Regression of vascular remodeling in renovascular hypertensive rats by tetrandrine and enalapril / 药学学报

<p><b>AIM</b>To observe the regression effect of tetrandrine (Tet) and enalapril (Ena) on vascular morphological changes in renovascular hypertensive (RH) rats.</p><p><b>METHODS</b>Renovascular hypertension was induced by two kidney one clip (2K1C) operation. The morphometric measurements were performed in the aorta, caudal artery, renal arterioles, coronary arterioles and mesenteric arterioles.</p><p><b>RESULTS</b>The wet weight of aorta, caudal artery and femoral artery of RH rats (18 weeks after 2K1C operation) were greater than those of sham-operated rats. The media thickness, lumen diameter, cross section of media, media over lumen ratio and the wet weight of abdomen aorta, caudal artery, coronary arterioles, renal arterioles and mesenteric arterioles were significantly increased, which were more significant in arterioles with the diameter smaller than 70 microns. There were no significant change in the number of the smooth muscle cells (VSMC) in most vessel wall, except in renal arterioles, where the number of smooth muscle cells were significantly increased. After Tet (50 mg.kg-1.d-1, p.o.) or Ena (6 mg.kg-1.d-1, p.o.) treated for 9 weeks from week 9 after 2K1C operation, almost all the changes in the media thickness, the media to lumen ratio, the cross section of media and the wet weight were ameliorated.</p><p><b>CONCLUSION</b>In RH rats, mainly a hypertrophic and rearrangement remodeling in the wall of arteries and arterioles was observed with a proliferation of VSMC in renal arterioles. Tet and Ena were shown to regress vascular remodeling by markedly attenuating these changes in renovascular hypertensive rats.</p>

Effects of praeruptorin C on cell hypertrophy, intracellular Ca2+i, nitric oxide and signal transduction in isolated hypertrophied rat smooth muscle cells induced by angiotensin II / 药学学报

<p><b>AIM</b>To investigate the effects of praeruptorin C (Pra-C) on smooth muscle cell (SMC) hypertrophy, intracellular calcium ([Ca2+]i), nitric oxide (NO) content and influence on cellular signal transduction in isolated cultured rat smooth muscle cell (SMC).</p><p><b>METHODS</b>Hypertrophied smooth muscle cells (HSMCs) were induced by angiotensin II (Ang II), cell area was measured under inverted microscope. Nitric oxide (NO) concentration was measured using Griess method. [Ca2+]i was measured using Fura-2/AM. The responses to [Ca2+]i elevation stimulated by KCl (60 mmol.L-1 or norepinephrine (10 mumol.L-1) were observed by incubation with phorbol 12-myristate 13-acetate (PMA), staurosporine (ST), the agonist and inhibitor of protein kinase C (PKC), and pertussis toxin (PTX), the sensitive toxin of Gi.</p><p><b>RESULTS</b>The cell area of SMCs were decreased by 39.01% (P < 0.001) and NO content of SMCs were significantly increased in Pra-C + Ang II group. In presence of 60 mmol.L-1 KCl or 10 mumol.L-1 NE, [Ca2+]i of SMCs in Pra-C + Ang II group was significantly decreased than that of Ang II group (P < 0.001) and closed to the normal group. Incubation of SMCs with PMA, ST and PTX, [Ca2+]i of SMCs in Ang II group was increased by PMA and decreased by ST and PTX, but that of Pra-C + Ang II group was similar to the normal group.</p><p><b>CONCLUSION</b>These findings suggest that Pra-C can reduce vascular hypertrophy in isolated rat HSMCs, and this is associated with improvement of SMCs [Ca2+]i level, NO content and cellular signal transdution of PKC and Gi.</p>

Inhibitory effects of ginkgolide B on proliferation of bovine aortic smooth muscle cells / 药学学报

<p><b>AIM</b>To investigate the effects of ginkgolide B (GB) on proliferation of bovine aortic smooth muscle cells (SMC) and its related mechanisms.</p><p><b>METHODS</b>After pretreating with GB or the mixture of ginkgolide A and B (GA:GB) at 37 degrees C for 0.5 h, the VSMC were treated with or without angiotensin II (Ang II) for 24 h. The proliferation of SMC was evaluated by 3H-thymidine incorporation and the cell cycle phase was measured by flow cytometry. Cytotoxicity was reflected by MTT and lactate dehydrogenase (LDH) activity of the supernatant.</p><p><b>RESULTS</b>Whether or not treated with Ang II, GB and GA:GB were shown to suppress SMC proliferation in concentration-dependent fashion at concentrations ranging from 10(-9) mol.L-1 to 10(-5) mol.L-1. The inhibitory effects appeared to be related to a G1-->S block in cell cycle traverse.</p><p><b>CONCLUSION</b>The suppression of SMC proliferation by GB might not only be contributed by blockage of the PAF receptor activity.</p>

Effect of praeruptorum caumarin on cardiac mass, myocardial Ca2+i and Na+, K(+)-ATPase, Ca2+, Mg(2+)-ATPase activity in renovascular hypertensive rats / 药学学报

<p><b>AIM</b>To investigate the preventive and reversional effect of praeruptorum caumarin compound on left ventricular hypertrophy in renovascular hypertensive rats (RHR) and its mechanism.</p><p><b>METHODS</b>The two-kidney-one-clip (2K1C) RHR model was used. The blood pressure, wet weight of the left ventricle, surface area of myocardial cells, resting [Ca2+]i level and Na+, K(+)-ATPase, Ca2+, Mg(2+)-ATPase activity of myocardial membrane and mitochondria were measured.</p><p><b>RESULTS</b>Praeruptorum caumarin 30 mg.kg-1.d-1 was given ig for 9 weeks from the 6th or 9th week after operation in the preventive or regressive group. The blood pressure, left ventricle wet weight and area of myocardial cells of the preventive and regressive group were significantly reduced than that of the LVH group. The resting [Ca2+]i of the both praeruptorum caumarin treated groups (121 +/- 13, 133 +/- 9 nmol.L-1) were lower than that of the LVH group (158 +/- 7 nmol.L-1). The KCl-induced [Ca2+]i elevation was decreased more significantly in preventive and regressive group than that of the hypertrophic myocytes. The activity of Na+, K(+)-ATPase and Ca2+, Mg(2+)-ATPase increased by 40% and 93% in the preventive group, 28.4% and 48.8% in regressive group than that of the LVH group.</p><p><b>CONCLUSION</b>Praeruptorum caumarin was shown to prevent and reverse hypertrophy of LVH by lowering [Ca2+]i and increasing the ATPase activity.</p>