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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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