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This Article Full Text Full Text (PDF) All Versions of this Article: 563/3/821    most recent jphysiol.2004.080705v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lambert, D. G Articles by Thomas, G. D Search for Related Content PubMed PubMed Citation Articles by Lambert, D. G Articles by Thomas, G. D

¹ Department of Internal Medicine, Hypertension Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA

Vasoconstrictor responses to sympathetic nerve stimulation and their sensitivity to metabolic modulation reportedly differ in fast-twitch and slow-twitch muscles, but the underlying mechanisms are not known. Both ₁- and ₂-adrenoceptors mediate these vascular responses in fast-twitch muscle, while their roles in slow-twitch muscle are less well defined. In this study, the phosphorylation of smooth muscle myosin regulatory light chain (smRLC) was measured as an index of vasoconstriction in slow-twitch soleus muscles and fast-twitch extensor digitorum longus (EDL) muscles isolated from C57BL/6J mice. In soleus muscles, incubation with phenylephrine (PE) or UK 14,304 to selectively activate ₁- or ₂-adrenoceptors resulted in concentration-dependent increases in smRLC phosphorylation. To evaluate metabolic modulation of these responses, vasodilator pathways previously implicated in such modulation in fast-twitch muscle were activated in soleus muscles by treatment with the nitric oxide (NO) donor nitroprusside or the ATP-sensitive potassium (K_ATP) channel opener cromakalim. Both drugs inhibited responses to UK 14,304, but not to PE. The effect of nitroprusside to antagonize UK 14,304 responses was prevented by inhibition of guanylyl cyclase or by blockade of K_ATP channels, but not by blockade of other potassium channels. Results were similar in EDL muscles. These data provide the first evidence for ₂-adrenoceptor-mediated constriction in slow-twitch muscle, and show that it is sensitive to modulation by NO via a cGMP-dependent mechanism that requires K_ATP channel activation. Based on the similar findings in soleus and EDL muscles, fibre type does not appear to determine the innate vascular response to ₁- or ₂-adrenoceptor activation.

(Received 7 December 2004; accepted after revision 23 December 2004; first published online 23 December 2004)
Corresponding author G. D. Thomas: University of Texas Southwestern Medical Center, Hypertension Division, 5323 Harry Hines Blvd, Dallas, TX 75390-8586, USA. Email: gail.thomas{at}utsouthwestern.edu

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