Effect of central ras on one-kidney Grollman hypertension in rats and its mechanism

Sheng Xiao-yun , Wang Qing , Yang Kun

Current Medical Science ›› 1991, Vol. 11 ›› Issue (1) : 31 -35.

PDF
Current Medical Science ›› 1991, Vol. 11 ›› Issue (1) : 31 -35. DOI: 10.1007/BF02893184
Article

Effect of central ras on one-kidney Grollman hypertension in rats and its mechanism

Author information +
History +
PDF

Abstract

The effect of central renin-angiotensin system (RAS) on one-kidney Grollman hypertension during the maintaining phase and its mechanism were investigated in rats. The arterial blood pressure (ABP) and the content of angiotensin II (A II) and norepinephrine (NE) in brain regions was measured respectively. 4 weeks after operation the ABP was elevated significantly, and it sustained at high level 8 weeks post-operatively. However, ABP in the control group underwent no significant changes at the same period. The A II and the NE content in the brain regions of the operated group were significantly higher than in those of the age-matched control group. During the maintaining phase of hypertension captopril (150 μg/10 μ1) was injected into the lateral cerebroventricle at 0.5 h, 1.0 h and 1.5 h respectively, and ABP and content of A II and NE were determined at the corresponding time. The results showed that the above three parameters decreased consistently at 0.5 h and 1.0 h, and increased gradually at 1.5 h, suggesting that the central RAS might play an important role in the maintaining phase of onekidney Grollman hypertension in rats.

Keywords

one-kidney Grollman hypertension / angiotensin II / norepinephrine / arterial blood pressure / captopril

Cite this article

Download citation ▾
Sheng Xiao-yun, Wang Qing, Yang Kun. Effect of central ras on one-kidney Grollman hypertension in rats and its mechanism. Current Medical Science, 1991, 11(1): 31-35 DOI:10.1007/BF02893184

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

GantenD, et al. . Iso-renins of extrare- nal origin “The tissue angiotensino- genase systems”. Am J Med, 1976, 60: 760-760

[2]

PhillipsMI, et al. . Evidence for an endogenous brain renin-angiotensin system. Fed Proc, 1979, 38: 2260-2260

[3]

GantenD, et al. . Genetic control of renin in the tissues of different strains of mice. Naunyn-Schmiedebergs Arch Pharmacol, 1986, 332: R59-R59

[4]

SchellingP, et al. . Regulation of brain angiotensinogen in renal hypertensive rats. Clin Exp Theory Practice, 1984, A6(10): 1755-9

[5]

BuggYT, et al. . Prevention of the development of renal hypertension by anterioventral third ventricle tissue lesions. Circ Res, 1977, 40: 1-110

[6]

RobertsonIIS, et al. . The pathophysiology of renovascular hypertension. J Hypertens, 1986, 4(4): S95-103

[7]

ThomasU, et al. . Brain converting enzyme inhibitions a possible mechanism for the antihypertensive action of captopril on SHR. Eur J Pharmacol, 1981, 70: 467-78

[8]

BarkerJL, et al. . BuckleyJP, FerrarioCM, et al. . Peptide regulation of neuronal excitability: evidence for a neurohormonal role. Central Action of Angiotensin and Related Hormones, 19772ed.New York, Pergamon Press: 29-51

[9]

SummersC, et al. . Central injection of angiotensin alters catecholamine activity in rat brain. Am J Physiol, 1983, 244: R257-61

AI Summary AI Mindmap
PDF

82

Accesses

0

Citation

Detail

Sections
Recommended

AI思维导图

/