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Articles in PresS, published online ahead of print August 29, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00549.2002
Submitted on July 2, 2002
Accepted on August 19, 2002
1 Institute of Physiology, University of Rostock, Rostock, Germany
2 Department of Pathophysiology, Moscow State University, Moscow, Russian Federation
* To whom correspondence should be addressed. E-mail: rudolf.schubert{at}medizin.uni-rostock.de.
The hypothesis that Rho-kinase is involved in myogenic reactivity was investigated in pressurized rat tail small arteries using videomicroscopic diameter determination and calcium fluorimetry. The potent Rho-kinase inhibitor, Y-27632, reversibly increased vessel diameter at 80 mmHg without changing the intracellular calcium concentration ([Ca]i) shifting the relationship between diameter change and [Ca]i to higher calcium levels. Neither endothelium removal nor inhibition of neural transmission affected the Y-27632-induced effect. Y-27632 at 3*10-6 mol l-1 attenuated the myogenic response in the pressure range from 10 to 120 mmHg shifting the relationship between vessel tone and [Ca]i to higher calcium levels. In addition, the Y-27632-induced shift of the relationship between vessel tone and [Ca]i was larger at 80 than at 10 mmHg. These results suggest that smooth muscle cell Rho-kinase in rat tail small arteries 1) is in an active state partly determining the level of the myogenic tone, and 2) alters the strength of the myogenic response by changing calcium sensitivity, probably caused by the pressure-induced activation of the kinase.
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