It is well established that MLC phosphorylation plays a key role in the regulation of smooth muscle contraction. It is also well established that All, and a number of other factors, at concentrations too low to initiate a direct contractile response, can enhance vascular smooth muscle contraction. We have previously shown that All can enhance the increase in Ca2+i; the signal (measured with Fura 2) initiated by a-adrenoceptor agonists. We have also shown that the same low concentration of All can enhance phosphorylation of MLC without initiating a contraction of the tissue. In the present study we have investigated the dose dependency on the effects of All on MLC phosphorylation in rat tail artery tissues.
|Number of pages||1|
|Journal||Proceedings of the Western Pharmacology Society|
|Publication status||Published - 1 Dec 1997|
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