Objective To investigate the effect of hypert riglyceridemia on vascular endothelial function. Methods With high-resolution ultrasound, flow and nitroglycerin-induced dilatation of the brachial artery were determined in thirty hypertriglyceridemic patients and thirty healthy subjects as controls. Serum lipid and plasma endothelin (ET) were determined. Results In patients with hypertriglyceridemia,flow-induced vasodilatation was much reduced compared with that in the control subjects[(2.7±2.0)% vs (15.0±8.0)%, P<0.001］.However, vasodilatation in response to nitroglycerin were similar in both groups［(15.0±5.0)% vs (16.8±9.0)%, P>0.05].Plasma ET level in the hypertriglyceridemic group was significantly higher than that in the control group［(106.22±19.16) μg/L vs (72.37±14.06) μg/L, P<0.001].ConclusionEndothelium-dependent vasodilatation was impaired in patients with hypertriglyceridemia.

Objective To study the role of atrial natriuretic peptide (ANP) and renin-angiotensin-aldosterone system (RAAS) in the pathogenesis of salt-sensitive (SS) hypertension and mechanism of the hypotensive effect of benazepril and ANP in patients with SS essential hypertension. Methods Sixty-four patients with essential hypertension were divided into SS (n=30) and non-salt-sensitive (NSS, n=34) groups by modified Sulliran's method. Plasma ANP, angiotensin Ⅱ (AⅡ) and aldosterone (ALD) were determined before and during the period of salt loading test. Thirty healthy subjects as controls were also enrolled. A self-comparative study of benazepril with the placebo was performed in SS group. Before and after the placebo and benazepril therapy, blood pressure (BP) and plasma ANP were determined. Results (1)Basal plasma ANP level in the SS group was significantly lower than that in the NSS group. Basal plasma ANP level in the NSS group was also significantly lower than that in the control group [(110.28±15.40) pmol/L vs NSS (145.52±26.53) pmol/L and control (197.74±26.20) pmol/L]. Plasma ANP in both SS and NSS groups [(133.56±34.03) pmol/L and (169.20±35.91) pmol/L respectively, both P<0.05 vs control]. Percentage of increase of plasma ANP in SS and NSS groups was of no difference (P>0.05) . (2) No significant difference of basal plasma AⅡ and ALD levels were found between SS and NSS groups (P>0.05). There were no significant changes of plasma AⅡ and ALD during salt loading in both SS and NSS groups ( both P>0.05). (3) After the benazepril treatment, plasma ANP was increased significantly [(146.74±31.86) pmol/L , P<0.01]; both systolic and diastolic BP were reduced significantly in SS group. (4) Basal plasma ANP level was negatively correlated with the magnitude of increase of mean arterial pressure (MAP) by salt loading (b=-0.06, P<0.05). Conclusion Deficiency of circulating endogenous ANP may play an important role in the pathogenesis of SS hypertension. Benazepril could reduce BP and increase plasma ANP significantly in patients with SS hypertension.

Objective To evaluate the factors affecting the treatment of old persons diagnosed hypertension. Method A sample of 55566 persons from the community of Yanji area of Shanghai was recruited. Results Among the 19295 persons over sixty there are 5842 patients with hypertension, the morbidity was 30.3%. Among the 36271 persons aged fifteen to fifty-nine there are 3536 patients with hypertension, the morbidity is 9.7%. The ratio of non-treatment in the old age group is 3.1% and in younger group is 8.8%. However,the compliance to the treatment was better in the younger than in old group(73.7% vs 56.2%). The age,hypertension grade and sex were all accounted for the differences in the regularity of the hypertension treatment. Conclusion Further effort on the education of non-old hypertensive patients is essential to decrease the damage from hypertension.

Objective To investigate the effect of cilazapril on reactivit y of blood vessels in diabetic rats. 　Methods The mesenteric vessels of streptozotocin induced diabetic rats wer e perfused with Kreb-Ringer's solution in vitro,the mesenteric vessels reactivi ty of diabetic rats was measured by physiological recorder. 　Results The responsive continual time to norepinephrine was delay ed signific antly(9.4±3.1 vs 5.2±2.1,P<0.01) and the highest perfusion pressu re decrease significantly in diabetic rats(5.12±0.87 vs 7.81±0.92 kPa, P<0.01); When taken cilazapril showed no difference in these indexes in diabetic animal s.

Objective To investigate the role of angiotensin Ⅱ receptors in metabolism of m yocardial collagen. 　Methods The collagen volume fraction(CVF), perivascular circumferential area(PVCA), hydroproline concentration(HC), ratio o f collagen type Ⅰto type Ⅲ(Ⅰ/Ⅲ),angiotensin Ⅱ(AngⅡ) content and the maximal binding capaci ty (Bmax) of ATRs were studied. The methods of radioimmunoassay(RIA),biochemistry assay, and pathological examin ation were used. 　Results Ventricular myocardial CVF, PVCA, HC, Ⅰ/Ⅲ, AngⅡ and B max of ATRs in WKY rats were significantly higher than those in sham -operation(SO)(P<0.05 or P<0.01),suggesting the collagen was abnormal ly accumulated in rats heart muscles. AngⅡ was positivily correlated with HC(r1=0.9045, P<0.01). After treament of Irbesartan, All above parameter were reduced significantly(P<0.05 or P<0.01), abnormally accumulated collagen was disap peared. While after treament of CGP42112A,an ATR2 antagonist, Bmax of ATRs was markedly decreased(P<0 .01), but CVF, PVCA, HC,Ⅰ/Ⅲ, AngⅡ showed little changes(P >0.05). 　Conclusion Obvious hyperplasia of myocardial collagens and remode ling of collagen network occurred after pressure overload. Local produced AngⅡ involves in the process,it's effects is mainly mediated by angiotensin Ⅱ 1 type receptor(ATR1)

