(Hypertension. 2001;37:66.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
From the Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee.
Correspondence to Nancy J. Rusch, PhD, Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail nrusch{at}mcw.edu
AbstractThe purpose of this study was to provide the first membrane potential profile in coronary endothelial cells from normotensive sham-operated control and 1-kidney, 1-clip renal hypertensive rats. Dilator responses were assessed in cannulated coronary arteries from control and 1-kidney, 1-clip rats, and the perforated patch-clamp method was used to compare membrane potential responses between the intact endothelial cells. Under these conditions, acetylcholine (100 pmol/L to 10 µmol/L) induced similar large dilations of coronary arteries from control and 1-kidney, 1-clip rats that were associated with endothelial cell hyperpolarizing responses of 16±3 and 18±2 mV, respectively. Substance P (10 fmol/L to 1 nmol/L) and bradykinin (100 fmol/L to 10 nmol/L) also substantially dilated coronary arteries from control rats but only induced small (2 to 4 mV) endothelial cell hyperpolarizing responses. These dilations, which appeared independent of membrane potential changes, were highly blunted or absent in arteries from 1-kidney, 1-clip rats. Thus, dilator responses to acetylcholine that are associated with large endothelial hyperpolarizing responses are normal in the small coronary arteries of 1-kidney, 1-clip rats. However, dilator response to substance P and bradykinin, which apparently are not heavily dependent on endothelial cell hyperpolarizations, are selectively targeted for impairment in the coronary arteries of this model of hypertension
Key Words: endothelium hypertension, renal coronary artery disease muscle, smooth, vascular membranes potassium channels
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