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Objective: To study influence of acute hypoxia on the current of voltage-gated potassium channel (IK) in pulmonary artery smooth muscle cells (PASMC) of rats. Methods: A total of 20 male SD rats were randomly and equally divided into normoxic control group and acute hypoxia group. The rats in acute hypoxia group were kept in hypoxic chamber for 8 h before experiment. Whole cell patch-clamp technique was used to record IK in PASMC. Results: Acute hypoxia significantly decreased the IK density in PASMC of rats. During -60mV to -10mV of resting membrane potential（RMP）, acute hypoxia did not significantly decrease peak IK density in PASMC of rats, P>0.05; At 0 mV, acute hypoxia significantly decreased the peak IK density in PASMC [from（38.1 ± 5.2） pA / pF decreased to（9.82 ± 2.1） pA / pF ,P<0.05], then along with RMP increase in PASMC, the decreasing amplitude of peak IK density in PASMC gradually increased（P<0.05）; From + 30 mV to+ 60 mV, the decreasing amplitude of peak IK density in PASMC further significantly increased（P<0.01）; At + 60 mV the peak IK density decreased from（38.1 ± 5.2） pA / pF to（9.82 ± 2.1） pA / pF , and the decreasing amplitude reached (46.8±3.3)%. Conclusion: Acute hypoxia can decrease Kv current in PASMC of rats, leading to hypoxic pulmonary vasoconstriction.
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Objective To work out a proper treatment regimen for hypertension in elderly patients with type 2 diabetes mellitus. Methods Sixty-five elderly patients 〔aged (68.3?4.4) yrs old〕 with hypertension and type 2 diabetes were randomized into three arms of antihypertensive treatment: arm A, n=20, treated with nifedipine in long-acting gastrointestinal-transport system (nifedipine-GITS) 60 mg/d; arm B, n=22, treated with nifedipine-GITS 30 mg/d and valsartan (angiotensin Ⅱ receptor blocker, ARB) 80mg/d; and arm C, n=23, treated with nifedipine-GITS 30mg/d, Valsartan 80mg/d and sustained-releasing indapamide (diuretics)1.5 mg/d. Results Eight weeks later, both systolic blood pressure (SBP) and diastolic blood pressure (DBP) were decreased significantly in all of the patients ( P
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Objective: To construct the eurokaryotic expression vector of KCNE1 gene and express recombinant KCNE1 in HEK293 cells.Methods:Human KCNE1 gene fragment was amplified from human placenta total RNA by RT-PCR and cloned into the vector of pCR2.1 TOPO by means of T-A cloning.KCNE1 cDNA was obtained from pCR2.1-KCNE1 by restriction enzyme digestion and inserted into the same restriction site of pEGFP-N1.Thus pEGFP-N1-KCNE1 was constructed and transfected into HEK293 cells with Effectene transfection reagent.Results:The eukaryotic expression vector pEGFP-N1-KCNE1 was successfully constructed by gene cloning and recombinant method and expressed in HEK293 cells.Conclusion:The cloning of KCNE1 gene and the construction and expression of its eukaryotic expression vector may shed some light on further functional study of KCNE1 gene.
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One hundred and sixteen senile patients (older than 65 years) with chronic heart failure (CHF) were analyzed retrospectively in order to verify if old patients with CHF would benefit from long-term (one year) angiotension-converting enzyme inhibitor (ACEI) treatment. The frequency of drugs (including ACEI, digitalis and diuretic) used was stratified into four degrees accordingly. Development of the CHF was scored with regard to relapse rate and severity of this disease. Stepwise regression analysis was applied to explore the relationship between the scored outcome of CHF and the frequency of individual drug administration. A significant relationship of the scored outcome of CHF to the frequency of ACEI usage but not to digitalis nor to diuretics was found (partial coefficient of the correlation r = 0.42, P = 0.002). It was concluded that the long-term administration of ACEI improves the outcome of CHF in senile patients.
Subject(s)
Aged , Female , Humans , Male , Angiotensin-Converting Enzyme Inhibitors , Chronic Disease , Heart Failure , Drug Therapy , Hypertension , Myocardial Ischemia , Retrospective Studies , Treatment OutcomeABSTRACT
One hundred and sixteen senile patients (older than 65 years) with chronic heart failure (CHF) were analyzed retrospectively in order to verify if old patients with CHF would benefit from long-term (one year) angiotension-converting enzyme inhibitor (ACEI) treatment. The frequency of drugs (including ACEI, digitalis and diuretic) used was stratified into four degrees accordingly. Development of the CHF was scored with regard to relapse rate and severity of this disease. Stepwise regression analysis was applied to explore the relationship between the scored outcome of CHF and the frequency of individual drug administration. A significant relationship of the scored outcome of CHF to the frequency of ACEI usage but not to digitalis nor to diuretics was found (partial coefficient of the correlation r = 0.42, P = 0.002). It was concluded that the long-term administration of ACEI improves the outcome of CHF in senile patients.
Subject(s)
Angiotensin-Converting Enzyme Inhibitors/administration & dosage , Chronic Disease , Heart Failure/drug therapy , Heart Failure/etiology , Hypertension/complications , Myocardial Ischemia/complications , Retrospective Studies , Treatment OutcomeABSTRACT
AIM:To determine the role of Kv1 2, Kv1 5, Kv2 1 in the hypoxia pulmonary vasoconstriction (HPV). METHODS: Male Wistar rats were divided into two groups: normoxic group and hypoxic group. The single smooth muscle cell was obtained from pulmonary artery of Wistar rats with acute enzymatic digestion method. The conventional whole-cell patch clamp technique was used to record the resting membrane potential (Em) and the potassium currents of voltage-gated potassium channel (IKv) in rat pulmonary arterial smooth muscle cells (PASMC). Intracellular application of Kv1 2/Kv1 5/Kv2 1 antibodies (1∶125) was conducted through the whole-cell patch clamp system. RESULTS: ① Em of PASMC was depolarized after 24 h hypoxia compared with that of control cells [from (-51 8?0 8) mV to (-47 2? 0 7) mV, P
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AIM: To study the effect of adrenomedullin (ADM) on L-type calcium currents (I Ca,L) and its signaling transduction process in guinea-pig ventricular myocytes. METHODS: By using whole-cell patch clamp technique, the effect of ADM(1-100 nmol?L -1) on I Ca,Lmyocyte. Furthermore, the possible signaling transduction process of ADM on I Ca,L was investigated by observing the effects of ADM 22-52 (a specific ADM-receptor antagonist,100 nmol?L -1)+ADM(100 nmol?L -1), H-89 (a specific protein kinase A inhibitor, 10 ?mol?L -1) + ADM(100 nmol?L -1), PKC 19-36 (a specific protein kinase C inhibitor, 10 ?mol?L -1) + ADM(100 nmol?L -1) and PMA (a specific protein kinase C activator, 1 ?mol?L -1) on I Ca,L, respectively. RESULTS: ADM at the concentrations of 1-100 nmol?L -1 decreased I Ca,L in a dose-dependent manner (P