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Articles in PresS, published online ahead of print March 21, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01016.2001
Submitted on November 21, 2001
Accepted on March 12, 2002
1 Pharmacy & Pharmacology, University of Bath, Bath, Bath, United Kingdom
* To whom correspondence should be addressed. E-mail: k.a.dora{at}bath.ac.uk.
Raising potassium ([K+]o) around mesenteric resistance arteries reverses depolarization and contraction to phenylephrine. As the smooth muscle depolarizes and intracellular Ca2+ and tension increase, this effect of K+ is suppressed while efflux of cellular K+ through calcium-activated K+ (KCa) channels is increased. We investigated whether K+ efflux through KCa suppresses the action of exogenous K+, and if it acts by pre-stimulating smooth muscle Na+/K+-ATPase. Under isometric conditions, 10.8 mM [K+]o had no effect on arteries contracted above 10 mN, unless iberiotoxin (IbTX, 100 nM), charybdotoxin (ChTX, 100 nM) and/or apamin (50 nM) were present. Simultaneous measurements of membrane potential and tension showed phenylephrine depolarised and contracted arteries to -32.2 ± 2.3 mV and 13.8 ± 1.6 mN (n=5) after blockade of KCa, but now 10.8 mM K+ reversed fully the responses (107.6 ± 8.6 % and 98.8 ± 0.6 %, respectively). Under isobaric conditions and pre-constriction with phenylephrine, 10.7 mM [K+]o reversed contraction at both 50 mmHg (77.0 ± 8.5 %, n=9) and 80 mmHg (83.7 ± 5.5 %, n=5). However, in four additional vessels at 80 mmHg, raising K+ failed to reverse contraction unless ChTX was present. Increases in isometric and decreases in isobaric tension with phenylephrine were augmented by either ChTX or ouabain (100 µM), whereas neither inhibitor altered tension under resting conditions. Inhibition of cellular K+ efflux facilitates hyperpolarization and relaxation to exogenous K+, possibly by indirectly reducing the background activation of Na+/K+-ATPase.
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