Kageyama Y, Suzuki H, Hayashi K, Saruta T
Clin Exp Hypertens A. 1986;8(3):355-70. doi: 10.3109/10641968609039610.
The effects of oral calcium loading on the blood pressure of spontaneously hypertensive rats (SHR) (n = 20) and age-matched normotensive Wistar-Kyoto rats (WKY) (n = 16) were investigated. Calcium loading was performed by adding 1.5% CaCl2 (Calcium chloride) to the drinking water. Calcium loading attenuated the development of hypertension in the SHR but not in the WKY, and at the end of a 3 week experiment, systolic blood pressure was 171+2 vs 197+3 mmHg (P less than 0.01). In spite of this reduction of blood pressure, there were no significant changes in sodium-water balance, plasma levels of norepinephrine and epinephrine, plasma renin activity, plasma aldosterone concentration and serum electrolytes due to the calcium treatment. On this basis, the depressor mechanism of calcium loading in the SHR was studied by observing the pressor response to norepinephrine and the vascular reactivity to norepinephrine in hind limb perfusion. It was found that both the pressor response and the vascular reactivity were significantly attenuated by the calcium treatment in the SHR but not in the WKY. These results suggest that the antihypertensive effects of calcium treatment in SHR may depend mainly on attenuation of the vascular reactivity.
研究了口服钙负荷对自发性高血压大鼠(SHR,n = 20)和年龄匹配的正常血压Wistar-Kyoto大鼠(WKY,n = 16)血压的影响。通过在饮用水中添加1.5%氯化钙(CaCl2)进行钙负荷。钙负荷减弱了SHR高血压的发展,但对WKY无效,在为期3周的实验结束时,收缩压为171±2 mmHg 对比197±3 mmHg(P < 0.01)。尽管血压有所降低,但钙治疗对钠水平衡、去甲肾上腺素和肾上腺素的血浆水平、血浆肾素活性、血浆醛固酮浓度和血清电解质均无显著影响。在此基础上,通过观察后肢灌注中对去甲肾上腺素的升压反应和血管反应性,研究了SHR中钙负荷的降压机制。发现钙治疗显著减弱了SHR中的升压反应和血管反应性,但对WKY无此作用。这些结果表明,钙治疗对SHR的降压作用可能主要取决于血管反应性的减弱。