Objective To investigate the roles of T GFβ1 and TGFβ1 typeⅠrecepter(TβRⅠ) in development of myocardial hypert rophy and myo cardial interstitium remodelling in renovascular hypertensive rat. 　Methods TGFβ1 and TβRⅠwere evaluated by qualitative and semi -qu antitative immunohistochemical staining to explore their distribution and ex peression in left ventricular tissue. Van Gieson staining were used in the stud y of total collagen in left ventricular interstitial tissue. 　Results Compared with sham-operated rat(SOR),the expression of T GFβ1 andTβRⅠ in left ventricular tissue were significantly increased in RHR(P <0.01 all). In RHR the antibody to TGFβ1 reacted primarily with cytoplasma a nd myo cardial interstitium while antibody to TβRⅠreacted mainly with myocyte membran es with weak labeling in myocardial interstitium. In SOR,very mild labeling for TGFβ1 and TβRⅠin myocardiun was found with no labeli ng in myocardial interstitium. Correlative analysis revealed that TGFβ1 or T βRⅠ was positively correlated with left ventricular mass index(LVMI),negativel y correlated with grey level of myocardial total collagen. Conclusions TGFβ1 and TβRⅠmay play important roles in develo pment of left ventricular hypertrophy and myocardial interstitial fibrosis.

Objective To investigate the gene expression of sodium pump α-subunit in aortic smooth muscle of 1-kidney-1-clip (1k1c) hypertensive rats. 　Methods 1k1c hypertensive rats were prepared by partially ligating the left renal artery and removing the right kidney. 4 weeks later, all the rats were killed and sodium pump α1- , α2-, and α3-subunit in aortic smooth muscles were detected with reverse transcription p ol ymerase chain reaction (RT-PCR) method and immunohistochemical assay at both mR NA and protein levels, respectively. 　Resulsts Changes in the expression of sodi um pump α-subunit gene were found in aortic smooth muscles of 1k1c hypertensiv e rats: α1-su bunit increased at both mRNA protein levels, while α2- and α3-subunits r emained without changes. 　Conclusions There were great changes in the gene expression of so dium pump α-subunit in aor tic smooth muscles of 1k1c hypertensive rats, which might be related to the development of hypertension in this hypertensive model.

Objective 1.To explore the role of environmental factors in the development and maintenance of hypertension . 2. To establish a hypertensive model without surgical or phar macologic intervention. 　Methods One hundreds male, 2-3-month-old Wistar rats were rand omly divided i nto 4 groups: 1. Cold-treated group(C, n=28): animals were exposed to cold (4±2)℃ for 4 hours per day for 8 weeks; 2. High salt-treated group (S, n=28): animals were given 8% NaCl di ets for 8 weeks. 3. Cold combined high salt-treated group (CS, n=28). Animals were given 8% N aCl diets for 8 weeks besides cold exposure. 4. Control group (N, n=16). Systolic blood pressur e(SBP, Tail-cuff technique) and heart rate were measured weekly in 4 groups throughout the experi ment. The thoracic aortas were extracted for morphologic studies. 　Results On the end of the first week, the average SBP and heart r ate of C, S, and CS group were sighificantly increased (P<0.01) than that of the N group. Blood pressure reached a maximal level by 3 weeks in C, S, and CS group (127.0±6.0, 125.9±5.5, 131±6.0)mmHg, respect ively, SBP remained significantly elevated for the remaining of the experiment. 　Conclusion Cold circumstance and high-salt intake play an impo rtant role in the development of hypertension. This model appears to be a successful model for the induction of hypertension in rats without surgical intervention or excessive doses of hormones.

Aim To investigate the change in neuropeptide Y(NPY) Y1 receptor level in infarcted myocardium tissues of (MI) rats. 　Method MI was induced by ligating the left descending anterior coronary artery (LAD) in the heart of rats. The techniques of reverse transcription polymerase chain reaction (RT-PCR) were used to identify the exist of NPY Y1 receptor mRNA in myocardial tissues. The technique of semi-quantitative PCR wa s used to observe the change of NPY Y1 receptor mRNA level. 　Results NPY Y1 receptor mRNA distributed in the heart tissues of rat. Compared with sham operated rats ,the NPY Y1 receptor mRNA level both in infarction area and non-infarction area was increased significantly after MI fo r 1d and 3d. The NPY Y1 receptor mRNA level in the heart tissues of sham-op erated rats was also significantly increased compared with that in control rats . 　Conclusion These results suggest that MI may result in increase NPY Y1 receptor level in the heart tissues of rats. Stre ss stimulation such as surgery may also increase the NPY Y1 receptor level in the heart.

Aim To investigate the effects of angiotensin Ⅱ(AngⅡ),AT1 receptor antagonist losartan and AT2 receptor antagonist PD123177 on protein synthesis rate and AT1 receptor mRNA expression in cultured neonatal rat cardi ac myocytes. 　Methods The protein synthesis rate in cultured cardiac myocytes w as determined by the3H-leucine incorporation,AT1 receptor mRNA expressi on of cardiac myocytes was assessed by reverse transcription-polymerase chain reaction(RT-PCR). 　Results AngⅡ increased the 　3H-leucine incorporation in cultured cardiac myocytes in a dose dependent manner,losartan but not PD12317 7 could significantly inhibit AngⅡ induced protein synthesis,;AT1 receptor mRNA expression was upregulated after AngⅡ,and inhibited by losartan,but not PD123177. 　Conclusion AngⅡ can induce cardiac myocytes hypertrophy via upregulating AT1 receptor,and AT1 receptor antagonist can decrease AT1 rec eptor expression,reduce cardiac myocytes hypertrophy.