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Evidence thatmechanisms dependentand independent ofnitric oxide mediateendothelium‐dependentrelaxation tobradykinin in humansmallresistance‐like… B. KempThomas M. Cocks1997 год

Evidence that mechanisms dependent and independent of nitric oxide mediate endothelium‐dependent relaxation to bradykinin in human small resistance‐like coronary arteries
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Аннотация: The effects of the nitric oxide (NO) synthase inhibitor, N G ‐nitro‐ l ‐arginine ( l ‐NOARG), the NO scavenger, oxyhaemoglobin (HbO) and high extracellular K + upon endothelium‐dependent relaxation to bradykinin were investigated in human isolated small coronary arteries. Endothelium‐dependent relaxations to bradykinin were compared in vessels contracted to ∼50% of their maximum contraction to 124 m m KCl Krebs solution, regardless of treatments, with the thromboxane A 2 mimetic, U46619 and acetylcholine. All relaxations were expressed as percentage reversal of the initial level of active force. l ‐NOARG (100 μ m ) caused a small but significant, 12% ( P <0.01), decrease in the maximum relaxation (R max : 91.5±5.4%) to bradykinin but did not significantly affect the sensitivity (pEC 50 : 8.08±0.17). Increasing the concentration of l ‐NOARG to 300 μ m had no further effect on the pEC 50 or R max to bradykinin. HbO (20 μ m ) and a combination of HbO (20 μ m ) and l ‐NOARG (100 μ m ) reduced R max to bradykinin by 58% ( P <0.05) and 54% ( P <0.05), respectively. HbO (20 μ m ) and l ‐NOARG (100 μ m , combined but not HbO (20 μ m ) alone, caused a significant 11 fold ( P <0.05) decrease in sensitivitiy to bradykinin. HbO (20 μ m ) decreased the sensitivity to the endothelium‐independent NO donor, S‐nitroso‐N‐acetylpenicillamine (SNAP), approximately 17 fold ( P <0.05). Raising the extracellular concentration of K + isotonically to 30 m m , reduced the R max to bradykinin from 96.6±3.1% to 43.9±10.1% ( P <0.01) with no significant change in sensitivity. A combination of HbO, l ‐NOARG and high K + (30 m m ) abolished the response to bradykinin. High K + did not change either the sensitivity or maximum relaxation to SNAP. In conclusion, l ‐NOARG does not completely inhibit endothelial cell NO synthesis in human isolated small coronary arteries. By comparison, HbO appeared to block all the effects of NO in this tissue and revealed that most of the relaxation to bradykinin was due to NO. The non‐NO ‐dependent relaxation to bradykinin in the human isolated small coronary arteries appeared to be mediated by a K + ‐sensitive vasodilator mechanism, possibly endothelium‐derived hyperpolarizing factor (EDHF). British Journal of Pharmacology (1997) 120 , 757–762; doi: 10.1038/sj.bjp.0700928
Год издания: 1997
Авторы: B. Kemp, Thomas M. Cocks
Издательство: Wiley
Источник: British Journal of Pharmacology
Ключевые слова: Nitric Oxide and Endothelin Effects, Renin-Angiotensin System Studies, Cardiovascular Issues in Pregnancy
Другие ссылки: British Journal of Pharmacology (HTML)
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