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Am J Physiol Heart Circ Physiol (October 3, 2002). doi:10.1152/ajpheart.00419.2002
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Articles in PresS, published online ahead of print October 3, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00419.2002
Submitted on May 17, 2002
Accepted on September 27, 2002

ß-adrenergic receptor blockade impairs shear stress/NO-dependent dilation of large coronary arteries during exercise

Masaki Okajima1, Masayuki Takamura1, Philippe Vequaud1, Robert Parent1, and Michel Lavallee2*

1 Department of Physiology, Institut de Cardiologie de Montreal, Montreal, Quebec, Canada
2 Department of Physiology, Institut de Cardiologie de Montreal, Montreal, Quebec, Canada; Faculty of Medicine, Universite de Montreal, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: lavallem{at}icm.umontreal.ca.

Shear stress-dependent nitric oxide (NO) formation prevents immoderate vascular constriction. We examined if shear stress-dependent NO formation limits exercise-induced coronary artery constriction after ß-adrenergic receptor blockade in dogs. Control exercise led to increases (p<0.01) in coronary blood flow (CBF) by 38±5 from 41±5 ml/min and in external diameter of epicardial coronary arteries (CD) by 0.24±0.03 from 3.33±0.20 mm. CD and shear stress were linearly related. After propranolol, CD fell (p<0.01) during exercise (0.08±0.03 from 3.23±0.19 mm) and the slope of the relationship between CD and shear stress was reduced (p<0.01). This slope was not further altered by the additional blockade of NO formation. In propranolol-treated resting dogs, flow-dependent effects of intracoronary (ic) adenosine to mimic exercise-induced increases in shear stress (after propranolol), led to increases (p<0.01) in CD (0.09±0.02 from 3.68±0.27 mm). Thus, both shear stress-dependent NO formation and ß-adrenergic receptor activation are required to cause CD dilation during exercise. Suppression of ß-adrenergic receptor activation leads to impaired shear stress-dependent NO formation and allows {alpha}-adrenergic constriction to become dominant.




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