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Exp Biol Med (Maywood)
October 2023
Department of Physiology, Faculty of Medicine, Universiti Malaya, Kuala Lumpur 50603, Malaysia.
An increase in blood pressure by a high-salt (HS) diet may change the expression levels of renal epithelial sodium channels (ENaCs) and aquaporins (AQPs). Spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats were exposed to HS and regular-salt (RS) diets for 6 weeks. Mean arterial pressure (MAP) and plasma atrial natriuretic peptide (ANP), angiotensin II (Ang II), aldosterone, and arginine vasopressin (AVP) levels were determined.
View Article and Find Full Text PDFFunction (Oxf)
August 2023
Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Non-enzymatic activation of renin via its interaction with prorenin receptor (PRR) has been proposed as a key mechanism of local renin-angiotensin system (RAS) activation. The presence of renin and angiotensinogen has been reported in the rostral ventrolateral medulla (RVLM). Overactivation of bulbospinal neurons in the RVLM is linked to hypertension (HTN).
View Article and Find Full Text PDFAm J Physiol Renal Physiol
July 2023
Department of Physiology, Medical College of Georgia, Augusta University, Augusta, Georgia, United States.
Histamine is involved in the regulation of immune response, vasodilation, neurotransmission, and gastric acid secretion. Although elevated histamine levels and increased expression of histamine metabolizing enzymes have been reported in renal disease, there is a gap in knowledge regarding the mechanisms of histamine-related pathways in the kidney. We report here that all four histamine receptors as well as enzymes responsible for the metabolism of histamine are expressed in human and rat kidney tissues.
View Article and Find Full Text PDFJ Pharmacol Sci
July 2022
Department of Pharmacology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
We have recently reported that the urea osmolyte-associated water conservation system is activated in fluid loss models such as high salt-induced natriuresis, renal injury-induced impaired renal concentrating ability, or skin barrier dysfunction-induced transepidermal water loss. The system consists of the interaction of multiple organs including renal urea recycling, hepato-muscular ureagenesis, and suppression of cardiovascular energy expenditure. Here, we determined the effect of pharmacological fluid loss induced by tolvaptan, a selective vasopressin V receptor antagonist, on water conservation.
View Article and Find Full Text PDFJ Cell Physiol
May 2022
Group of Neuroendocrinology, Diabetes and Metabolism Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
Chronic high salt intake is one of the leading causes of hypertension. Salt activates the release of the key neurotransmitters in the hypothalamus such as vasopressin to increase blood pressure, and neuropepetide Y (NPY) has been implicated in the modulation of vasopressin levels. NPY in the hypothalamic arcuate nucleus (Arc) is best known for its control in appetite and energy homeostasis, but it is unclear whether it is also involved in the development of salt-induced hypertension.
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