摘要
Potassium (K+) in high concentrations have been shown to attenuate endothelium-dependent vasodilation. The purpose of the present study was to determine if small changes in K- concentration (within physiological range)affected nitric oxide(NO)release/effect in isolated blood vessels. Rings(4mm)of canine femoral arteries were continually suffused with a modified Krebs-bicarbonate solution (normal Krebs<4.smmol/L K+ >or low K+ Krebs<2.4mmol/L K+>), and tension changes were monitored with a force-displacement transducer. Norepinephrine (NE, 1μmol/L) was used to precontract the arteries F(7.7±0.9) g in 4. 8mmol/L K+ medium, n= 7 and (7.8±0.5)g in 2. 4μmol/ L K+ medium, n=7]. Acetylcholine (ACh, 1nmol/L￣1μmol/L) was a more potent relaxant of the precontraction in low K+ than in normal K+ medium. The ACh concentrations that produced 50% relaxation (IC50) were, respectively,(36± 10.9) nmol/L(n= 7)and(16±1.7) nmol/L (n=7) in normal and low K+ Krebs solution (P< 0. 05). The inhibitor of nitric oxide synthase, Nw-nitro-L-arginine (Nitroarg,0.1mmol/L) produced a greater shift (P < 0. 05) to the left of the NE-response curves in the low K+ medium compared to the normal K+ Krebs. On the other hand,concentration-dependent relaxations produced by nitroprusside (1μmol/L-1μmol/L)in precontracted arteries were not significantly different in normal and low K+ mediums(n=5).The results indicate that the release of NO by ACh or NE is enhanced in a low K+ medium.
Potassium (K+) in high concentrations have been shown to attenuate endothelium-dependent vasodilation. The purpose of the present study was to determine if small changes in K- concentration (within physiological range)affected nitric oxide(NO)release/effect in isolated blood vessels. Rings(4mm)of canine femoral arteries were continually suffused with a modified Krebs-bicarbonate solution (normal Krebs<4.smmol/L K+ >or low K+ Krebs<2.4mmol/L K+>), and tension changes were monitored with a force-displacement transducer. Norepinephrine (NE, 1μmol/L) was used to precontract the arteries F(7.7±0.9) g in 4. 8mmol/L K+ medium, n= 7 and (7.8±0.5)g in 2. 4μmol/ L K+ medium, n=7]. Acetylcholine (ACh, 1nmol/L￣1μmol/L) was a more potent relaxant of the precontraction in low K+ than in normal K+ medium. The ACh concentrations that produced 50% relaxation (IC50) were, respectively,(36± 10.9) nmol/L(n= 7)and(16±1.7) nmol/L (n=7) in normal and low K+ Krebs solution (P< 0. 05). The inhibitor of nitric oxide synthase, Nw-nitro-L-arginine (Nitroarg,0.1mmol/L) produced a greater shift (P < 0. 05) to the left of the NE-response curves in the low K+ medium compared to the normal K+ Krebs. On the other hand,concentration-dependent relaxations produced by nitroprusside (1μmol/L-1μmol/L)in precontracted arteries were not significantly different in normal and low K+ mediums(n=5).The results indicate that the release of NO by ACh or NE is enhanced in a low K+ medium.
