Minami N, Head G A
Neuropharmacology Laboratory, Baker Medical Research Institute, Melbourne, Victoria, Australia.
Auton Neurosci. 2000 Aug 14;82(3):115-22. doi: 10.1016/S0165-1838(00)00098-9.
In the present study we sought to determine the effect of age, hypertension and endogenous angiotensin on the chronotropic responses to vagal stimulation in urethane anesthetized-normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). After beta-adrenoceptor blockade with atenolol, the right and left vagal nerves were stimulated with graded frequencies between 1 and 32 Hz in 5-, 8- and 22-week-old animals. At all ages and in both strains, there was a strong linear relationship between the degree of bradycardia and the log of the stimulation frequency. At the age of 5 weeks, the bradycardia to stimulation of the right vagus was greater in SHR than that observed in WKY (P<0.05). However, in 8- and 22 week-old animals, no differences were observed between the response to vagal stimulation in WKY and SHR. Thus, there was an age-dependent increase in the response to right vagal stimulation in WKY, but no such trend in SHR. No significant age-dependent changes in left vagal responses were observed in either strain. Left vagal responses were approximately half of the response to right vagal stimulation at all ages in SHR and in 8-22 week WKY, but similar to right vagal responses in 5 week WKY. Administration of the angiotensin converting enzyme inhibitor perindopril, which effectively blocked the formation of endogenous angiotensin, did not affect responses to vagal stimulation at any age, in either strain. These results suggest that the baroreflex vagal deficit observed in adult SHR compared to WKY is not due to a difference in the responsiveness of the cardiac vagal neuroeffector mechanism nor due to an effect of circulating angiotensin II. Furthermore, the enhanced vagal bradycardia observed in very young SHR which was due primarily to the earlier establishment of the adult vagal response pattern may indicate accelerated vagal development in this strain compared to WKY.
在本研究中，我们试图确定年龄、高血压和内源性血管紧张素对氨基甲酸乙酯麻醉的正常血压Wistar-Kyoto（WKY）大鼠和自发性高血压大鼠（SHR）迷走神经刺激变时反应的影响。在用阿替洛尔进行β-肾上腺素能受体阻断后，对5周、8周和22周龄的动物，以1至32Hz的分级频率刺激左右迷走神经。在所有年龄组和两种品系中，心动过缓程度与刺激频率的对数之间存在很强的线性关系。在5周龄时，SHR对右迷走神经刺激的心动过缓程度大于WKY（P<0.05）。然而，在8周龄和22周龄的动物中，WKY和SHR对迷走神经刺激的反应没有差异。因此，WKY对右迷走神经刺激的反应存在年龄依赖性增加，但SHR中没有这种趋势。在这两种品系中，均未观察到左迷走神经反应有明显的年龄依赖性变化。在SHR以及8至22周龄的WKY中，所有年龄组的左迷走神经反应约为右迷走神经刺激反应的一半，但在5周龄的WKY中与右迷走神经反应相似。给予血管紧张素转换酶抑制剂培哚普利可有效阻断内源性血管紧张素的形成，但在任何年龄组和任何品系中均不影响对迷走神经刺激的反应。这些结果表明，与WKY相比，成年SHR中观察到的压力反射性迷走神经缺陷既不是由于心脏迷走神经效应机制反应性的差异，也不是由于循环血管紧张素II的作用。此外，在非常年幼的SHR中观察到的迷走神经心动过缓增强主要是由于成年迷走神经反应模式的较早建立，这可能表明与WKY相比，该品系的迷走神经发育加速。
