Objective To investigate the possible roles of hemodynamics, circulating hormones, cell cation transport and cyclic nucleotides in left ventricular hypertrophy (LVH) of essential hypertension (EH) in vivo. Methods Blood pressure, total peripheral resistance (TPR) and plasma norepinephrine (NE), endothelin (ET), angiotensin Ⅱ (AngⅡ), endogenous digitalis like substances (EDLS) and atrial natriuretic peptide (ANP) were determined, along with the measurements of lymphocytic membrane ion pumps, cations and cyclic nucleotides in 45 EH patients with LVH (12 concentric hypertrophy, 33 eccentric hypertrophy), 30 normal subjects and 45 EH patients without LVH (as double concurrent controls). Multiple stepwise regression analysis was computed using left ventricular mass index (LVMI) as dependent variable and 22 parameters as independent variables. Results (1) In EH patients with LVH, increases were seen in systolic blood pressure, mean arterial pressure (MAP) and NE, ET, AngⅡ, EDLS and ANP as well as lymphocytic Na +, Ca 2+ , cAMP and cAMP/cGMP ratio, while Na + K + ATPase and Ca 2+ ATPase activities, K + and Mg 2+ decreased. (2) Five hormones were related respectively to ion pumps, Na +, Ca 2+ and cyclic nucleotides. (3) LVMI were correlated with NE, ET, AngⅡ and EDLS, Ca 2+ ATPase, Na +, cAMP and cAMP/cGMP ratio. (4) The regression equation revealed that NE, ET, Ca 2+ ATPase, Mg 2+ and cAMP were the independent factors affecting LVH. (5) TPR and AngⅡ were higher, K + was lower in concentric LVH than those in eccentric LVH. Conclusion The changes of hemodynamics, circulating hormones, cell cation transport and cyclic nucleotides, or their interaction may be involved in the pathogenesis of LVH in EH. NE, ET. Ca 2+ ATPase, Mg 2+ and cAMP seem to play more important parts in LVH . TPR , whereas AngⅡ and K + may relate to cocentric LVH.

BACKGROUND:Although the nickel-titanium occluder in the treatment of congenital heart disease has a better clinical effect, arrhythmia wil be more likely to develop in late stage. OBJECTIVE:To investigate the effect of nickel-titanium wire on expression of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor of rat myocardial cels. METHODS:Thirty Sprague-Dawley rats were obtained and randomly divided into two groups: experimental and control groups. The nickel-titanium wire was implanted to the apex of heart of rats in the experimental group. Rats in the control group received no special treatment. Rat mycardial cels were harvested at the 1th, 3rdand 6th months after operation. The gene and protein expressions of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor of rat myocardial cels were detected using RT-PCR and immunohistochemistry, respectively. The inflammatory reactions were detected using hematoxylin-eosin staining. RESULTS AND CONCLUSION:After the nickel-titanium wire was implanted into the rat myocardium, inflammatory reaction was induced by inflammatory cel infiltration in the experimental group, with hyperplasia of fibrous tissue. The inflammatory reaction gradualy disappeared as the implanted time extended. No inflammatory cel infiltration was visible in the control group. There was no significant difference in the gene and protein expressions of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor of rat myocardial cels at different time points after operation between these two groups. It showed that nickel-titanium wire had no influence on the expressions of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor of rat myocardial cels. These results suggest that nickel-titanium occluder-related arrhythmia may have little relationship with abnormal protein expression of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor.

Objective To investigate the role of transforming growth factor-β1 (TGF-β1), Smad2/3 and Smad7 expressions in carotid artery remodeling in renovascular hypertensive rats, and also the therapeutic effect of Enalapril and Amlodipine. Methods The renovascular hypertensive rat (RHR) models with two-kidney and one-clip were established, including model group (n = 6), sham-operated group (n = 6), Enalapril group (10 mg/kg per day, n = 6), Amlodipine group (5 mg/kg per day, n = 6) and combination group (Amlodipine 2.5 mg/kg per day + Enalapril 5mg/kg per day, n = 6). The medication were continuous administrated for six weeks. Carotid artery morphological and structural changes in the media were observed by HE staining, Masson staining and immuno histochemical staining. Media thickness (MT), MT and lumen diameter ratio (MT/LD), and the expression levels of media α-smooth muscle actin (α-actin), proliferating cell nuclear antigen (PCNA), TGF-β1, phosphorylated Smad2/3 (p-Smad2/3) and Smad7 in carotid arteries were measured. Results The media of carotid arteries in RHR model group was significantly thickened, the volume of smooth muscle cell was increased, and the array was in disorder; MT, MT/LD, the proliferation index of smooth muscle cell and collagen fiber area percentage of carotid arteries in the model group were significantly higher than those in the sham-operated group (P < 0.01). Compared to sham-operated group, the model group had significantly higher expressions of TGF-β1 and p-Smad2/3 (P < 0.05) and lower Smad7 expression. Both Enalapril and Amlodipine improved smooth muscle hypertrophy and collagen deposition, reduced RHR carotid MT, MT/LD, proliferation index of smooth muscle cell, collagen fiber area percentage and the expressions of TGF-β1 and p-Smad2/3 (P < 0.05), increased Smad7 expression (P < 0.05). Moreover, the combination treatment of Enalapril and Amlodipine had significantly better effects than single Amlodipine group (P < 0.05), but not single Enalapril group. Conclusions TGF-β1/Smads pathway may participate in the mechanism of carotid artery remodeling in RHR; the role of Amlodipine and Enalapril in inversing carotid artery remodeling may be related to the change of TGF-β1/Smads pathway, the combination treatment of Amlodipine and Enalapril had better effects than single administration of Amlodipine.