The Effect Of Antihypertensive NO.1 On Kidney Rennin Angiotensin System In Spontaneous Hypertensive Rat

There are about 1.6 hundred million hypertension patient in our country and the prevalence is 18.8%. The control rate of hypertension is only 6.1%, the uncontrol rate is 18.6%.There are 69.8% patient who did not know he is hypertension, and 5.5% patient who know he is hypertension refuse to take medicine.So the hypertension is the main killer of health for humanbeings.The renin-angiotensin system(RAS) is the main regulator for blood pressure regulation. The researcher has found that there was location RAS expcept circulation RAS with the development of cellular and molecular biology technical. It was demonstated that the component in location RAS can be synthesized in location tissue. The location RAS is independent of circulation RAS. But it is not clear that the role of location RAS in hypertension and the target organ injury induced by location RAS. Then the spontaneous hypertensive rat (SHR)was used as object to explore the role of kidney RAS in hypertension then to explore the mechanism of antihypertensive NO.1.Methods: RT-PCR were used to measure the expression of angiotensin-converting enzyme (ACE), angiotensin type 1 receptor (AT1), angiotensin receptor type 2 (AT2) , Bax and the aquaporins 4 (AQP4) mRNA in kidney of SHR treated with antihypertensive NO.1.Results and discussion: Antihypertensive NO.1 can decrease the blood pressure of spontaneously hypertensive rat significantly, and it has a dose-effect relation. Antihypertensive NO.1 has no effect on the ACE mRNA expression, but it could increase the ratio of AT2/AT1 in kidney of SHR. It suggested that antihypertensive NO.1 has no effect on the concentation of Angâ…¡, but can affect its binding with receptor(AT1 or AT2). When Angâ…¡bind with AT2 receptor, it will decrease the blood pressure through vasodilation. In addition to, when SHR treated with antihypertensive NO.1, the exprssion of AQP4 mRNA in kidney is decreased, then decreased reabsorption of water in collecting duct. This maybe one of the mechanism for decreasing blood pressure by antihypertensive NO.1. Antihypertensive NO.1 can also decrease the expression of Bax mRNA in kidney of SHR, then lessen the kidney injury. It is related to the RAS activation regulated by antihypertensive NO.1. It maybe the result of direct antiapoptosis by antihypertensive NO.1Conclusion: 1)Antihypertensive NO.1 decreased the blood pressure through increasing the ratio of AT2/AT1 which resulted in vasodilation. 2) Antihypertensive NO.1 decreased the exprssion of AQP4 mRNA in kidney, then decreased reabsorption of water in collecting duct. This maybe one of the mechanism for decreasing blood pressure by antihypertensive NO.1. 3) Antihypertensive NO.1 can also decrease the expression of Bax mRNA in kidney of SHR, then lessen the kidney injury. It is related to the RAS activation regulated by antihypertensive NO.1. It maybe the result of direct antiapoptosis by antihypertensive NO.1...