Impaired endothelium-dependent relaxation in large, but not small arteries in rats after coronary ligation
| Autor: | David L. Prior, Jaye Chin-Dusting, Pamela J. Arnold, Xiao-Jun Du, Garry L. Jennings |
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| Rok vydání: | 1998 |
| Předmět: |
Male
Nitroprusside medicine.medical_specialty Vasodilation Aorta Thoracic Coronary Disease Nitroarginine Rats Sprague-Dawley Norepinephrine medicine.artery Internal medicine medicine Thoracic aorta Animals Enzyme Inhibitors Mesenteric arteries Pharmacology Aorta Chemistry medicine.disease Acetylcholine Mesenteric Arteries Rats medicine.anatomical_structure Endocrinology Heart failure Anesthesia Circulatory system Sodium nitroprusside Endothelium Vascular Nitric Oxide Synthase Artery medicine.drug |
| Zdroj: | European journal of pharmacology. 355(2-3) |
| ISSN: | 0014-2999 |
| Popis: | Vascular responses were studied in both large and small arteries of rats following 8 weeks of heart failure produced by coronary ligation. Responses to noradrenaline, acetylcholine and sodium nitroprusside were studied in isolated thoracic aorta and mesenteric arteries. In the aorta, concentration-response curves for noradrenaline were similar between heart failure and sham animals and unaffected by the nitric oxide synthase inhibitor, NG-nitro-L-arginine (L-NOARG). Relaxation by acetylcholine was impaired in heart failure rats (EC50-6.79 log M heart failure vs. -7.15 log M sham). In the presence of L-NOARG, relaxation by acetylcholine was completely abolished in rings from sham rats, whereas constriction was observed in rings from heart failure rats. Relaxation by sodium nitroprusside was not different between sham and heart failure rats. In mesenteric arteries, responses to noradrenaline, acetylcholine and sodium nitroprusside were not different between heart failure and sham rats. L-NOARG reduced the maximum response to acetylcholine in both heart failure (82% to 50%) and shams (89% to 49%) by a similar magnitude, with no effect on relaxation to sodium nitroprusside. These data suggest that acetylcholine-induced relaxation is impaired in the aorta, but not mesenteric arteries in rats with heart failure. The mechanism is not solely due to impaired nitric oxide release and may be due to acetylcholine-induced contraction. |
| Databáze: | OpenAIRE |
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