| The etiology and pathogenesis of essential hypertension have not been clarified until now. Since mosaic theory suggested in 1940s essential hypertension probably results from combination of genetic, environmental, neural, endocrine and hemodynamic factors. Many researches have identified that essential hypertension belongs to a complicated polygentic disease. Genes contributing to hypertension are being sought by analytic experiments aimed at identifying candidate genes associated or segregating with the phenotype in humans and animals and by synthetic experiments in which changes are made in candidate genes in animals and their effects on blood pressure are determined.Calcium plays an important role in the pathogenesis of essential hypertension. Calcium mobilization is associated with electrical activity and contraction of the heart and vascular smooth muscle. Calcium transport defect is closely correlated with hypertension. Most of the intracellular calcium is stored in the SR. SR controls contraction and relaxation of smooth muscle cell through regulating the free calcium concentration in the cell. When the calcium release channel open, calcium is put into the cytoplasm from SR. When the concentration of the free calcium up to 10-5 M in the cytoplasm, troponin I is activated and the conformation is changed so that contraction appears at the moment globulin contacts with actin. Then the free calcium is pumpedinto SR by the SERCA. When the concentration of the free calcium down to 10-7M, globulin and actin detach with each other, then relaxation happens. This is an intact contraction-relaxation procedure. Ca2+ homeostasis will be disequilibrated after the abnormal expression of SERCA and calcium release channels, and that leads to disfunction of contraction and relexation, hence heart failure occurs. The funtion of SERCA is regulated by phosphorylation and dephosphorylation of phospholamban. There are two types of calcium release channels. One is inositol triphosphate receptor calcium channels, the other is ryanodine receptor calcium channels. The SERCA and these two kinds of calcium release channels are closely cooperated in the maintenance of calcium homeostasis.Though Boknik et al found that there were not any changes in the expression of SERCA and phospholamban, the procedure of protein phosphorylation enhanced. Lompre et al found that during the early and medium phase of the heart development, the expression of SERCA was increased with the age, but decreased obviously when became old. The increased and decreased expression of SERCA will lead to changes of the function of contraction and relaxation. Arai et al observed dual phenomena of the expression of SERCA that the expression of SERCA increased significantly in the model of cardiac hypertrophy after ligating the aorta of the rats. And decreased when the hypertrophy became serious. So the mRNA level of SERCA expression is an index of the degree of cardiac hypertrophy and its systolic function, In our experiments that before the occurrence of arterial hypertension, the expression of SERCA raised. The result indicated that it may have close effects on the occurrence, development and maintenance of genetic hypertension.Owing to the different experimental conditions, subjective or objective, different results were provided. Some studies showed that during the early and medium time of the arterial hypertension, there were not any changes in the expression of calcium release channels. But some other researchs prove the evidence that it is a dual results of calcium release channel in the model of cardiac hypertrophy. At the early time of hypertrophy, the mRNA expression of RyR2 upregulated and downregulated at the middle and end stage.G proteins are cell membrane proteins which have the activity of GTP binding and hydrolysis. G proteins were made up of three subunit as a, |3 and Y , that link cell surfacee receptors to intracellular effector systems, such as phospholipase C(PLC), leading to the formation of second messengers as inositol pho...
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