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The function of kidney is maintaining water balance of our body through regulation of urine concentration and dilution. The aquaporins are molecular basis of renal urine production and water transport, and their expression and membrane translocation are regulated delicately. Nuclear receptors are a superfamily of ligand-activated transcription factors consisting of 48 members in human. They widely participate in a variety of physiological and pathophysiological regulation including growth and development, glucose and lipid metabolism, inflammation, immunology by regulating target gene transcription and expression. Increasing evidence demonstrates that these receptors are involved in the regulation of aquaporins expression and membrane translocation in kidney, thereby playing a major role in water homeostasis. Here we review the role of nuclear receptors in regulating renal water transport.

Aquaporins (AQPs), mainly distributed in epithelial and endothelial cells, are a family of channel-forming membrane proteins, originally confirmed to mediate the cellular water-transportation. AQPs are essential for maintaining homeostasis of the body water. Recently, studies have shown that AQPs may be involved in vascular function regulation and the development of related diseases, especially in cerebral ischemia, congestion heart failure, hypertension and tumor angiogenesis. Therefore, further studies are needed to elucidate mechanism accounting for the association between AQPs and vascular function related diseases, which may lead to novel approaches to the prevention and treatment of these diseases. In this review, we will discuss the expression and physiological roles of AQPs in vascular tissues and summarize recent progress in the relationship between AQPs and vascular function related diseases.

Objective: Many studies have shown that tissue development is closely correlated with fluid transport. Aquaporins (AQPs) are a group of cell membrane proteins that actively and selectively transport water. This study aimed to investigate the changes of AQPs expression during lung development in rats in order to elucidate the role of AQPs in the rat lung development., Methods: AQP1, AQP3, AQP4 and AQP5 proteins and mRNA in the lung cell membrane were measured by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) respectively in the 20-day-old embryo (E20), 7-day-old newborn rat, and one-month-old young and adult rats. The correlation between AQPs expression and lung development was studied., Results: With increasing age, the lung development showed a dynamic and successive course, with the most rapid from the fetus to the newborn rat, and then a slowed down afterwards. AQPs mRNA was weakly expressed in the lung of the E20 group. Lung AQPs mRNA and protein increased rapidly after birth until adulthood. The AQPs distribution patterns in the lung were unique with no duplication. There was a positive correlation between AQPs expression and lung development (P<0.05)., Conclusions: In addition to being involved in the transepithelial transport of water in the lung, AQPs is also related to its development.

Objective: To explore the effects of aquaporins (AQP) 1, 4 on water transport between airspace and pulmonary capillary and high pressure pulmonary edema. The other purpose was to study the active alveolar fluid transport as well as alveolar fluid clearance (AFC) in different pH of airspace., Methods: The effects of AQP1, 4 on water transport between airspace and pulmonary capillary and high pressure pulmonary edema were studied by surface fluorescence methods and gravimetric method respectively, AFC and AFC in airspace with different pH were measured by isotope method., Results: AQP1 knockout inhibited water transport through pulmonary capillary and also reduced high pressure pulmonary edema. Salbutamol increased AFC, but it was reduced when propranolol was used together. AFC was improved by terbutaline, isoproterenol, salmeterol when pH > 2.5 in airspace, but the effect was reduced after pH < 2.5 in airspace. Sodium channel inhibitor, Benzamil, could also inhibit AFC., Conclusions: AQP1 knockout significantly reduced water transport through alveolar capillary, and also reduced high pulmonary edema slightly. beta adrenergic stimulant improved AFC in mechanically ventilated rats. Intact airspace is very important for the function of AFC, however, the effect of AFC was impaired after lung injury induced by pH < 2.5 in airspace.