Vascular effect of hydroxyl-safflor yellow A and underlying mechanism / 上海第二医科大学学报

Objective To investigate the vascular effect of hydroxyl-safflor yellow A(HSYA) on rat thoracic aorta and its underlying mechanism. Methods The tension of isolated thoracic aorta rings of rats perfused with different concentrations of HSYA(1?10-6-1?10-4 mol/L) was measured using organ bath technique.The effects of HSYA on the vasocontraction induced by cumulative phenylephrine(PE)(1?10-6-1?10-4 mol/L),KCl(6?10-2 mol/L) and CaCl2(1?10-5-3?10-3 mol/L) were recorded respectively. Results HSYAcaused a concentration-dependent anti-contraction effects by KCl or PE in endothelium-intact and endothelium-denuded aortic rings.HSYA inhibited the CaCl2-induced contraction and downward shifted concentration-response curve of aortic rings.HSYA+HP resulted in more significant anti-contraction effect than single use of HSYA(P0.05).There were significant differences in anti-contraction effect between HSYA+RR and RR or HSYA(P

Detection of serum autoantibodies against AT₁A-receptor during the development of the four types of hypertensive rat models / 生理学报

Using two-kidney one-clip renal hypertensive (2K1C group), stress-induced hypertensive (neural group), DOCA-salt treated hypertensive (DOCA group) and spontaneously hypertensive rats (SHR group), to investigate the change in AT(1A)-receptor autoantibodies (AT(1A)-AAs) during the development of the four types of hypertension. The biological activities of AT(1A)-AAs were examined. It was shown that the frequency of occurrence and titres of AT(1A)-AAs increased significantly during the development of hypertension. In the four hypertensive groups studied, the occurrence of AT(1A)-AAs was most prominent in SHR, 2K1C and neural groups. The biological effects of AT(1A)-AAs were shown to increase the beating frequency of cultured neonatal myocardial and vascular contractile tension. It is suggested that autoimmune mechanisms are involved the pathogenesis of different types of hypertension and the AT(1A)-AAs may be one of the mechanisms leading to cardiac hypertrophy.

Comparative studies of vasodilating effects of angiotensin-(1-7) on the different vessels / 生理学报

The purpose of this study was to compare the vasodilating effects of angiotensin-(1-7) [Ang-(1-7)] on the different vessels and to clarify its mechanisms by using relaxing responses of preconstricted vascular rings. The results showed: (1) Ang-(1-7) dose-dependently induced vasorelaxation in all the vessels studied. However, there is apparent heterogeneity in the responsiveness of vessels from different origin. (2) The Ang-(1-7)-induced vasorelaxation was endothelium dependent and largely mediated by NO system. (3) The vasodilator action of Ang-(1-7) was not mediated by AT1 or AT2 receptor subtypes. It is suggested that the Ang-(1-7)-induced vasorelaxation is endothelium dependent by some other unclarified angiotensin receptor subtypes and is largely mediated by NO system.

Effect of losartan on produce of sera autoantibodies to angiotensin II-1 receptor in renovascular hypertension rats / 中国应用生理学杂志

<p><b>AIM AND METHODS</b>The effects of losartan (after operation 2 week to 10 week, 5 mg/kg d ig) on generation of AT1R-AA in sera were observed during development of hypertension in rats. The renovascular hypertension (RVH) model was established by two-kidney one-clip method, a synthetic peptide corresponding to amino acid sequence 165-191 of the second extracellular loop of the angiotensin II-1 receptor (AT1R) was used as antigen, SA-ELISA were used to examine sera AT1R autoantibody (AT1R-AA).</p><p><b>RESULTS</b>The frequencies and titres of AT1R-AA after operation one week rats were significantly increased (P < 0.05). The treatment with losartan not only inhibited structural and functional changes, but also the frequencies and titres of AT1R-AA was significantly lower (P < 0.05) than RVH group.</p><p><b>CONCLUSION</b>It is suggested that the losartan significantly inhibits generation of the AT1R-AA.</p>

Changes in autoantibody against cardiovascular AT1-receptor during development of renovascular hypertension in rats / 生理学报

The aim of this study was to observe the change in angiotensin II receptor subtype 1 (AT(1)) autoantibody during the development of renovascular hypertension (RVH). The Goldblatt renovascular hypertension model was established by the two-kidney one-clip method, and a synthetic peptide corresponding to amino acid sequence 165-191 of the second extracellular loop of the AT(1)-receptor was used as the antigen. Sera AT(1)-receptor autoantibody was detected by SA-ELISA. It was shown that two weeks after operation both the frequency of occurrence and the titre of autoantibodies to AT(1)-receptor were significantly increased as compared with the pre-treatment control. The increase in autoantibodies lasted several weeks and then decreased gradually to the pre-clipping level at 12 weeks. It is suggested that autoimmune mechanisms are involved in the pathogenesis of renovascular hypertension and the AT(1) autoantibodies may be one of the mechanisms leading to cardiac hypertrophy.