一氧化氮在灌注心脏对乙酰胆碱和缓激肽的血管舒张反应中的作用。

Role of nitric oxide in the vasodilatory responses to acetylcholine and bradykinin in perfused hearts.

作者信息

Yoshiyama M, Miura K, Nishikimi T, Teragaki M, Todi I, Akioka K, Takeuchi K, Takeda T

机构信息

First Department of Internal Medicine, Osaka City University Medical School, Japan.

出版信息

Jpn Circ J. 1993 Dec;57(12):1159-63. doi: 10.1253/jcj.57.1159.

DOI:10.1253/jcj.57.1159

PMID:8283608

Abstract

The role of nitric oxide in the coronary vasodilation caused by acetylcholine or bradykinin in perfused guinea-pig hearts was investigated by using 1 mM L-NG-nitro arginine (L-NNA), a specific inhibitor of the formation of nitric oxide from L-arginine. L-NNA increased coronary perfusion pressure and inhibited the vasodilator responses to acetylcholine and bradykinin. The extent of vasodilation was evaluated in terms of the reduction of perfusion pressure from the initial baseline that had been induced by U-46619. L-NNA markedly attenuated coronary vasodilation caused by 5 x 10(-11) mol of acetylcholine from 15 +/- 1 to 4 +/- 1 mmHg (p < 0.01), and that caused by 1 x 10(-11) mol bradykinin from 21 +/- 2 to 8 +2- 1 mmHg (p < 0.01). On the other hand, L-NNA only weakly inhibited coronary vasodilation caused by 5 x 10(-7) mol of acetylcholine from 40 +/- 3 to 27 +/- 4 mmHg (p < 0.01), and that caused by 1 x 10(-9) mol of bradykinin (from 39 +/- 2 to 32 +/- 2 mmHg (p < 0.01). L-NNA had no effect on the vasodilation induced by 1 x 10(-8) mol of bradykinin. Ibuprofen, cyclooxygenase inhibitor, did not affect these vasodilatory responses. These results suggest that the formation of nitric oxide from L-arginine in coronary resistance vessels helps to regulate vascular tone, and that prostaglandins are not related to the vasodilatory responses to acetylcholine or bradykinin.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

采用1 mM L-NG-硝基精氨酸（L-NNA），一种从L-精氨酸形成一氧化氮的特异性抑制剂，研究了一氧化氮在灌注豚鼠心脏中由乙酰胆碱或缓激肽引起的冠状动脉舒张中的作用。L-NNA增加冠状动脉灌注压，并抑制对乙酰胆碱和缓激肽的血管舒张反应。血管舒张程度根据由U-46619诱导的初始基线灌注压的降低来评估。L-NNA显著减弱由5×10⁻¹¹ mol乙酰胆碱引起的冠状动脉舒张，从15±1 mmHg降至4±1 mmHg（p<0.01），以及由1×10⁻¹¹ mol缓激肽引起的冠状动脉舒张，从21±2 mmHg降至8±1 mmHg（p<0.01）。另一方面，L-NNA仅微弱抑制由5×10⁻⁷ mol乙酰胆碱引起的冠状动脉舒张，从40±3 mmHg降至27±4 mmHg（p<0.01），以及由1×10⁻⁹ mol缓激肽引起的冠状动脉舒张（从39±2 mmHg降至32±2 mmHg，p<0.01）。L-NNA对由1×10⁻⁸ mol缓激肽诱导的血管舒张无影响。环氧合酶抑制剂布洛芬不影响这些血管舒张反应。这些结果表明，冠状动脉阻力血管中从L-精氨酸形成一氧化氮有助于调节血管张力，并且前列腺素与对乙酰胆碱或缓激肽的血管舒张反应无关。（摘要截短至250字）