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

作　　者：Dinesh Aryal Keith E. Jackson 

机构地区：[1]School of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana at Monroe, Monroe, LA, USA

出　　处：《Journal of Biosciences and Medicines》2020年第4期26-44,共19页生物科学与医学（英文）

摘　　要：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-3?cotransporters, 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.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-3?cotransporters, 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.

关 键 词：ACID-BASE Transporters Hypertension PROXIMAL TUBULE ANGIOTENSIN II 

分 类 号：O61[理学—无机化学]