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1 Department of Anesthesiology and Physiology, Medical College of Wisconsin and VAMC, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: pcliff{at}mcw.edu.
We hypothesized that elevated temperatures would attenuate, but reduced temperatures would potentiate the tension mediated by vascular P2X receptors. Twenty-four rats were sacrificed. The femoral arteries were dissected out and placed in modified Krebs-Henseleit buffer. Arteries were cut into 2mm sections and mounted in organ tissue baths. Maximal tension (grams) was measured during a KCl and norepinephrine challenge. Tension was measured during doses of
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-methyleneATP (10-7 to 10-3M), phenylephrine (10-7 to 10-4M), and acetylcholine (10-9 to 10-5M), with tissue bath temperature adjusted to 35, 37, and 41oC. Dose response curves were fit using non-linear regression analysis to calculate the EC50 and slope. The peak tension was lower with
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-methylene ATP during 41oC (1.49±0.14grams) compared to 35oC (2.08±0.09grams) and 37oC (1.94±0.09grams; p<0.05). Slope and EC50 were not affected by temperature. Tension produced by phenylephrine and relaxation to acetylcholine were not affected by temperature. These data indicate that the vasoconstrictor response to
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-methylene ATP is sensitive to temperature. Moderate cooling does not potentiate P2X mediated vasoconstriction, but elevated temperature attenuates the vasoconstrictor response to P2X purinergic receptors.
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