Heterogeneity of endothelium-dependent mechanisms in different rabbit arteries.
The possible endothelial factors involved in endothelium-dependent relaxations induced by acetylcholine (ACh) in aorta, mesenteric and femoral arteries of rabbit were analyzed. In thoracic aorta precontracted with noradrenaline, NG-nitro-L-arginine methyl ester (L-NAME) and methylene blue (MB), inhibitors of nitric oxide (NO) synthase and guanylate cyclase, practically abolished ACh relaxation. This relaxation was reduced by the Na+ pump inhibition with ouabain and K(+)-free solution, and by the blockade of Ca(2+)-dependent K+ channels with tetraethylammonium (TEA). Ouabain reduced the relaxation produced by the NO donor, sodium nitroprusside (SNP). In the mesenteric artery, L-NAME and MB produced a small reduction of ACh relaxation. However, ouabain, K(+)-free medium and TEA markedly decreased this relaxation. SNP induced a relaxation which was diminished by ouabain. In segments precontracted with high K+, ACh relaxation was abolished by L-NAME and MB. In femoral arteries, L-NAME and MB reduced ACh relaxation. The stimulated cGMP concentrations caused by ACh or SNP were less in the aorta than in mesenteric and femoral arteries. These results suggest that ACh relaxation is mediated: in aorta by endothelial NO which may hyperpolarize to some extent the smooth muscle cells through the sodium pump activation, in mesenteric artery by endothelium-derived hyperpolarizing factor and NO, the latter being clearly expressed in segments contracted with high K+, and in femoral artery essentially by endothelial NO release.
Ferrer
M
M
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, España.
Encabo
A
A
Conde
M V
MV
Marín
J
J
Balfagón
G
G
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology*; D006152:Cyclic GMP / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004727:Endothelium / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005263:Femoral Artery / Q000502:physiology*; D005905:Glyburide / Q000494:pharmacology; D006162:Guanylate Cyclase / Q000502:physiology; D008084:Lipoxygenase / Q000502:physiology; D016859:Lipoxygenase Inhibitors / Q000494:pharmacology; D008638:Mesenteric Arteries / Q000502:physiology*; D008751:Methylene Blue / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology; D011451:Prostaglandin-Endoperoxide Synthases / Q000502:physiology; D011817:Rabbits; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*
D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D016859:Lipoxygenase Inhibitors; D015221:Potassium Channels; D014665:Vasodilator Agents; D009599:Nitroprusside; D009569:Nitric Oxide; D010042:Ouabain; D008084:Lipoxygenase; D019001:Nitric Oxide Synthase; D011451:Prostaglandin-Endoperoxide Synthases; D006162:Guanylate Cyclase; D000254:Sodium-Potassium-Exchanging ATPase; D006152:Cyclic GMP; D000109:Acetylcholine; D005905:Glyburide; D008751:Methylene Blue