LAUSR

Arterial hypertension is a serious medical condition that significantly increases the risks of heart, brain, kidney, and other diseases affecting 1.28 billion adults worldwide. Hypertension is a major cause of premature death worldwide. This pathological condition is also called a “silent killer.” Most people with hypertension are unaware of the problem because it may have no symptoms until the first complications occur. This is why it is so important that blood pressure is measured on a regular basis.1 The aim of the following contribution is to highlight some of recent papers that appeared in Acta Physiologica with focus on articles that might be of importance to the field of arterial hypertension research and related topics. The scope that was covered in this field in Acta Physiologica ranged from basic research conducted in animal models to studies closely related to clinical questions. Form a historic perspective, comparative physiology models have been a hallmark of studies on animal osmoregulation.2 The basic idea is that animal experiments might be used to study fundamental mechanisms that are involved also in humans in the following particular example case for mechanisms relating to blood pressure regulation such as sodium and potassium transporters. In this specific case Clifford et al3 determined whether Na+ uptake in adult zebrafish (Danio rerio) exposed to acidic water adheres to traditional models reliant on Na+/ H+ Exchangers (NHEs), Na+ channels and Na+/Cl− Cotransporters (NCCs) or if it might occur through a novel mechanism. In order to achieve this the zebrafish were exposed to control or acidic (pH 4.0) water for 0– 12 h during which radioactive Na+ uptake, ammonia excretion, net acidic equivalent flux, and net K+ flux were measured. The involvement of the possible transporters was evaluated by exposure to Cl− free or elevated [K+] water, or to pharmacological inhibitors. The presence of NCKXs in gill was examined using RTPCR. The authors found that the uptake of sodium was strongly attenuated by acid exposure, but gradually recovered to control rates. The systematic elimination of each of the traditional models led the authors to consider K+ as a counter substrate for Na+ uptake during acid exposure. The elevated environmental potassium inhibited sodium uptake during acid exposure in a concentrationdependent manner. Analysis of mRNA revealed that six NCKX isoforms were present in zebrafish gills. The main conclusion of this article is that during acid exposure, zebrafish engage a novel Na+ uptake mechanism that utilizes the outwardly directed K+ gradient as a countersubstrate for Na+ and is sensitive to tetraethylammonium. NKCXs are promising candidates to mediate this potassiumdependent sodium uptake. How these findings relate to human physiology remains to be determined. One possible approach is to check whether the genes analyzed in the study are present in humans as well. To this end, it is interesting that the tissue distributions of the human NCKX2 (SLC24A2) (http://www.genome.ucsc.edu/cgibin/hgGen e?hgg_ gene=ENST0 00003 41998.7), for example is focused on brain tissue whereas the human NCKX1, (SLC24A1) (http://www.genome.ucsc.edu/cgibin/hgGen e?hgg_ gene=ENST0 00005 46330.1) shows a much broader tissue distribution involving kidney tissue as well. One of the most powerful regulation systems of osmolarity involves the release of ADH and one of its target tissues – the kidney with the appropriate receptors and targeting of aquaporins. Regulation of the plasma membrane location of aquaporins is important for water reabsorption in the collection duct of the kidney. Once the aquaporins are targeted to the plasma membrane and then more present, the cell layer becomes more permeable for water and water can follow the concentration gradient leading to an increased reabsorption of water. The molecule cAMP is an important second messenger in transmitting the signal for water reabsorption. The dysregulation of AQP2 is associated with water balance disorders. In a study by Ernstsen et al.,4 the authors aimed to analyze AQP2 trafficking in response to acute pyelonephritis. From clinical observations it is known that children and adults with acute pyelonephritis have a urinary concentration defect and studies in children revealed increased AQP2 excretion in the urine. This study aimed to analyze AQP2 trafficking in response to acute pyelonephritis. To address this, the authors used immunofluorescence imaging to analyze the subcellular