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1 Physiology, New York Medical College, Valhalla, NY, USA; Pathophysiology, Semmelweis University, Budapest, Hungary
2 Physiology, New York Medical College, Valhalla, NY, USA; Division of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary
* To whom correspondence should be addressed. E-mail: koller{at}nymc.edu.
The role of metabolic factors derived from cardiac muscle in the development of reactive hyperemia following brief occlusions of the coronary circulation seems to be well established. However, the contribution of occlusion-induced changes in hemodynamic forces to eliciting reactive hyperemia is less known. We hypothesized that in isolated coronary arterioles changes in intraluminal pressure (P) and flow (F), during and after release of occlusion (O/R), via activating intrinsic mechanosensitive mechanisms, elicit release of vasoactive factors resulting in reactive dilations. Thus, in isolated coronary arterioles (diameter: 88±8 µm) changes in diameter to changes in P or P+F during and after brief period (30, 60 and 120s) of O/R of cannulating tube were measured by videomicroscopy. In response to both types of O/R, diameter first decreased, then subsequently increased during occlusions. When only P was changed (form 80-10-80 mmHg) after release of occlusion peak dilations increased as a function of the duration of occlusions. After establishing flow (30 µL/min) O/R elicited changes in both P and F (form 80-10-80 mmHg and from 0 to 30 µL/min). In these conditions after release of occlusions not only the peak but also the duration of reactive dilation increased significantly as a function of the length of occlusions. The dilations during, and peak dilations after occlusions both in P and P+F protocols were significantly reduced by the inhibition of NO synthase with L-NAME or by endothelium removal, whereas duration of post-occlusion dilations were reduced by L-NAME or by endothelium removal only in P+F protocol. Furthermore, in both protocols catalase significantly reduced the peak, but not the duration of reactive dilations. Thus, mechanosensitive mechanisms that are sensitive to deformation, pressure, stretch and shear stress elicit release of NO and hydrogen peroxide resulting in reactive dilation of isolated coronary arterioles.
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