Nonvasomotor influence of sodium nitroprusside on arteriolar remote response to methacholine

Vascular communication functions to facilitate blood distribution within tissues and can be demonstrated as conducted vasomotor responses. This study was designed to determine if local application of sodium nitroprusside (SNP) would affect arteriolar function at remote sites. In the cheek pouch of anesthetized hamsters, local application of SNP and nifedipine caused arteriolar dilation only at the site of application (7.1 +/- 0.5 and 7.4 +/- 0.6 microm), but not at remote sites. The application of SNP enhanced subsequent remote, nitric oxide (NO)-independent dilation in response to methacholine, which was applied at a site upstream from the SNP application site (6.7 +/- 0.7 versus 4.5 +/- 0.7 microm for methacholine alone). This potentiating effect was also observed following application of 3-morpholinosydnonimine, but not following nifedipine. This nonvasomotor influence of SNP was not affected by N(omega)-nitro-L-arginine (L-NA), tetrodotoxin (TTX), Gap 27 peptide or halothane. Attenuated local dilation in response to methacholine by L-NA could be partially recovered following downstream application of SNP, suggesting that SNP-induced potentiation was associated with enhanced vasodilatory signals at the methacholine application site. Thus, our results suggest that SNP induces nonvasomotor signals in arterioles to affect the network distribution of blood flow. Intrinsic NO, TTX-sensitive Na(+) channels and gap junctional communication do not seem to play a major role in the conduction of the nonvasomotor signals.