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      Differential Distribution of Mechanosensitive Nonselective Cation Channels in Systemic and Pulmonary Arterial Myocytes of Rabbits

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          The mechanosensitive nonselective cation channel (NSC<sub>MS</sub>) is a key player in vascular myogenic contraction. The functional channel density and pressure sensitivity of NSC<sub>MS</sub> in vascular myocytes were compared between pulmonary and systemic arteries (coronary, mesenteric and cerebral arteries) in the rabbit. In cell-attached condition, a negative pressure via patch pipettes commonly activated NSC<sub>MS</sub> with weak voltage dependence. The threshold pressure for activation was lower, and the density of NSC<sub>MS</sub> was higher in the pulmonary than the systemic arteries. When the pulmonary arteries were divided into small-diameter (outer diameter, OD < 0.5 mm) and large-diameter (OD > 1.5 mm) arteries, the low threshold and high density of NSC<sub>MS</sub> were observed only in small-diameter ones. No such difference was observed between the small- and large-diameter coronary arteries. The higher stretch sensitivity and denser functional expression of NSC<sub>MS</sub> in small pulmonary arteries might suggest an adaptive tuning for the relatively low pulmonary blood pressure in vivo.

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          Pressure-induced actin polymerization in vascular smooth muscle as a mechanism underlying myogenic behavior.

          We hypothesize that actin polymerization within vascular smooth muscle (VSM) in response to increased intravascular pressure is a novel and previously unrecognized mechanism underlying arterial myogenic behavior. This hypothesis is based on the following observations. 1) Unlike skeletal or cardiac muscle, VSM contains a substantial pool of unpolymerized globular (G) actin whose function is not known. 2) The cytosolic concentration of G-actin is significantly reduced by an elevation in intravascular pressure, demonstrating the dynamic nature of actin within VSM and implying a shift in the F:G equilibrium in favor of F-actin. 3) Agents that inhibit actin polymerization and stabilize the cytoskeleton (cytochalasins and latrunculin) inhibit the development of myogenic tone and decrease the effectiveness of myogenic reactivity. 4) Depolymerization of F-actin with cytochalasin D causes VSM relaxation and increased G-actin content, whereas polymerization of F-actin with jasplakinolide causes VSM contraction and decreased G-actin content. These results are consistent with observations in other cell types in which actin dynamics have been implicated in contractility and/or motility. Actin filament formation in VSM may therefore underlie mechanotransduction and, by providing additional sites for interaction with myosin, enhance force production in response to pressure. Although the mechanism by which actin polymerization is stimulated by pressure is not known, it likely occurs via integrin-mediated activation of signal transduction pathways previously associated with VSM contraction (e.g., PKC activation, Rho A, and tyrosine phosphorylation).
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            Swelling-activated cation channels mediate depolarization of rat cerebrovascular smooth muscle by hyposmolarity and intravascular pressure.

            1. Increases in intravascular pressure depolarize vascular smooth muscle cells. Based on the attenuating effects of Cl- channel antagonists, it has been suggested that swelling-activated Cl- channels may be integral to this response. Consequently, this study tested for the presence of a swelling-activated Cl- conductance in both intact rat cerebral arteries and isolated rat smooth muscle cells. 2. A 50 mosmol l-1 hyposmotic challenge (300 to 250 mosmol l-1) constricted rat cerebral arteries. This constriction contained all the salient features of a pressure-induced response including smooth muscle cell depolarization and a rise in intracellular Ca2+ that was blocked by voltage-operated Ca2+ channel antagonists. The hyposmotically induced depolarization was attenuated by DIDS (300 microM) and tamoxifen (1 microM), a response consistent with the presence of a swelling-activated Cl- conductance. 3. A swelling-activated current was identified in cerebral vascular smooth muscle cells. This current was sensitive to Cl- channel antagonists including DIDS (300 microM), tamoxifen (1 microM) and IAA-94 (100 microM). However, contrary to expectations, the reversal potential of this swelling-activated current shifted with the Na+ equilibrium potential and not the Cl- equilibrium potential, indicating that the swelling-activated current was carried by cations and not anions. The swelling-activated cation current was blocked by Gd3+, a cation channel antagonist. 4. Gd3+ also blocked both swelling- and pressure-induced depolarization of smooth muscle cells in intact cerebral arteries. 5. These findings suggest that swelling- and pressure-induced depolarization arise from the activation of a cation conductance. This current is inhibited by DIDS, tamoxifen, IAA-94 and gadolinium.
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              Lipid and mechano-gated 2P domain K+ channels


                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                July 2006
                28 July 2006
                : 43
                : 4
                : 347-354
                Department of Physiology and Biophysics, Seoul National University College of Medicine, Seoul, Korea
                93607 J Vasc Res 2006;43:347–354
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 4, References: 16, Pages: 8
                Research Paper


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