Lin Yingzi, Tsuchihashi Takuya, Matsumura Kiyoshi, Fukuhara Masayo, Ohya Yusuke, Fujii Koji, Iida Mitsuo
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Hypertens Res. 2003 Oct;26(10):839-45. doi: 10.1291/hypres.26.839.
We have previously reported that urotensin II acts on the central nervous system to increase blood pressure in normotensive rats. In the present study, we have determined the central cardiovascular action of urotensin II in spontaneously hypertensive rats (SHR). Intracerebroventricular (ICV) injection of urotensin II elicited a dose-dependent increase in blood pressure in both SHR and normotensive Wistar-Kyoto rats (WKY). The changes in mean arterial pressure induced by ICV urotensin II at doses of 1 and 10 nmol in the WKY were 8 +/- 2 and 23 +/- 3 mmHg, respectively. ICV administration of urotensin II caused significantly greater increases in blood pressure in SHR (16 +/- 3 mmHg at 1 nmol and 35 +/- 3 mmHg at 10 nmol, respectively) compared with those in WKY. Urotensin II (10 nmol) elicited significant and comparable increases in heart rate in SHR (107 +/- 10 bpm) and WKY (101 +/- 21 bpm). Plasma epinephrine concentrations after ICV administration of 10 nmol urotensin II were 203 +/- 58 pmol/ml in SHR and 227 +/- 47 pmol/ml in WKY, which tended to be higher than those in artificial cerebrospinal fluid-injected rats (73+/- 7 and 87 +/- 28 pmol/ml, respectively, p < 0.1). The immunoreactivity of urotensin II receptor GPR 14 was expressed extensively in the glial cells within the brainstem, hypothalamus, and thalamus. These results suggest that central urotensin II may play a role in the pathogenesis of hypertension in SHR. Since GPR 14 was expressed in the glial cells of the brain, urotensin II may act as a neuromodulator to regulate blood pressure.
我们之前曾报道,尾加压素II作用于中枢神经系统可使正常血压大鼠的血压升高。在本研究中,我们测定了尾加压素II对自发性高血压大鼠(SHR)的中枢心血管作用。脑室内(ICV)注射尾加压素II可使SHR和正常血压的Wistar-Kyoto大鼠(WKY)的血压呈剂量依赖性升高。在WKY中,ICV注射1和10 nmol剂量的尾加压素II引起的平均动脉压变化分别为8±2和23±3 mmHg。与WKY相比,ICV给予尾加压素II使SHR的血压升高更为显著(1 nmol时为16±3 mmHg,10 nmol时为35±3 mmHg)。尾加压素II(10 nmol)使SHR(107±10次/分钟)和WKY(101±21次/分钟)的心率显著且同等程度升高。ICV给予10 nmol尾加压素II后,SHR的血浆肾上腺素浓度为203±58 pmol/ml,WKY为227±47 pmol/ml,均高于注射人工脑脊液的大鼠(分别为73±7和87±28 pmol/ml,p<0.1)。尾加压素II受体GPR 14的免疫反应性在脑干、下丘脑和丘脑的神经胶质细胞中广泛表达。这些结果表明,中枢尾加压素II可能在SHR高血压发病机制中起作用。由于GPR 14在脑的神经胶质细胞中表达,尾加压素II可能作为一种神经调节剂来调节血压。