Whall C W, Havlik R J, Halpern W, Bohr D F
Blood Vessels. 1983;20(1):23-33. doi: 10.1159/000158456.
We characterized the function of adrenergic nerve varicosities in mesenteric resistance arteries from spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats by observing contractile responses to depolarization with a high potassium solution (HiK). Intact rings of resistance arteries were mounted in a specialized muscle chamber for measurement of circumferential contractile forces. Contractile responses to exogenous norepinephrine (NE), to HiK, and to the combination of NE plus HiK were significantly greater in SHR compared to WKY vessels. Using either phentolamine or 6-hydroxydopamine-treated vessels to eliminate a neurogenic adrenergic response, we determined that a part of the HiK-induced contraction was due to NE released from nerve varicosities (i.e., the adrenergic component). In order to compare these adrenergic components for possible nerve-related differences, they were first normalized to their maximum exogenous NE responses. This normalized adrenergic component of SHR vessels (52 and 58% for phentolamine and 6-hydroxydopamine treatment, respectively) was significantly greater than that of the WKY vessels (35 and 37%). This greater adrenergic component could reflect either a greater vascular smooth muscle sensitivity to NE in arteries from SHR or an increase in NE concentration, or both.
我们通过观察用高钾溶液（HiK）去极化后的收缩反应，对自发性高血压（SHR）大鼠和血压正常的Wistar Kyoto（WKY）大鼠肠系膜阻力动脉中肾上腺素能神经膨体的功能进行了表征。将完整的阻力动脉环安装在专门的肌肉腔室中，以测量圆周收缩力。与WKY血管相比，SHR对外源性去甲肾上腺素（NE）、HiK以及NE加HiK组合的收缩反应明显更大。使用酚妥拉明或6-羟基多巴胺处理的血管消除神经源性肾上腺素能反应后，我们确定HiK诱导的收缩部分是由于神经膨体释放的NE（即肾上腺素能成分）所致。为了比较这些肾上腺素能成分是否存在与神经相关的差异，首先将它们标准化为最大外源性NE反应。SHR血管的这种标准化肾上腺素能成分（酚妥拉明和6-羟基多巴胺处理分别为52%和58%）明显大于WKY血管（35%和37%）。这种更大的肾上腺素能成分可能反映了SHR动脉中血管平滑肌对NE的敏感性更高、NE浓度增加，或者两者兼而有之。
