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J Appl Physiol 86: 963-969, 1999;
8750-7587/99 $5.00
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Vol. 86, Issue 3, 963-969, March 1999

Modulation of temperature-induced tone by vasoconstrictor agents

Michael P. Massett1, Stephen J. Lewis2, James N. Bates3, and Kevin C. Kregel1

Departments of 1 Exercise Science, 2 Pharmacology, and 3 Anesthesia, The University of Iowa, Iowa City, Iowa 52242

One of the primary cardiovascular adjustments to hyperthermia is a sympathetically mediated increase in vascular resistance in the viscera. Nonneural factors such as a change in vascular tone or reactivity may also contribute to this response. Therefore, the aim of this study was to determine whether vascular smooth muscle tone is altered during heating to physiologically relevant temperatures >37°C. Gradually increasing bath temperature from 37°C (normothermia) to 43°C (severe hyperthermia) produced graded contractions in vascular ring segments from rat mesenteric arteries and thoracic aortae. In untreated rings these contractions were relatively small, whereas hyperthermia elicited near-maximal increases in tension when rings were constricted with phenylephrine or KCl before heating. In phenylephrine-treated mesenteric arterial rings, the contractile responses to heating were markedly attenuated by the Ca2+ channel antagonists nifedipine and diltiazem. Diltiazem also blocked the contractile responses to heating in thoracic aortic rings. These results demonstrate that hyperthermia has a limited effect on tension generation in rat vascular smooth muscle in the absence of vascular tone. However, in the presence of agonist-induced tone, tension generation during heating is markedly enhanced and dependent on extracellular Ca2+. In conclusion, these data suggest that local regulation of vascular tone can contribute to the hemodynamic adjustments to hyperthermia.

calcium channels; contraction; diltiazem; hyperthermia; mesenteric artery; nifedipine; temperature; thoracic aorta


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