Possible role of sodium-hydrogen antiport in acetylcholine-induced relaxation of rat aorta.
The decreased extracellular Na concentration (25mM) attenuated vasodilator effect of acetylcholine (ACh) in norepinephrine-treated aortic ring. This attenuation was greater in the low Na medium substituted by Li, which can exchange intracellular H through Na-H antiport, as compared with that substituted by choline, which cannot. 10 microM amiloride canceled the difference between the two low Na mediums. Thus the inhibition of Na-H antiport may counteract the suppressive effect of decreased intracellular Na on ACh vasodilation, suggesting a possible role of Na-H antiport in a release of vasoactive substance(s) from endothelial cells.
Ando
K
K
Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Japan.
Takahashi
K
K
Ono
A
A
Shimosawa
T
T
Ogata
E
E
Fujita
T
T
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology*; D002352:Carrier Proteins / Q000502:physiology*; D004730:Endothelium, Vascular / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D005996:Nitroglycerin / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000494:pharmacology*; D017923:Sodium-Hydrogen Exchangers; D014664:Vasodilation / Q000187:drug effects*
D002352:Carrier Proteins; D017923:Sodium-Hydrogen Exchangers; D012964:Sodium; D005996:Nitroglycerin; D000109:Acetylcholine; D009638:Norepinephrine