocation. This Na,K-ATPase-Src signaling has been shown in the kidney and heart, and seems perfectly suited for modulation of vasoconstriction, but has never been studied in smooth muscle cells.
Several findings indirectly suggest the importance of Na,K-ATPase-Src complex for vascular remodeling and elevated contraction in resistance arteries in ouabain-induced and other forms of hypertension. Familial hemiplegic migraine type 2 (FHM2), associated with the loss-of-function mutation in the Na,K-ATPase, is characterized by elevated vascular contractility which might depend on Src activation.
We have shown that the Na,K-ATPase-dependent Src activation could increase arterial contraction via sensitization of the contractile machinery to intracellular Ca2+, modulation of gene expression and smooth muscle cell phenotype. The novel signaling pathway initiated from the Na,K-ATPase in the vascular wall could be of substantial physiological significance and increase our understanding of the mechanisms of hypertension and provide a new anti-hypertensive target.
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