Kusano S, Seto S, Akahoshi M, Kitamura S, Nagao S, Ozeki S, Yano K, Hashiba K
Third Department of Internal Medicine, Nagasaki University School of Medicine, Japan.
Brain Res. 1993 Jul 30;618(1):63-70. doi: 10.1016/0006-8993(93)90429-q.
The role of central Ca2+ in the regulation of blood pressure (BP) was investigated in conscious spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). Ten microliters of a high Ca2+ solution (Ca2+: 32.6 mM) administered intracerebroventricularly (i.c.v.) decreased the mean arterial pressure (MAP) for more than 20 min in SHR (n = 7, P < 0.005), while no change of MAP was observed in the WKY (n = 6). This depressor response to Ca2+ i.c.v. was dose-dependent at Ca2+ concentrations between 16.3 and 65.2 mM. We also investigated the effect of high Ca2+ i.c.v. in SHR after pretreatment with Ca2+ channel blockers, diltiazem (60 micrograms/10 microliters) or nisoldipine (4, 8, 16 and 32 micrograms/10 microliters), administered i.c.v., the autonomic ganglion blocker, hexamethonium (50 mg/kg), administered i.v. and alpha-methyl-p-tyrosine (100 and 400 micrograms/10 microliters) delivered i.c.v. Pretreatment with i.c.v. diltiazem (n = 8) or nisoldipine (n = 5 for 8 micrograms, n = 6 for 4, 16, 32 micrograms) abolished and/or blunted the decrease of MAP due to high Ca2+. Hexamethonium administered i.v. (n = 6) also canceled the depressor action of i.c.v. Ca2+. Pretreatment with 100 micrograms of i.c.v. alpha-methyl-p-tyrosine could not prevent the depressor action of i.c.v. Ca2+; however, 400 micrograms of alpha-methyl-p-tyrosine administered i.c.v. abolished the effect of i.c.v. Ca2+. Furthermore Ca2+ channel blockers administered i.c.v. in themselves increased MAP in SHR (P < 0.05). These results suggest that central Ca2+ is involved in the central regulation of BP in SHR. This effect may be mediated through changes in sympathetic activity.
在清醒的自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）中研究了中枢Ca2+在血压（BP）调节中的作用。向脑室内（i.c.v.）注射10微升高Ca2+溶液（Ca2+：32.6 mM）可使SHR（n = 7，P < 0.005）的平均动脉压（MAP）降低超过20分钟，而WKY（n = 6）的MAP未观察到变化。这种对i.c.v. Ca2+的降压反应在Ca2+浓度为16.3至65.2 mM之间时呈剂量依赖性。我们还研究了在i.c.v.给予Ca2+通道阻滞剂地尔硫䓬（60微克/10微升）或尼索地平（4、8、16和32微克/10微升）、静脉注射自主神经节阻滞剂六甲铵（50毫克/千克）以及i.c.v.给予α-甲基对酪氨酸（100和400微克/10微升）预处理后，i.c.v.给予高Ca2+对SHR的影响。i.c.v.给予地尔硫䓬（n = 8）或尼索地平（8微克时n = 5，4、16、32微克时n = 6）预处理可消除和/或减弱由于高Ca2+引起的MAP降低。静脉注射六甲铵（n = 6）也可消除i.c.v. Ca2+的降压作用。100微克i.c.v.给予α-甲基对酪氨酸预处理不能预防i.c.v. Ca2+的降压作用；然而，400微克i.c.v.给予α-甲基对酪氨酸可消除i.c.v. Ca2+的作用。此外，i.c.v.给予Ca2+通道阻滞剂本身可使SHR的MAP升高（P < 0.05）。这些结果表明，中枢Ca2+参与了SHR中BP的中枢调节。这种作用可能是通过交感神经活动的变化介导的。
