Decreased skeletal muscle vasodilation in patients with congestive heart failure.
In congestive heart failure (CHF), excessive vasoconstriction is present, which is due to overactive vasoconstrictor mechanisms although vasodilator mechanisms may be impaired. In the present study, we examined vasodilation in CHF by measuring forearm blood flow with a strain gauge plethysmograph. Patients with CHF had higher forearm vascular resistance than normal control subjects. Patients with CHF had decreased forearm vasodilation in response to intra-arterial infusions of atrial natriuretic peptide (ANP) and acetylcholine, but not in response to sodium nitroprusside or nitroglycerin. Oral captopril did not alter the degree of forearm vasodilation during handgrip exercise. These results suggest that endothelium-dependent and ANP-induced forearm vasodilation is impaired in patients with CHF but the decreased vasodilation is not due to impaired vascular smooth muscle responsiveness to a vasodilator. The renin-angiotensin system does not seem to play a major role in the maintenance of vascular resistance during exercise in CHF.
Imaizumi
T
T
Research Institute of Angiocardiology and Cardiovascular Clinic, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Hirooka
Y
Y
Takeshita
A
A
D000109:Acetylcholine / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D002216:Captopril / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000503:physiopathology; D015444:Exercise; D005542:Forearm / Q000098:blood supply; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000098:blood supply*; D005996:Nitroglycerin / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D009599:Nitroprusside; D009320:Atrial Natriuretic Factor; D002216:Captopril; D005996:Nitroglycerin; D000109:Acetylcholine