NG-nitro-l-arginine-resistant endothelium-dependent relaxation induced by acetylcholine in the rabbit renal artery
| Autor: | Motohatsu Fujiwara, Emiko Sameshima, Yu Yamaguchi, Satomi Kitagawa, Masaru Kunitomo |
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| Rok vydání: | 1994 |
| Předmět: |
Male
medicine.medical_specialty Vascular smooth muscle Drug Resistance In Vitro Techniques Arginine Nitroarginine General Biochemistry Genetics and Molecular Biology Ouabain Nitric oxide chemistry.chemical_compound Internal medicine medicine Animals Channel blocker General Pharmacology Toxicology and Pharmaceutics Tetraethylammonium General Medicine Hyperpolarization (biology) Acetylcholine Methylene Blue Vasodilation Endocrinology chemistry Biochemistry Endothelium Vascular Rabbits medicine.drug |
| Zdroj: | Life Sciences. 55:491-498 |
| ISSN: | 0024-3205 |
| Popis: | Studies were designed to determine the extent of the involvement of endothelium-derived relaxing factor(s) other than nitric oxide (NO) in vascular relaxation in response to acetylcholine (ACh) in the rabbit renal artery. ACh (10(-9)-10(-6) M) induced concentration-dependent relaxation of isolated endothelium-intact arterial rings preconstricted with noradrenaline. NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, partly inhibited the ACh-induced endothelium-dependent relaxation, whereas it almost completely abolished the production of cyclic-3', 5'-guanosine monophosphate (cGMP) in these rings in response to ACh. Methylene blue, an inhibitor of guanylate cyclase, had an essentially similar effect to L-NAME on the relaxation. Indomethacin, an inhibitor of cyclooxygenase, had no effect. High concentrations of potassium chloride (to inhibit endothelium-dependent hyperpolarization), tetraethylammonium (TEA) or 4-aminopyridine (4-AP), a voltage-dependent or Ca(2+)-dependent K+ channel blocker, partly inhibited the relaxation while, in contrast, glibenclamide, an ATP-sensitive K+ channel blocker, had no effect. Ouabain, an inhibitor of Na+, K(+)-ATPase, also partly inhibited the ACh-induced relaxation, especially the higher concentration effect. Application of L-NAME together with ouabain, TEA, or a high concentration of potassium chloride completely abolished the relaxation. These results suggest that ACh-induced endothelium-dependent relaxation in the rabbit renal artery is mediated by NO, and by an other factor(s), which relaxes the vascular smooth muscle through opening K+ channels other than ATP-sensitive ones, and/or through the activation of a Na+, K(+)-pump. |
| Databáze: | OpenAIRE |
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