Epithelial Sodium Channel δ Subunit Is Expressed in Human Arteries and Has Potential Association With Hypertension.

BACKGROUND: Elevated expression and increased activity of vascular epithelial sodium channel (ENaC) can result in vascular dysfunction in small animal models. However, there is limited or no knowledge on expression and function of ENaC channels in human vasculature. Hence, this study explored the expression and function of ENaC in human arteries and their association with hypertension. METHODS: Human internal mammary artery (IMA) and aorta were obtained from cardiovascular patients undergoing coronary artery bypass graft surgery. Expression of the ENaC subunit was analyzed by polymerase chain reaction, Western blot, and immunohistochemistry. ENaC function was observed by patch-clamp electrophysiology in endothelial cells isolated from IMA. Levels of ENaC subunit expression levels were compared between arteries from normotensive, uncontrolled hypertensive, and controlled hypertensive patients. RESULTS: For the first time, expression of α, ß, γ, and δ was detected at mRNA and protein levels in human IMA and aorta. Single-channel patch-clamp recordings identified both αßγ- and δßγ-like channel conductance in primary endothelial cells isolated and cultured from IMA. Reduced expression of the δ subunit was observed in controlled hypertensive IMA, whereas reduced expression of γ-ENaC was observed in controlled hypertensive aorta. CONCLUSIONS: These data suggest that functional ENaC channels are expressed in human arteries and their expression levels are associated with hypertension.

The δ subunit of epithelial sodium channel in humans-a potential player in vascular physiology.

Vascular epithelial sodium channels (ENaCs) made up of canonical α, ß, and γ subunits have attracted more attention recently owing to their physiological role in vascular health and disease. A fourth subunit, δ-ENaC, is expressed in various mammalian species, except mice and rats, which are common animal models for cardiovascular research. Accordingly, δ-ENaC is the least understood subunit. However, the recent discovery of δ subunit in human vascular cells indicates that this subunit may play a significant role in normal/pathological vascular physiology in humans. Channels containing the δ subunit have different biophysical and pharmacological properties compared with channels containing the α subunit, with the potential to alter the vascular function of ENaC in health and disease. Hence, it is important to investigate the expression and function of δ-ENaC in the vasculature to identify whether δ-ENaC is a potential new drug target for the treatment of cardiovascular disease. In this review, we will focus on the existing knowledge of δ-ENaC and implications for vascular physiology and pathophysiology in humans.

Capsazepine in rats′lateral ventricles:Effect of different doses on LPS-induced fever / 中国药理学通报

Aim To observe the effects of the transient receptor potential vanilloid receptor 1 ( TRPV1 ) antago-nist Capsazepine on the LPS-induced fever process. Methods Three doses of Capsazepine were respec-tively injected into rats’ lateral ventricles before the in-traperitoneal injection of LPS caused fever. An emitter was implanted inside the rat’ s abdominal cavity to mo-nitor the body temperature changes during the fever process. Then the changes of calcium ion in the hypo-thalamus were detected by fluorescence and the expres-sions of TRPV1 protein were detected by Western blot. Results The higher dosage of Capsazepine was injec-ted, the higher the level of LPS-induced fever was, and the lower the concentration of calcium ion in the hypothalamus as well as the TRPV1 expressions were. Conclusion Capsazepine could increase the level of fever induced by LPS via acting on the rats’ hypothala-mus. This effect might be related to the functions of TRPV1 .