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Received October 3, 2005
Revised October 26, 2005
Accepted after revision February 20, 2006
1 Medical College of Wisconsin
2 Pepperdine University
* To whom correspondence should be addressed. E-mail: pcliff{at}mcw.edu.
To date, no satisfactory explanation has been provided for the immediate increase in blood flow at the onset of exercise. We hypothesized that rapid vasodilatation is a consequence of release of a vasoactive substance from the endothelium due to mechanical deformation of the vasculature during contraction. Rat soleus feed arteries were isolated, removed, and mounted on micropipettes in a sealed chamber. Arteries were pressurized to 68 mmHg and luminal diameter was measured using an inverted microscope. Pressure pulses of 600 mmHg were delivered for 1 sec, 5 sec, and as a series of 5 repeated 1 sec pulses with 1 sec between pulses. During application of external pressure the lumen of the artery was completely closed, but immediately following release of pressure, diameter was significantly increased. In intact arteries (Series 1, n=6) for the 1 sec pulse, 5 sec pulse, and series of 5-1 sec pulses, the peak increases in diameter were (mean±SEM) 16_2%, 14_2%, and 27_3% with times from release of pressure to peak diameter of 4.1±0.3 sec, 4.6±0.7 sec and 2.8±0.4 sec. In series 2 (n=9) arteries increased diameter by 15_2%, 15_2%, and 30_3% before and 8_1%, 8_1%, and 21±2% after removal of the endothelium with air. The important new finding in these experiments is that mechanical compression caused dilatation of skeletal muscle feed arteries with a time course similar to the change in blood flow after a brief muscle contraction. The magnitude of dilatation was not affected by the increasing the duration of compression but was enhanced by increasing the number of compressions. Since removal of the endothelium reduced but did not abolish the dilatation to mechanical compression, it appears that the dilatation is mediated by both endothelium-dependent and independent signaling pathways.
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