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Baum, M., Twombley, K., Gattineni, J., Joseph, C., Wang, L., Zhang, Q., Dwarakanath, V., et al. (2012) Proximal Tubule Na+/H+ Exchanger Activity in Adult NHE8-/-, NHE3-/-, and NHE3-/-/NHE8-/- Mice. American Journal of Physiology-Renal Physiology, 303, 1495-1502.
https://doi.org/10.1152/ajprenal.00415.2012

has been cited by the following article:

• TITLE: Association of Acid-Base Balance in the Renal Proximal Tubule and Blood Pressure Alterations: Potential Role of Local Mediators

  AUTHORS: Dinesh Aryal, Keith E. Jackson

  KEYWORDS: Acid-Base Transporters, Hypertension, Proximal Tubule, Angiotensin II

  JOURNAL NAME: Journal of Biosciences and Medicines, Vol.8 No.4, April 2, 2020

  ABSTRACT: Disturbances in acid-base balance leading to the development of hypertension are currently gaining increased attention among researchers. Perturb acid-base balance characterized by metabolic acidosis has been demonstrated in hypertensive animals and humans. Research suggests that acid-base changes are not only the consequences of elevated blood pressure but can precede the development of hypertension. However, no exact mechanism has been identified to link acid-base imbalance with alterations in blood pressure. The kidney proximal tubule is the major site for maintaining normal bicarbonate concentrations which is an important component of acid-base balance. Acid-base transporter proteins in the renal proximal tubule such as Na+/HCO-3cotransporters, Na+/H+ exchangers, and anion-exchangers play important roles in controlling acid secretion, ammonia production and bicarbonate reabsorption for maintaining acid-base balance. It is well known that sodium retention in the renal tubules leads to increase in blood volume and consequently increases in blood pressure. Therefore, it is the purpose of this review to discuss the role of sodium-coupled acid-base transporters in regulating proximal tubular sodium retention and controlling blood pressure homeostasis. We will also focus on the capacity of local mediators; angiotensin II, cortisol, prosta-glandin and aldosterone, to regulate acid-base and blood pressure homeostasis.