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Am J Physiol Heart Circ Physiol 282: H1334-H1340, 2002. First published December 13, 2001; doi:10.1152/ajpheart.00327.2001
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Vol. 282, Issue 4, H1334-H1340, April 2002

Increased coronary perfusion augments cardiac contractility in the rat through stretch-activated ion channels

R. R. Lamberts1, M. H. P. van Rijen1, P. Sipkema1, P. Fransen2, S. U. Sys2, and N. Westerhof1

1 Institute for Cardiovascular Research, Laboratory for Physiology, 1081 BT Amsterdam, The Netherlands; and 2 Department of Physiology and Medicine, University of Antwerp, B2020 Antwerp, Belgium

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), 10 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 (means ± SE, P < 0.05), respectively. The increase in developed force after a perfusion pulse is transient, whereas developed force during a 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 Nomega -nitro-L-arginine [nitric oxide (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 the 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.

mechanotransduction; gadolinium; nitric oxide; papillary muscles; streptomycin


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