Role of nitric oxide in the regulation of coronary vascular tone in hearts from hypertensive rats. Maintenance of nitric oxide-forming capacity and increased basal production of nitric oxide.
Role of nitric oxide in the regulation of coronary vascular tone in hearts from hypertensive rats. Maintenance of nitric oxide-forming capacity and increased basal production of nitric oxide.
复制标题
一氧化氮在高血压大鼠心脏冠状血管张力调节中的作用。
作者：
M. Kelm;M. Feelisch;T. Krebber;A. Deussen;W. Motz;B. Strauer
在动脉高血压中，冠状动脉血流储备（由自动调节和最大冠状动脉血流之间的差异表示）经常受损。以前的实验和临床研究使用乙酰胆碱作为刺激的生产内皮衍生的舒张因子表明，受损的内皮依赖性血管舒张，可能是由一氧化氮（NO）的形成减少，可能会导致这种微血管功能障碍。然而，到目前为止，还没有研究已经进行量化的高血压心脏的冠状循环内的NO的形成，以评估其在设置冠状动脉血管紧张度在高血压心脏的作用。因此，我们定量NO的形成内的冠状动脉循环的恒定流量灌注，从自发性高血压大鼠（SHR，第16至第26周），作为高血压性心脏病的模型，和从血压正常的控制应变（Wistar-Kyoto，WKY）使用氧合血红蛋白技术的分离的心脏。与WKY心脏相比，SHR的冠状动脉灌注压和血管阻力几乎高出30%。冠状动脉内应用NO降低冠状动脉血管阻力的最大45%的静息值在两组中的浓度依赖性的方式。缓激肽诱导的冠状动脉血管阻力的降低和NO释放的平行增加在SHR和WKY心脏中是可比的，并且落在外源性应用NO的血管扩张剂范围内。此外，与WKY心脏相比，SHR中标准化为心脏湿重的NO基础释放高出50%。两组基础NO释放率与冠状动脉灌注压和血管阻力变化呈负相关（r分别为-0.85和-0.84，P <0.05）。（250字处删节）
In arterial hypertension, coronary flow reserve, expressed by the difference between autoregulated and maximal coronary flow, is frequently impaired. Previous experimental and clinical investigations using acetylcholine as a stimulus for the production of endothelium-derived relaxing factor suggested that an impaired endothelium-dependent vasodilation, presumably caused by a decreased formation of nitric oxide (NO), may account for this microvascular dysfunction. However, so far no study has been performed that quantifies the formation of NO within the coronary circulation of hypertensive hearts to assess its role in setting coronary vascular tone in the hypertensive heart. We therefore quantified NO formation within the coronary circulation of constant flow-perfused, isolated hearts from spontaneously hypertensive rats (SHR, 16th to 26th week), as a model for hypertensive heart disease, and from the normotensive control strain (Wistar-Kyoto, WKY) using the oxyhemoglobin technique. Coronary perfusion pressure and vascular resistance were almost 30% higher in SHR compared with WKY hearts. Intracoronarily applied NO decreased coronary vascular resistance by maximally 45% of resting values in a concentration-dependent manner in both groups. The bradykinin-induced decrease in coronary vascular resistance and the parallel increase in NO release were comparable in SHR and WKY hearts and fell within the vasodilator range of exogenously applied NO. Moreover, basal release of NO normalized to heart wet weight was 50% higher in SHR compared with WKY hearts. Rates of basal NO release were correlated inversely with changes in coronary perfusion pressure and vascular resistance in both groups (r = -.85 and -.84, respectively, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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DOI：
10.1073/pnas.89.16.7674
发表时间：
1992-08-15
影响因子：
11.1
作者：
STAMLER, JS;JARAKI, O;LOSCALZO, J
通讯作者：
LOSCALZO, J
高血压和左心室肥厚对冠状动脉自动调节范围较低的影响。
影响因子：
37.8
作者：
Harrison,DG;Florentine,MS;Brooks,LA;Cooper,SM;Marcus,ML
通讯作者：
Marcus,ML
系统性高血压血管肥大的细胞生物学。
DOI：
10.1016/0002-9149(88)90029-x
发表时间：
1988
期刊：
The American journal of cardiology
影响因子：
--
作者：
Dzau,VJ;Gibbons,GH
通讯作者：
Gibbons,GH
影响因子：
--
作者：
KATUSIC, ZS;VANHOUTTE, PM
通讯作者：
VANHOUTTE, PM