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Articles in PresS, published online ahead of print December 13, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00327.2001
Submitted on April 24, 2001
Accepted on December 6, 2001
1 Laboratory for Physiology, Institute for Cardiovascular Research, Amsterdam, Netherlands
2 Department of Physiology and Medicine, University of Antwerp, Antwerp, Belgium
* To whom correspondence should be addressed. E-mail: lamberts{at}physiol.med.vu.nl.
The role of stretch-activated ion channels (SACs) in coronary perfusion-induced increase in cardiac contractility was investigated in isolated isometrically contracting perfused papillary muscles from Wistar rats. A brief increase in perfusion pressure (3-4 s, perfusion pulse, n=7), ten repetitive perfusion pulses (n=4) or a sustained increase in perfusion pressure (150-200 s, perfusion step, n=7) increase developed force by 2.7±1.1, 7.7±2.2 and 8.3±2.5 mN/mm2 (mean±SEM, p<0.05), respectively.The increase in developed force after a perfusion pulse is transient, whereas developed force during perfusion step remains increased by 5.1±2.5 mN/mm2 (p<0.05) in the steady state. Inhibition of SACs by addition of gadolinium (10 µmol/L) or streptomycin (40 and 100 µmol/L) blunts the perfusion-induced increase in developed force. Incubation with 100 µmol/L N
-nitro-L-arginine (NO-synthase inhibition), 10 µmol/L sodium nitroprusside (NO-donation) and 0.1 µmol/L verapamil (L-type Ca2+ channel blockade) are without effect on perfusion-induced increase of developed force. We conclude that brief, repetitive or sustained increases in coronary perfusion augment cardiac contractility through activation of stretch-activated ion channels, whereas endothelial NO release and L-type Ca2+ channels are not involved.
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