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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of NO and angiotensin II in the early development of endothelial functions impairment and cardiac hypertrophy in deoxycorticosterone acetate-salt hypertension.
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Role of NO and angiotensin II in the early development of endothelial functions impairment and cardiac hypertrophy in deoxycorticosterone acetate-salt hypertension.

机译：NO和血管紧张素II在醋酸脱氧皮质酮盐酸盐高血压中内皮功能损害和心脏肥大的早期发展中的作用。

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This study was designed to investigate the effects of chronic inhibition of NO synthesis as well as chronic angiotensin receptor blockade with losartan in the development of hypertension, on mesenteric arterial bed reactivity as well as on the development of cardiac and kidney hypertrophy in deoxycorticosterone-salt (DOCA) hypertension. Uninephrectomized rats were divided in four experimental groups all receiving saline water to drink and treated or not with losartan over a period of 9 days. Two of these groups were administered DOCA, one of which received also N(G)-nitro-L-arginine-methyl ester (L-NAME) to drink. A third group received only L-NAME, while another group received only saline. Systolic blood pressure was similarly increased in L-NAME, DOCA, DOCA-L-NAME groups. Cardiac and kidney weights were increased in DOCA but significantly reduced in DOCA-L-NAME. Losartan prevented the development of hypertension in all groups and also prevented cardiac and kidney hypertrophy in DOCA. The hyperreactivity of mesenteric arteries to phenylephrine, measured in the presence of indomethacin, was endothelium-dependent in both L-NAME groups but not in DOCA rats. Pretreatment with BQ 123 did not modify these endothelium-dependent responses in L-NAME rats. Chronic losartan prevented endothelium-dependent phenylephrine hyperreactivity only in DOCA, whereas only the removal of the endothelium attenuated the responsiveness in both L-NAME-treated groups. Vasorelaxations to acetylcholine and isoproterenol were attenuated in the three hypertensive groups and were normalized only in DOCA and L-NAME treated with losartan. In summary, in all hypertensive groups, blood pressure was normalized by losartan independently of its effects on endothelial functions. In DOCA, losartan normalized the phenylephrine hyperreactivity through an endothelial-dependent mechanism. However, in L-NAME-treated groups an endothelial-derived contracting factor, other than angiotensin II, endothelin, or vasoconstrictor prostanoids, appears to be activated. Both NO and angiotensin II seem to play a role in the early development of hypertension and organ hypertrophy in DOCA hypertension.
机译：这项研究旨在研究氯沙坦对NO合成的慢性抑制以及氯沙坦对慢性血管紧张素受体的阻滞在高血压发展，肠系膜动脉床反应性以及脱氧皮质酮盐对心脏和肾脏肥大发展的影响（ DOCA）高血压。未切开直肠的大鼠分为四个实验组，每组均接受盐水饮用，并在9天的时间内不使用氯沙坦治疗。这些组中有两个进行了DOCA给药，其中一组还接受了N（G）-硝基-L-精氨酸甲酯（L-NAME）饮用。第三组仅接受L-NAME，而另一组仅接受生理盐水。 L-NAME，DOCA，DOCA-L-NAME组的收缩压也同样升高。 DOCA中心脏和肾脏的重量增加，而DOCA-L-NAME中心脏和肾脏的重量显着减少。氯沙坦预防了所有人群的高血压发展，还预防了DOCA中的心脏和肾脏肥大。在吲哚美辛存在下测得的肠系膜动脉对苯肾上腺素的高反应性在两个L-NAME组中均依赖于内皮，而在DOCA大鼠中则不然。用BQ 123预处理不会改变L-NAME大鼠的这些内皮依赖性反应。慢性氯沙坦仅在DOCA中预防了内皮依赖性苯肾上腺素的过度反应，而在两种L-NAME治疗组中，只有去除内皮才能减弱其反应性。在三个高血压组中，对乙酰胆碱和异丙肾上腺素的血管舒张作用减弱，仅在氯沙坦治疗的DOCA和L-NAME中正常化。总之，在所有高血压组中，氯沙坦可独立于其对内皮功能的影响而使血压正常化。在DOCA中，氯沙坦通过内皮依赖性机制使苯肾上腺素过反应性正常化。但是，在L-NAME治疗组中，除血管紧张素II，内皮素或血管收缩素类前列腺素外，内皮衍生的收缩因子似乎已被激活。 NO和血管紧张素II似乎都在DOCA高血压的高血压早期发展和器官肥大中起作用。

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