The present experiments were designed to compare the antihypert-ensive effects of nitrendipine, m-nifedipine and their oil preparation in conscious renal hypertensive rats The left renal artery was narrowed by a silver clip of 0.2mm diameter under anaesthesia.The systolic blood pressure was measured by the tail cuff method. Nitrendipine and m-nifedipine dissolved in peanut oil ( 20mg/ml ) ; 20mg/kg were given im every other day for 4 weeks.Using sum of squares of deviations from mean in comparison with the untreated control animals the results showed that the 2 drugs reduced the blood pressure significantly (P

In left ventricular hypertrophied hypertensive rats (LVH), effects of alcohol extract of Peucedanum praeruptorum(QHJG)on left ventricular(LV)compliance and Ca2+content in left ventricular myocardial mito chondria and tail artery were studied.QHJG 0.6g/100g(body weight).d was given for 9 weeks (ig). The LV compliance in LVH group was significantly decreased as compared with that in the sham-operated group. The Ca2+ content in left ventricular myocardial mitochondria and tail artery of LVH group was markedly raised. But QHJG could mardedly im prove the LV compliance and decrease the Ca2+ of left ventricular myocardial mitochondria and tissues of tail artery from LVH rats.These results suggest that QHJG can improve the LV compliance in LVH rats,which maybe related to its reduction of Ca2+ content of LV myocardial mitochondria and tissues of tail artery

Renovascular hypertensive rats were treated with either medipine (m-Nif) or nifedipine (Nif) for 9 weeks. In all groups the antihypertive therapies significantly reduced both mean arterial blood pressure and left ventricular hypertrophy. In LVH rats contractions caused by NE were increased on rings both with endothelium and without endothelium, and NE-ratio was greater than 1. The increase in NE induced contraction and the decrease in Ach induced relaxation in LVH rats were due to bothendothelium and smooth muscle dysfuction. In the m-Nif and Nif treated groups, these NE-ra-tio were significantly decreased and had lower maxtimal response and higher IC50. These indicate m-Nif and Nif had direct effect on smooth muscle and endothelium. Our results show that m-Nif and Nif has no influence on the endotheli-um-dependent relaxation to Ach.

AIM　To study the effects of praeruptorin C (pra-C), a pure constituent isolated from “Qian-Hu”, the roots of Peucedanum praeruptorum Dunn. (Umbelliferae), on vascular hypertrophy, collagen content, transient ［Ca2+］i, NO and vascular response of the thoracic aorta of renovascular and spontaneously hypertensive rats (RHR, SHR). METHODS　RHR and SHR were given pra-C 20 mg.kg-1.d-1 for 9 weeks, ig. Blood pressure of both rats were measured using tail cuff manometry. Under inverted microscopy the length and width of the smooth muscle cells were measured by using computer software MICC (Dongnan University). ［Ca2+］i of smooth muscle cell (SMCs) was measured with Fura-2/AM. By measuring the specific aminoacid hydroxyproline content, the collagen content was obtained. By using Griess reagent, the NO in the smooth muscle cells (SMCs) was measured. RESULTS　The intermedia of the thoracic aorta in RHR was enlarged than that of the normal and pra-C groups. The size (length×width) of the SMCs of thoracic aorta from RHR increased 73.4 μm vs nomal 34.5 μm and pra-C 34 μm. The collagen content of thoracic aorta was 39%±6.8% dry weight in RHR, they were 26.5%±3% dry weight in normal and 25.6%±1.1% dry weight in pra-C, RHR vs pra-C. The resting ［Ca2+］i of single cell of SMCs was (62±6) nmol.L-1. In Hanks solution containing CaCl2 1 mmol.L-1, the resting ［Ca2+］i of SMCs was (150±8) nmol.L-1 in normal. (226±11) nmol.L-1 in RHR. In presence of KCl 60 mmol.L-1, NE 10 μmol.L-1, ANG II 100 nmol.L-1 and ATP 30 μmol.L-1 the ［Ca2+］i of SMCs were increased by 128%; 132%; 233% and 152% in RHR, respectively. The pra-C group was similar to the normal group. The resting ［Ca2+］i of SMCs was (71±6) nmol.L-1 in control of SHR, in Hanks solution containing CaCl2 1 mmol.L-1. The resting ［Ca2+］i of SMCs was (160±8) nmol.L-1 in normal, and (362±18) nmol.L-1 in SHR. In presence KCl 60 mmol.L-1 and NE 10 μmol.L-1 the ［Ca2+］i of SMCs were increased by 235% and 200% in SHR, respectively. Pra-C group was similar to normal group. NO of SMCs was decreased 76% in SHR, pra-C group was nearly normal. The pra-C improved vascular responses of the thoracic aorta of RHR. CONCLUSION　These results indicate that pra-C improved the vacular hypertrophy by decreasing the size of SMCs cells, collagen content. SMCs ［Ca2+］i and increasing NO production.

