作者: Joanne M. Doughty , Alastair L. Miller , Philip D. Langton
DOI: 10.1111/J.1469-7793.1998.433BT.X
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摘要: Resistance arteries respond to increases in transmural pressure by actively contracting, thus maintaining a constant blood flow an organ despite changes pressure. This mechanism, termed the myogenic response, was first described early years of century (Bayliss, 1902). In pressurized vessels, response is strongly temperature dependent, that it absent at room (18–21°C). At 37°C, pressure-dependent membrane depolarization from approximately -65 -40 mV associated with has been observed renal and cerebral (Harder, 1984; Harder, Gilbert & Lombard, 1987). sufficient increase significantly open probability (Po) dihydropyridine (DHP)-sensitive calcium channels, leading calcium-dependent contraction. However, ionic mechanism underlying this poorly understood. Evidence chloride channels are present smooth muscle (e.g. Pacaud, Loirand, Baron, Mironneau Mironneau, 1991; Large Wang, 1996), combined estimated reversal potential for -20 -30 (Aickin, 1990) makes conductance obvious candidate mediating pressure-induced depolarization. Indeed, channel blockers have demonstrated inhibit (Nelson, Conway, Knot Brayden, 1997). paper evidence presented some not selective isolated resistance arteries, effects on may be, least part, due block channels. Thus, should be used caution evaluating possible function response.