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Articles in PresS, published online ahead of print August 22, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01033.2001
Submitted on November 27, 2001
Accepted on August 13, 2002
1 Department of Physiology, Charles University Second Medical School, Prague, Czech Republic; Centre for Experimental Cardiovascular Research, Prague, Czech Republic
2 Institute for the Care of Mother and Child, Prague, Czech Republic
3 Vascular Biology Group, Cardiology Division, University of Alberta School of Medicine, Edmonton, Alberta, Canada
4 Vascular Biology Group, Cardiology Division, University of Alberta School of Medicine, Edmonton, Alberta, Canada; Physiology Department, University of Alberta, Edmonton, Alberta, Canada
* To whom correspondence should be addressed. E-mail: vaclav.hampl{at}lfmotol.cuni.cz.
Fetal-to-maternal blood flow matching in the placenta, necessary for optimal fetal blood oxygenation, may occur via hypoxic fetoplacental vasoconstriction (HFPV). We hypothesized that HFPV is mediated by potassium (K+) channel inhibition in fetoplacental vascular smooth muscle, as occurs in several other oxygen sensitive tissues. Using an isolated human placental cotyledon perfused at constant flow rate, we found that hypoxia reversibly increased perfusion pressure by over 20%. HFPV was unaffected by cyclooxygenase or nitric oxide synthase inhibition. HFPV and 4-aminopyridine, an inhibitor of voltage-dependent K+ (Kv) channels, increased pressure in a non-additive manner, suggesting they act via a common mechanism. Iberiotoxin, a calcium-sensitive K+ channel inhibitor, had little effect on normoxic pressure. Immunoblotting and RT-PCR showed expression of several putative oxygen-sensitive K+ channels in peripheral fetoplacental vessels. In patch clamp experiments with smooth muscle cells isolated from peripheral fetoplacental arteries, hypoxia reversibly inhibited Kv, but not calcium- or ATP-dependent K+ currents. We conclude that human fetoplacental vessels constrict in response to hypoxia. This response is largely mediated by hypoxic inhibition of Kv channels in smooth muscle of peripheral fetoplacental arteries.
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