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

Hypertension is one of the clinical syndrome of systolic blood pressure and diastolic blood pressure surge in circulation, Ultimately leading to the heart, brain, kidneys and other series of target organ damage. At present the incidence of hypertension in China is dramatically on the rise, We should further promote the prevention and treatment of hypertension in order to reduce the incidence of hypertension and actively control the occurrence of various complications. Mechanisms of hypertension and some antihypertensive drugs is still not fully illuminated. However, RAS played an important role in the process of generation and maintenance of hypertension. How to do an effective study in the causes of hypertension and mechanism of antihypertensive drugs to control the blood pressure is the core of the treatment of hypertension, and is great significance of reducing cardiovascular mortality and improving the quality of life.The pathogenesis of hypertension is not clear, but the pressure to RAS and develop the key role has been reached. In recent years, with biochemistry and molecular biology technology development, people found that rennin is not only a cycle of kidney secrete hormones, in renal tissues, especially the brain, cardiovascular system and adrenal itself, still exist in a local renin-angiotensin system. It is distributed throughout the organization organs, including the circulatory system and central nervous system and the stress response system with classic closely relationship. At present, the circulation of blood plasma RAS already known, and the influence on local organization RAS system of primary hypertension relation is unclear. This experiment can be known step-down no.l in the hypotensive based on the established models, step-down no.l SHR after the intervention of SHR observation RAS cortex AGT ingredient, ACE, AT1, AT2 expression level change, further defined step-down size, its mechanism of step-down more extensive clinical application provides a scientific experiment basis.Experimental methods:60 spontaneously hypertensive rats (SHR) and 12 Wistar rat only healthy weight evenly (male),200±20g randomly divided into six groups, and 12, respectively in model group, and SHR positive-controlled group, one of the low-dose, step-down 1 dose group, step-down no.l in the high-dosage groups. In fourteen weeks, form spontaneously hypertensive cerebral specimens, and used in through the retrovirus-the polymerase chain reaction (PCR) and Western RT-Blotting detecting spontaneously hypertensive rats (SHR) therapy RAS cortex AGT system components, such as AT1 AT2 mRNA ACE, and the expression level of change.Results:the hypertensive rats in the cortex and the expression is ATI AT2 model was increased, and the group with the increase of higher doses. Rising above the AT2 expression AT1 (P<0.01), Use antihypertensive drug after 1 spontaneously hypertensive rats in the cortex is the expression of ACE was increased, and the model group with higher doses, and compared with the model group, step-down no.l AGT group expression level significantly reduced.Conclusion:Drugs can reduce the level of substrate expression of RAS system, causing increased expression of AT1 and AT2, AT2 receptor expression in particular. AT2 plays an a role in antihypertensive effect by expansion of blood vessels. Expression of ACE in cerebral cortex of SHR is creasing compared with the model group, expression increased with The higher dose of drug. but expression level of ACE has little effect on blood pressure.