Submitted on July 16, 2007
Accepted on October 3, 2007
Changes in Forearm Muscle Temperature Alter Renal Vascular
Responses to Isometric Handgrip
Nathan T Kuipers1, Charity L. Sauder1, Matthew L. Kearney1, and Chester A. Ray1*
1 Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: caray{at}psu.edu.
The purpose of the present study was to examine the effect of heating and cooling the forearm muscles on renal vascular responses to ischemic isometric handgrip (IHG). It was hypothesized that heating and cooling the forearm would augment and attenuate renal vascular responses to IHG, respectively. Renal vascular responses to IHG were studied during forearm heating at 39 °C (n=15, 26±1 yr) and cooling at 26 °C (n=12, 26±1 yr). For a control trial subjects performed the experimental protocol while the forearm was normothermic (~34 °C). Muscle temperature (measured by intramuscular probe) was controlled by changing the temperature of water cycling through a water-perfused sleeve. The experimental protocol was: 3-min baseline, 1 min of ischemia, ischemic IHG to fatigue, and 2 min of postexercise muscle ischemia. At rest, renal artery blood velocity (RBV; Doppler ultrasound) and renal vascular conductance (RVC; RBV / mean arterial blood pressure) were not different between normothermia and the two thermal conditions. During ischemic IHG there were greater decreases in RBV and RVC in the heating trial. However, RBV and RVC were similar during postexercise muscle ischemia during heating and normothermia. During cooling, RVC decreased less compared to normothermia during ischemic IHG. During postexercise muscle ischemia, RVC was greater during cooling compared to the normothermic trial. These results indicate that heating augments mechanoreceptor-mediated renal vasoconstriction whereas cooling blunts metaboreceptor-mediated renal vasoconstriction.
