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Am J Physiol Heart Circ Physiol (July 22, 2005). doi:10.1152/ajpheart.00568.2005
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Submitted on May 31, 2005
Accepted on July 15, 2005

ACETYLCHOLINE AND SODIUM NITROPRUSSIDE CAUSE LONG-TERM INHIBITION OF EDCF-MEDIATED CONTRACTIONS

Eva H.C. Tang1, Michel Feletou2, Yu Huang3, Ricky Y.K. Man1, and Paul M Vanhoutte1*

1 Department of Pharmacology, University of Hong Kong, Hong Kong
2 Institut de Recherches Internationales Servier, Paris, France
3 Department of Physiology, Chinese University of Hong Kong, Hong Kong

* To whom correspondence should be addressed. E-mail: vanhoutte.hku{at}hku.hk.

Preliminary studies suggested that previous exposure to acetylcholine exerts a delayed inhibition of subsequent contractions mediated by endothelium-derived contracting factor (EDCF). To confirm this long-term inhibitory effect of acetylcholine and to determine whether or not nitric oxide (NO) mediates the phenomenon, rings of spontaneously hypertensive rat (SHR) aortae were suspended in organ chambers for the recording of isometric force. The rings were incubated in the absence or presence of N{omega}-nitro-L-arginine methyl ester (L-NAME; inhibitor of NO synthases) or ODQ (inhibitor of soluble guanylyl cyclase) before exposure to increasing concentrations of acetylcholine or sodium nitroprusside (SNP) during contractions to phenylephrine. Thereafter, EDCF-mediated contractions to acetylcholine or the calcium ionophore A23187 were elicited. If the rings were pre-exposed to acetylcholine or SNP, the subsequent acetylcholine-induced EDCF-mediated contractions were reduced compared to those obtained in rings of the same arteries not previously exposed to either agent. ODQ did not affect the inhibition caused by pre-exposure to acetylcholine, but significantly reduced that due to pre-exposure to sodium nitroprusside. Previous exposure to SNP reduced but previous exposure to acetylcholine did not affect endothelium-dependent contractions to A23187. Previous exposure to either acetylcholine or SNP did not affect the contractions to the thromboxane mimetic U46619. Thus, acetylcholine and SNP exert delayed inhibition of EDCF-mediated contractions via distinct pathways. The effect of acetylcholine is NO-independent and upstream of the increase in calcium concentration that triggers the release of EDCF. That of SNP is downstream of the calcium rise and is mainly NO dependent.




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