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Abstract. Experimental evidence indicates that hypertension is a multifactorial disorder and that the products of several genes may contribute to its development. The aim of this study was to investigate the expression of hypertension-related genes in spontaneous hypertensive rats (SHRs). A microarray screening for hypertension-related genes was conducted in SHRs and Wistar-Kyoto (WKY) rats using total-RNA extracted from second-order mesenteric arteries and kidneys. The FXYD5 mRNA expression in vascular smooth muscle cells (VSMCs) was silenced by RNA interference (RNAi). Meanwhile, the FXYD5 mRNA overexpression in renal tubular epithelial cells (RTECs) was induced by the recombinant plasmid pcDNA3.1(+)-FXYD5. The expression of FXYD5 mRNA was found to be 14.8-fold lower in SHR rats compared to that in WKY rats (P<0.01). The levels of FXYD5 mRNA expression were the highest in kidneys of SHR 13-week-old rats when the blood pressure reached the highest levels. The down-regulated FXYD5 mRNA expression inhibited the migration of smooth muscle cells (P<0.01) and cell membrane Na + -K + -ATPase activity (P<0.01). Up-regulated FXYD5 mRNA expression enhanced the renal tubular epithelial cell membrane Na + -K + -ATPase activity (P<0.05) and cell proliferation (P<0.05). FXYD5 is related to the migration of smooth muscle cells and cell membrane Na + -K + -ATPase activity in rodents. The results of the present study suggest that FXYD5 may have profound impact on the regulation of blood pressure, and that this gene may be a potential target for anti-hypertensive therapy. IntroductionThe prevalence of hypertension has been reported to be 21.1% among Canadians >18 years old and 20.1% in the United States (1). With high incidence, hypertension significantly influences the health in elderly people and the morbidity of this disease has been increasing over the past few decades. Although many advances in drug development and therapy have been achieved, thus far, the pathogenesis of hypertension has not been completely clarified.Recent experimental evidence indicates that hypertension is predominantly a multifactorial disorder involving a complicated interaction between environmental influences and polygenetic defects. In particular, patients with familial aggregation hypertension display a strong trend in genetic predisposition. This raises the possibility that the products of several causal genes may work together in the development of hypertension, which contribute to a 30-50% variation in blood pressure among those hypertensive individuals (2,3).In this study, gene-chip was used to compare the gene expressions in second-order mesenteric arteries and kidneys between two rat models, the spontaneously hypertensive rat (SHR) and the Wistar-Kyoto (WKY) rat. Furthermore, real-time RT-PCR was used to confirm that FXYD5 was down-regulated in SHR in kidney and second-order mesenteric arteries. Northern blot results also suggested that the gene expression level was significantly different in the different stages of hypertension and differe...

Pheochromocytoma associated with pregnancy is not common. Caesarean section may induce pheochromocytoma crisis, resulting in a lethal condition. The clinical picture of pheochromocytoma crisis is extremely variable. In this report, we describe a case of severe pheochromocytoma crisis induced by caesarean section presenting with hyperpyrexia, haemodynamic collapse, muscle weakness, heart failure, and acute kidney injury. Furthermore, we report that the muscle weakness was a manifestation of rhabdomyolysis, resulting from the pheochromocytoma crisis. Standard medical therapy failed to halt the patient's rapidly deteriorating condition. Continuous renal replacement therapy removed catecholamines from the circulation, resulting in improvement of haemodynamics and abrogation of rhabdomyolysis.

Purpose: As the number of patients with chronic obstructive pulmonary disease continues to increase, it is increasingly important to understand the impact of cardiovascular risk on the progression of chronic obstructive pulmonary disease, which can provide guidance for clinical medication and recommendations for patient care and rehabilitation. The purpose of this study was to investigate the relationship between cardiovascular risk and the progression of chronic obstructive pulmonary disease (COPD). Methods: Selected COPD patients admitted to hospital from June 2018 to July 2020 were included in the study for prospective analysis, and patients who showed more than two instances of moderate deterioration or severe deterioration within one year before the consultation were defined as COPD patients, and all participants underwent relevant tests and assessments. Results: Multivariate correction analysis showed that a worsening phenotype improved the risk of carotid artery intima-media thickness exceeding 75% by nearly three times, and it had no relation with the degree of COPD severity and global cardiovascular risk; in addition, the relationship between a worsening phenotype and high carotid intima-media thickness (c-IMT) was more pronounced in patients under 65 years of age. Conclusions: The existence of subclinical atherosclerosis is individually related to the worsening phenotype, and the difference is more obvious in young patients. Therefore, the control of vascular risk factors in these patients should be strengthened.