DIVERGENT EFFECTS OF ACUTE AND CHRONIC ETHANOL EXPOSURE ON CONTRACTION AND CA2+ MOBILIZATION IN CULTURED VASCULAR SMOOTH-MUSCLE CELLS

被引：12

作者：

BRINER, VA ^{[1
]}

TSAI, P ^{[1
]}

WANG, XN ^{[1
]}

SCHRIER, RW ^{[1
]}

机构：

[1] UNIV COLORADO,SCH MED,DEPT MED,C281,4200 E 9TH AVE,DENVER,CO 80262

来源：

AMERICAN JOURNAL OF HYPERTENSION | 1993年 / 6卷 / 04期

关键词：

ETHANOL; VASCULAR SMOOTH MUSCLE CELL; CA2+ MOBILIZATION;

D O I：

10.1093/ajh/6.4.268

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

In cultured rat vascular smooth muscle cells (VSMC), acute preincubation of 100 mmol/L ethanol for 30 min attenuated the number of contracting cells in response to (10(-7) mol/L) arginine vasopressin (AVP) (P < .01). In contrast, VSMC cultured chronically for 3 days in medium supplemented with 100 mmol/L ethanol enhanced (10(-7) mol/L) AVP-induced shape change (P < .01). Specific H-3-AVP binding to VSMC after acute or chronic exposure to 100 mmol/L ethanol did not differ from those of control experiments. Acute ethanol pretreatment attenuated basal, 10(-7) mol/L AVP-, 65 mmol/L K+-stimulated Ca2+ uptake, in a dose-dependent manner. In contrast, 100 mmol/L ethanol for 4 days enhanced the (P < .001) AVP- 10(-7) mol/L and (P < .01) 65 mmol/L K+-stimulated Ca-45(2+) uptake. Acute ethanol exposure inhibited and chronic ethanol administration enhanced Ca2+ uptake stimulated by 6 X 10(-7) mol/L Bay K 8644, an activator of voltage-sensitive Ca2+ channels. Nifedipine, a blocker of these Ca2+ channels, diminished AVP-stimulated (P < .02) and K+-induced (P < .001) Ca2+ uptake more potently in VSMC pretreated for 4 days with 100 mmol/L ethanol than in control cells. Acute ethanol preexposure for 30 min attenuated AVP-stimulated inositol trisphosphate (IP3) formation (P < .05) and the rise in cytosolic free Ca2+ ([Ca2+]i) (p < .01) . In contrast, chronic ethanol-treated VSMC enhanced IP, formation (P < .05) and the rise in [Ca2+]i (p < .01) in response to AVP. In conclusion, the inhibitory effect of acute ethanol exposure on AVP-induced contraction in VSMC results from attenuation of receptor- and depolarization-induced transmembrane Ca2+ uptake via voltage-sensitive Ca2+ channels and reduction of post-receptor PI breakdown. In contrast, chronic ethanol exposure increases VSMC contraction in response to AVP by enhancing Ca2+ uptake via voltage-sensitive Ca2+ channels as well as increasing IP3 formation and rise in [Ca2+]i.

引用

页码：268 / 275

页数：8

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