Open AccessVariations of Endothelium-Dependent Vasoresponses in Congestive Heart Failure
Author(s) -
Keiko Takahashi,
Mitsumasa Ohyanagi,
Kiyomitsu Ikeoka,
Atsunori Ueda,
Satsuki Koida
Publication year - 2005
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-200501000-00004
Subject(s) - bradykinin , vasodilation , heart failure , medicine , sodium nitroprusside , cardiology , vascular resistance , acetylcholine , endothelium , nitric oxide , vascular smooth muscle , endocrinology , blood pressure , smooth muscle , receptor
Endothelium-dependent vasodilation decreases in patients with congestive heart failure (CHF). Whether this decreased vasodilation occurs simultaneously in different vascular beds has not been elucidated. We studied the vasomotor reactivity in both coronary and peripheral resistance vessels in a rat CHF model produced by ligating the left coronary artery. Variations in vessel diameter in response to vasoactive drug administration were measured using an in vitro system of coronary resistance vessels from cardiac muscle and peripheral resistance vessels from cremaster muscle. Vascular responses to acetylcholine were impaired in the early stage of CHF (at 2 weeks), whereas the reaction to bradykinin was preserved. NG-monomethyl-L-arginine (L-NMMA) inhibited the responses of acetylcholine; however, L-NMMA only partially inhibited the responses to bradykinin. Vascular reactivity to A23187 was preserved in the early stage and was impaired in the late stage of CHF (at 8 weeks). These reactions were inhibited by L-NMMA. The response to sodium nitroprusside remained constant in both stages of CHF. The responses were similar in the coronary resistance and peripheral resistance vessels. This suggests that acetylcholine transmission is impaired in the early stages of CHF but that with CHF of longer duration there is progressive impairment of nitric oxide production and release in both coronary and peripheral resistance vessels.