[The inhibition of acetylcholine- and sodium nitroprusside-induced pulmonary artery relaxation by chronic hypoxia].
This experiment was designed to investigate whether chronic hypoxia could reduce pulmonary artery relaxation induced by acetylcholine and sodium nitroprusside (endothelium-dependent and endothelium-independent vasodilator, respectively). Male Wistar rats were divided into 3 groups: control, kept in air; CH4, in hypobaric chamber (8000 m above sea level) for 4 days; CH20, in hypobaric chamber (5000 m above sea level) for 20 days. All the hypoxic rats developed pulmonary hypertension. Rings of extra- (EPPA) or intra- (IPPA) pulmonary artery were suspended in an organ bath containing oxygenated Kreb's solution at 37 degrees C for relaxation/inhibition studies. The results showed that chronic hypoxia, CH4 and CH20, inhibited the relaxation response of both IPPA and EPPA to both acetylcholine and sodium nitroprusside. It is suggested that chronic hypoxia might attenuate the sensitivity and reactivity of the pulmonary artery to both acetylcholine and sodium nitroprusside through the inhibition of guanyl cyclase activity in smooth muscle.
Rui
L
L
Institute of Basic Medical Science, Beijing.
Cai
Y
Y
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009126:Muscle Relaxation / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009599:Nitroprusside / Q000494:pharmacology*; D011651:Pulmonary Artery; D051381:Rats; D011919:Rats, Inbred Strains
D009599:Nitroprusside; D000109:Acetylcholine