TY - JOUR
T1 - Acetylcholine induces vasoconstriction in the microcirculation of cardiomyopathic hamsters
T2 - Reversal by L-arginine
AU - Mayhan, William G.
AU - Rubinstein, Israel
N1 - Funding Information:
The authors thank E. M. White at Canadian Hybrid Farms for providing the cardiomyopathic hamsters. We thank Glenda M. Sharpe for technical assistance. We thank Dr. Irving H. Zucker for helpful suggestions. This study was supported by National Heart, Lung, and Blood Institute Grant HL-40781, a Research Career Development Award HL-02124, Seed Grants from the University of Nebraska College of Medicine (91-10 and 92-41), a Grant-in-Aid from the American Heart Association, National Affiliate (91006230), a Grant-in-Aid from the American Heart Association, Nebraska Affiliate (NE-91-G-16), and support from the Nebraska Cancer and Smoking Disease Research Program (92-32).
PY - 1992/5/15
Y1 - 1992/5/15
N2 - The goal of this study was to determine whether endothelium-dependent responses of the microcirculation are altered during cardiomyopathy. We examined in vivo responses of cheek pouch arterioles to an endothelium-dependent agonist (acetylcholine) and an endothelium-independent agonist (nitroglycerin) in normal and in cardiomyopathic hamsters. In normal hamsters, acetylcholine produced dose-related dilatation of arterioles. In contrast, acetylcholine produced constriction of arterioles in cardiomyopathic hamsters. Nitroglycerin produced similar dose-related dilatation in normal and cardiomyopathic hamsters. We also examined whether impaired responses to acetylcholine in cardiomyopathic hamsters were related to an alteration in the L-arginine/nitric oxide pathway. We found that L-arginine (100 μM) restored endotheliumdependent vasodilatation to acetylcholine in cardiomyopathic hamsters. Thus, cardiomyopathy impairs endothelium-dependent responses of the microcirculation which is reversed by L-arginine.
AB - The goal of this study was to determine whether endothelium-dependent responses of the microcirculation are altered during cardiomyopathy. We examined in vivo responses of cheek pouch arterioles to an endothelium-dependent agonist (acetylcholine) and an endothelium-independent agonist (nitroglycerin) in normal and in cardiomyopathic hamsters. In normal hamsters, acetylcholine produced dose-related dilatation of arterioles. In contrast, acetylcholine produced constriction of arterioles in cardiomyopathic hamsters. Nitroglycerin produced similar dose-related dilatation in normal and cardiomyopathic hamsters. We also examined whether impaired responses to acetylcholine in cardiomyopathic hamsters were related to an alteration in the L-arginine/nitric oxide pathway. We found that L-arginine (100 μM) restored endotheliumdependent vasodilatation to acetylcholine in cardiomyopathic hamsters. Thus, cardiomyopathy impairs endothelium-dependent responses of the microcirculation which is reversed by L-arginine.
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U2 - 10.1016/S0006-291X(05)80034-8
DO - 10.1016/S0006-291X(05)80034-8
M3 - Article
C2 - 1590798
AN - SCOPUS:0026736386
SN - 0006-291X
VL - 184
SP - 1372
EP - 1377
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -