Clinical and Experimental Hypertension最新文献

Background: At present, no early diagnostic markers for essential hypertension (EH)-induced subclinical target organs damage (such as carotid plaque) are available. This study aimed to identify the circular RNAs (circRNAs) in EH with carotid plaques, and assess their utility as biomarkers.

Methods: First, circRNAs were identified through microarry analysis and database prediction. Second, a case-control study of EH patients with carotid plaque (n = 100) and healthy controls (n = 100) was performed to evaluate circRNAs expression in peripheral blood. Finally, receiver operating characteristic (ROC) curve was established to evaluate the diagnostic value.

Results: Five circRNAs (hsa_circ_0105130, hsa_circ_0109569, hsa_circ_0072659, hsa_circ_0079586 and hsa_circ_0064684) were identified as the candidate circRNAs. We found that circRNAs were increased in case group compared with controls (P < .05). The results of ROC shown that these five circRNAs, especially hsa_circ_0109569 (AUC = 0.741), all had the moderate predictive value.

Conclusions: Our study revealed circulating circRNAs may act as promising noninvasive biomarkers for early detection and population screening of EH-induced subclinical target organ injury.

Purpose: The present study was designed to observe the vasoreactivity in retina and choroid after calcium channel blocker (CCB) treatment in a group of hypertensive patients.

Method: The study was based on 56 hypertensive patients (56 eyes) and 56 control subjects (56 eyes). Choroidal scans and the measurement of peripapillary retinal vessel diameters was performed at baseline and optical coherence tomography (OCT) scans were also performed at first month . Subfoveal choroidal thickness (SFCT) and the diameters of superior temporal artery (STA), inferior temporal artery (ITA), superior temporal vein (STV), inferior temporal vein (ITV) were compared between the groups.

Results: The baseline diameters of the STA, ITA were significantly decreased in the patient group compared with the control group (all p < .05). There was a significant increase at first month after the CCB treatment in comparison to baseline measurements (all p < .05). When compared with the controls, the diameter of venules showed a decrease at baseline but was not significant. After the treatment, the diameters of venules were insignificantly increased compared with baseline measurements (p = .178 and p = .275) and there were also no significant differences between the control group and the patient group in first month (all p > .05). The average choroidal thickness measurements of the hypertensive group was lower than the control group (p = .404) and there was a tendency to increase after the treatment (p = .055).

Conclusion: This study demonstrates that, treatment with CCB seems to improve retinal arteries and has almost no affect on the choroidal thickness in newly diagnosed hypertensive patients.

Background: This study investigated oxidative damage to bone marrow cells in the pathogenesis of renovascular hypertension (RH).

Methods: Male C57BL/6 J mice (10-week-old and ~23 g) were divided into two groups: Sham-operated and 2K1C, which has a stainless-steel clip placed around the left renal artery. After twenty-eight days, the animals were anesthetized for hemodynamic measurements and bone marrow cells isolation. The intracellular production of ROS, DNA damage, and DNA repair kinetics were evaluated.

Results: Our results show that RH increases HSCs ROS production and that the 2K1C group showed a significant reduction of HSCs in the G0/G1 phase, increased p53 expression, DNA fragmentation, low DNA repair capacity, and a higher percentage of apoptotic cells when compared with the Sham group.

Conclusions: Our data imply that RH can compromise the hematopoiesis by increased oxidative stress leading to impaired DNA repair activity. Furthermore, this study provides new insights into the influence of hypertension on bone marrow homeostasis. This study showed for the first time that RH leads to oxidative damage, including genotoxic, to bone marrow cells. Thus, these findings provide new insights into the consequences of RH on bone marrow cells.

Introduction: Subclinical hyperthyroidism (SHT) is an endocrine disorder that is associated with abnormalities in heart structure and function. Oxidative stress plays an important role in the pathophysiology of cardiac disorders caused by SHT. Portulaca oleracea (P. Oleracea) is a herbaceous plant with many pharmacologic effects including antioxidant, and anti-inflammatory properties. In the present study, the effects of Portulaca oleracea and vitamin E on the biochemical, hemodynamic, and functional parameters of the cardiac tissue was studied in rats with subclinical hyperthyroidism.

Methods: Fifty-six male rats were divided into seven groups: 1-Control group: daily injection of saline, 2-SHT group: daily injection of levothyroxine sodium (LS) (20 µg/kg), 3- T4+Po groups were given LS and P. oleracea (100, 200, and 400 mg/kg in drinking water), 4- the T4+vit E groups received LS and a daily injection of vitamin E (100 and 200 mg/kg). Cardiac index, systolic blood pressure (SBP), also malondialdehyde and total thiol levels were measured in cardiac tissue.

Results: SBP and maximum dP/dt were significantly increased and minimum dP/dt was significantly decreased in SHT group. In P. oleracea groups, maximum dP/dt were significantly reduced and minimum dP/dt was increased. Malondialdehyde levels and cardiac index in groups receiving vitamin E and P. oleracea were significantly decreased. Maximum dP/dt was decreased in the group receiving LS+vitamin E. Minimum dP/dt was significantly higher in group received LS+ vitamin E.

Conclusion: This study showed that Portulaca oleracea has a positive effect on cardiac dysfunction caused by subclinical hyperthyroidism.

Background: Intimal hyperplasia contributed by phenotypic switching of vascular smooth muscle cell (VSMC) plays an important role in the pathogenesis of various cardiovascular diseases. MicroRNA-144 (miR-144) is recently reported to be implicated in the development of atherosclerosis. However, the individual role of miR-144 in VSMCs phenotypic modulation and intimal hyperplasia currently still remains unknown.

Methods and results: Here we found that miR-144 expression was upregulated in carotid arteries with intimal hyperplasia that subjected to wire injury and the consistent results were obtained with dedifferentiated VSMCs upon platelet-derived growth factor-BB (PDGF-BB) stimulation. Loss-of-function study showed that miR-144 knockdown decreased the ability of VSMC proliferation tested by Brdu and CCK8, and reduced the migrate capability analyzed by Transwell, whereas increased the differentiated SMC marker gene expression examined by RT-PCR. The above results were reversed by miR-144 overexpression. Mechanistically, we have demonstrated that PTEN was the direct target of miR-144 that was responsible for the alleviated effect of miR-144 inhibition on phenotypic switching of VSMCs. Notably, mice injected with miR-144 inhibitor attenuated the formation of neointimal lesions in response to wire injury and maintained the mature SMC marker expression inhibited the proliferation and migration of VSMCs.

Conclusion: Our research exhibited that miR-144 knockdown attenuated intimal hyperplasia through inhibiting the VSMC phenotypic switching, which was partially mediated by directly targeting to PTEN. Taken together, these evidences suggested that miR-144 may act as a promising therapeutic target for arterial restenosis.

Objectives: This study explored the miR-101 clinical significance in hypertensive disorder complicating pregnancy (HDCP).

Methods: Pregnant women with gestational hypertension (GH)/mild preeclampsia (mPE)/severe preeclampsia (sPE) were included. The miR-101 levels were measured. Correlation between miR-101 and soluble fmslike tyrosine kinase-1 (sFlt-1), miR-101 predictive value, and factors influencing HDCP grade were evaluated.

Results: Serum miR-101 was down-regulated and negatively correlated with sFlt-1. miR-101 was an independent risk factor for HDCP and decreased with HDCP severity. The area under the curve of miR-101 in differentiating GH from mPE and mPE from sPE was 0.7764 and 0.8529.

Conclusion: Serum miR-101 level may be a biomarker for grading HDCP.

Hypothyroidism disturbs redox homeostasis and takes part in cardiovascular system dysfunction. Considering antioxidant and cardio-protective effects of PPAR-γ agonists including pioglitazone (POG) and rosiglitazone (RSG), the present study was aimed to determine the effect of POG or RSG on oxidants and antioxidants indexes in the heart and aorta tissues of Propylthiouracil (PTU)-induced hypothyroid rats.

Materials and methods: The animals were divided into six groups: (1) Control; (2) propylthiouracil (PTU), (3) PTU-POG 10, (4) PTU-POG 20, (5) PTU-RSG 2, and (6) PTU-RSG 4. Hypothyroidism was induced in rats by giving 0.05% propylthiouracil (PTU) in drinking water for 42 days. The rats of PTU-POG 10 and PTU-POG 20 groups received 10 and 20 mg/kg POG, respectively, besides PTU, and the rats of PTU-RSG 2 and PTU-RSG 4 groups received 2 and 4 mg/kg RSG, respectively, besides PTU. The animals were sacrificed, and the serum of the rats was collected to measure thyroxine level. The heart and aorta tissues were also removed for the measurement of biochemical oxidative stress markers.

Results: Hypothyroidism was induced by PTU administration, which was indicated by lower serum thyroxine levels. Hypothyroidism also was accompanied by a decrease of catalase (CAT), superoxide dismutase (SOD) activities, and thiol concentration in the heart and aorta tissues while increased level of malondialdehyde (MDA). Interestingly, administration of POG or RSG dramatically reduced oxidative damage in the heart and aorta, as reflected by a decrease in MDA and increased activities of SOD, CAT, and thiol content.

Conclusion: The results of this study showed that administration of POG or RSG decreased oxidative damage in the heart and aorta tissues induced by hypothyroidism in rats.

Obejectives: Cardiac infarction is a dynamic, nonlinear and unpredictable course of disease, and who die of acute myocardial infarction, and coronary thrombosis. TRAF3 provide novel targets for the clinical prevention and treatment for tumors, viral infection, and so on.We investigated the mechanisms of TRAF3 gene, which plays a possible role in cardiac infarction and contributes to the pathogenesis of cardiac infarction-induced oxidative stress.

Methods: Serum samples of patients with cardiac infarction and normal healthy volunteers were obtained from the 920 Hospital of PLA joint service support force. C57BL/6 mice were ligated and H9C2 cells were induced with 1% O2,5%CO2 and 94% N2.

Results: The mRNA expression levels of TRAF3 in patients with cardiac infarction were increased, compared to healthy volunteers. Serum mRNA of TRAF3 was in positive correlation with serum CK levels in patients with cardiac infarction. Over-expression of TRAF3 heightened ROS-induced oxidative stress in vitro model of cardiac infarction. Then, TRAF3 recombinant protein could promote oxidative stress and aggravated cardiac infarction in mice model. Over-expression of TRAF3 induced ULK1 protein expression and reduced ULK1 ubiquitination in vitro model. The activation of ULK1 reduced the effects of TRAF3 on oxidative stress in vitro model of cardiac infarction. Meanwhile, the inhibition of ULK1 reversed the effects of si-TRAF3 on oxidative stress in vitro model of cardiac infarction.

Conclusions: This study identified that TRAF3 promoted ROS-induced oxidative stress in model of cardiac infarction through the regulation of ULK1 ubiquitination, which could potentially give rise to a new strategy for the treatment of cardiac infarction.

Objective: To investigate the effects of sacubitril/valsartan (S/V) on cardiopulmonary function and blood pressure response to exercise during hospitalization in patients with acute myocardial infarction (AMI) based on the cardiopulmonary exercise test (CPET).

Methods: A total of 265 AMI patients were treated with either perindopril or S/V within 24 hours of admission. CPET was completed for all patients before discharge. There were 182 cases in the perindopril group and 83 cases in the S/V group.

Results: The proportion of exercise oscillatory ventilation (EOV) was higher in the S/V group than in the perindopril group (10.8% vs 1.6%, X² = 11.148, P = .001). The resting heart rate (HR), resting diastolic blood pressure (DBP), and warm-up DBP were lower in the S/V group than in the perindopril group (P < .05). The resting systolic blood pressure (SBP) was 9.0 mmHg lower (115.7 ± 17.5 vs 106.7 ± 15.0, P < .001), the SBP during warm-up was 9.5 mmHg lower (124.8 ± 23.7 vs 115.3 ± 22.5,P = .002), the SBP at the anaerobic threshold (AT) was 10.5 mmHg lower (135.3 ± 24.8 vs 127.1 ± 25.1,P = .021),the SBP at max watts was 11.5 mmHg lower (148.9 ± 26.4 vs 137.4 ± 26.4,P = .001), and the SBP during one-minute recovery was 12.3 mmHg lower (146.5 ± 27.1 vs 134.2 ± 24.4, P = .001)in the S/V group than in the perindopril group. The S/V group had a higher oxygen ventilation equivalent and carbon dioxide ventilation equivalent (VE/VCO₂) at AT and a lower oxygen uptake-work rate relationship during max watts (P < .05). The differences in the oxygen pulse, stroke volume, peak oxygen uptake (VO_{2 peak}), and VE/VCO₂ slope were not statistically significant between the two groups.

Conclusion: Treatment with S/V was able to reduce the exercise blood pressure in patients with AMI during hospitalization, but did not significantly improve the VO_{2 peak}, VE/VCO₂ slope, or exercise tolerance.