To analyse the effect of tetrandrine(Tet) on proliferation of aortic vascular smooth muscle cells ( AVSMC), AVSMC were isolated and cultured from sham-operated rats(Sham), renovascular hypertensive rats〔RHR, 18 weeks after two kidney one clip(2K1C) operation〕, and Tet (50 mg*kg-1*d-1 po for 9 weeks from week 9 after 2K1C operation)treated RHR. The proliferation of AVSMC was detected by MTT method, and the DNA synthesis was evaluated by ［3H］-thymidine incorporation. The results showed that ①The ultrastructure of aorta suggested that AVSMC in RHR had transferred from contractile phenotype to synthetic phenotype; ②Compared to Sham, AVSMC from RHR showed a higher proliferative property with a higher cell number and an increased growth rate stimulated by norepinephrine(NE) or angiotensinⅡ(AngⅡ); ③Compared to untreated RHR, AVSMC from Tet treated RHR showed a reduced reactivity to NE- or AngⅡ-stimulated proliferation and growth rate; ④Tet(0.1－10 μmol*L-1) treated in vitro induced a concentration-dependent depression in ［3H］ thymidine-incorporation stimulated by NE or AngⅡ in AVSMC from either RHR or Sham. This study provides an evidence of increased reactivity to NE or AngⅡ in AVSMC of RHR. Tet inhibits the proliferation and DNA synthesis in AVSMC, depresses the susceptibility of AVSMC to AngⅡ and NE, both contribute to the regression effect on hypertensive vascular remodeling.

Effects of preconditioning(PC) and praeruptorine C(Pra-C) on intracellular free calcium level(［Ca2+］i) and NO content in hypertrophied vascular smooth muscle cells (VSMC) with hypoxia were studied. ①The aorta VSMC of rats with renovascular hypertension induced by two-kidney-one-clip(2K1C) were isolated and cultured. Fura-2/AM was as a calcium fluorescent indicator. It was seen that Pra-C(20 mg*kg-1*d-1，ig, for 9 weeks from week 9 after 2K1C) and PC (3 cycles of 5 min pure N2 and 5 min 95%O2+5%CO2) antagonisted the elevated activities(higher ［Ca2+］i) induced by KCl and norepinephrine in VSMC with hypo- xia (30 min pure N2). ② In hypertrophied VSMC stimulated by angiotensinⅡ, combination of Pra-C(10 μmol*L-1 for 24 h) and PC enhanced NO content to the normal level in hypertrophied VSMC with hypo- xia. The results suggest that combination of Pra-C and PC have cooperative protection for hypertrophied VSMC with hypoxia injury.

A study was made on the effects of Dephenetin on vascular resistance and cardiotonic action in anesthetized dogs. The results showed that Dephenetin reduced left coronary cifcumflexus, vertebral and femoral ateries resistance, it increased cardiac out put without significant heart rate changes.The results also showed that Dephenetin dilates peripheral vessels and produced positive inotropic action.

In the isolated rabbit aorta, like verapamil ( Ver ) anisodamine ( Ani ) might inhibit the contraction induced by phenylephrine ( PE ) and high K+ with IC50 value of 120 and 86 ? mol/L, respectively. PE/K+ ratio of IC50 was 1.4 which was less than that of Ver. It showed that although PDC may be more sensitive to Ani than ROC, the difference in sensitivity of Ani on 2 calcium chan- nel are less marked than that of some calcium antagonists. Ani had inhibitory effects on 2 contractile components of serotonin (5-HT ) . Ani and Ver could obviously inhibit post-resting potentiatipn and staircase phenomenon in guinea pig atria. Ani also might inhibit the contraction induced by calcium and shift concentration-response nonparallelly to right on both tissues above.The results suggest that Ani possesses nonspecific calcium antagonistic effect and reduces the tension by affecting PDC and ROC to decrease extracellular calcium influx and inhibiting intracellular calcium release.

The bovine basilar artery vascular smooth muscle cells(BAVSMC S) were isolated and cultured.The effects of chitosan and enalaprilat on the proliferation of BAVSMC S induced by angiotensin Ⅱ(AngⅡ) were evaluated with MTT method,the DNA synthesis in BAVSMC S was measured by thymidine incorporation and total protein of BAVSMC S was detected by coomassie brilliant blue method.The results showed that chitosan can inhibit the proliferation of BAVSMC S induced by AngⅡ in a time and concentration dependent manner,and depress thymidine incorporation of BAVSMC S induced by AngⅡ in a concentration dependent manner chitosan can reduce the content of protein in BAVSMC S induced by AngⅡ.These findings suggested that chitosan is capable of producing an inhibitory effect on proliferation of bovine basilar artery vascular smooth muscle cells induced by AngⅡ .

To study the effects of tetrandrine (Tet) on hypertrophied myocardial hydroxyproline content and myosin ATPase activity, left ventricular hypertrophy(LVH) was induced by renovascular hypertension (two-kidney, one-clip) in rats. Eight weeks after operation Tet 50 mg*kg-1*d-1 and enalapril(Ena) 6 mg*kg-1*d-1 were given by gavage for 8 weeks. The results showed that hydroxyproline content in LVH group was much higher than that of sham-operated one 〔(5.9±0.3) vs (3.6±0.4) mg*g-1 dry weight〕, and was decreased by 28.2% and 39.0% in Tet and Ena groups, respectively. Myosin ATPase activity in LVH group was much lower than that of sham-operated group 〔(0.43±0.09) vs (0.97±0.06) mmol Pi*min-1*g-1 protein, P<0.01〕. In Tet and Ena groups they were 60.5% and 118.6% higher than that of LVH group, respectively. The results suggest that Tet or Ena partially reduce the hydroxyproline content and elevate myosin ATPase activity of hypertrophied myocardium in renovascular hypertensive rats.