© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Signal transduction in spontaneous myogenic tone in isolated arterioles from rat skeletal muscle
Laboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit, Amsterdam, The Netherlands
* Corresponding author. Tel.: +31-20-566-5179; fax: +31-20-691-7233.
Objective: The mechanism of spontaneous myogenic tone was investigated in isolated arteriolar segments. Methods: Arterioles were isolated from rat cremaster muscle. Segments were endothelium-denuded and mounted in a pressure myograph at 75 mmHg. Under this condition, segments spontaneously constricted from a passive diameter of 167±3 to 82±4 µm (n=41). The effects of several inhibitors were tested on the maintenance of myogenic tone. Results: Gadolinium (10–6–10–4 M), a putative inhibitor of stretch-activated cation channels, was ineffective. The phospholipase C (PLC) inhibitor 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (NCDC) induced a dose-dependent inhibition of tone. NCDC inhibited phenylephrine- (10–6 M), but not potassium buffer-induced (100 mM) constriction. The protein kinase C (PKC) inhibitors staurosporine, chelerythrine and calphostin C inhibited myogenic tone in a concentration-dependent manner. At an intermediate concentration, calphostin C selectively inhibited phenylephrine-induced constriction. However, all PKC inhibitors abolished responses to phenylephrine and potassium buffer at higher concentrations. The cytochrome P450 inhibitor 17-ODYA (0.3–3x10–6 M) did not inhibit myogenic tone. Conclusions: No evidence was found for a role of gadolinium-sensitive, stretch-activated cation channels or cytochrome P450 metabolites. On the other hand, both PLC and PKC contribute to the maintenance of myogenic tone.
KEYWORDS Arteries; Mechanotransduction; Protein kinases; Smooth muscle; Vasoconstriction/dilation
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