Acid-base and endocrine effects of aldosterone and angiotensin II inhibition in metabolic acidosis in human patients

Henger, Annerose; Tutt, P; Riesen, Walter; Hulter, Henry N.; Krapf, Reto

doi:10.1067/mlc.2000.110371

Cited by 63 publications

(47 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ACTH release and a consequent increased production of cortisol and aldosterone. These adrenal hormones up-regulates the expression of glutaminase in kidney tubules, which evolves ammonia as a buffer for acid excretion [14][15][16]. In our study, waist circumference and HOMA-R as an index of visceral obesity and insulin resistance respectively reflected urine acidification.…”

Section: Measurementsmentioning

confidence: 77%

Association of urine acidification with visceral obesity and the metabolic syndrome

et al. 2011

View full text Add to dashboard Cite

It has been known that the composition of the diet affects acid-base balance in the body. Remer et al. showed that high intake of protein-rich diet was metabolized to yield free sulfuric acid, which induced metabolic acidosis and urine acidification [1,2]. High dietary protein intake and the associated metabolic acidosis have been shown to adversely affect bone health in humans because of increased excretion of urinary calcium [3,4]. Likewise, an excessive protein intake could be associated with other pathological conditions.The metabolic syndrome is characterized by visceral obesity causing insulin resistance, elevated blood pressure, and dyslipidemia, which is a common basis of cardiovascular diseases [5]. Although the exact mechanism remains unclear, one possible explanation is that Abstract. Urine acidification is induced by metabolic acidosis which is associated with a high intake of protein-rich diet. The purpose of this study was to investigate the relationship of urine acidification with visceral obesity and the metabolic syndrome. We recruited 1,051 male subjects who underwent health examinations at the Health Care Center in Kinki Central Hospital. Subjects who were treated for hypertension, dyslipidemia, diabetes mellitus, and hyperuricemia and had the past history of chronic liver disease, chronic kidney disease and cancer, were excluded in this study. All subjects were administered to urine pH, blood and physical examinations. Lower urine pH was associated with higher serum urea nitrogen which reflects high intake of protein-rich diet, whereas it had no relation to serum creatinine. Lower urine pH was also associated with an increase in waist circumference, homeostasis model assessment-R, fasting plasma glucose, HbA1c, serum triglyceride, serum uric acid and with a decrease in high density lipoprotein cholesterol. Urine pH was not associated with mean blood pressure. Urine acidification is a characteristic of visceral obesity and the metabolic syndrome. High intake of protein-rich diet may contribute urine acidification, which is associated with various metabolic abnormalities in visceral obesity.Key words: Urine acidification, Metabolic acidosis, Metabolic syndrome, Hyperuricemia the increased cortisol production induces visceral obesity and insulin resistance [6], and thereby may promote the metabolic syndrome [7]. It is known that metabolic acidosis relates an increased cortisol production from adrenal glands. The epidemiologic study has established a close link between the elevated levels of serum uric acid and the increasing prevalence of the metabolic syndrome [8]. The elevated levels of serum uric acid are associated with increased cardiovascular morbidity and mortality in the US adult population [9]. These results suggested that hyperuricemia is one of components of the metabolic syndrome.The purpose of this study was to investigate the relationship of urine acidification with visceral obesity and the parameters of the metabolic syndrome in men. Materials and Methods SubjectsWe initially re...

show abstract

Section: Measurementsmentioning

confidence: 77%

Association of urine acidification with visceral obesity and the metabolic syndrome

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Furthermore, aldosterone increases the activity of vacuolar H ϩ -ATPases in rat and rabbit cortical and medullary collecting ducts, and these effects are mimicked in isolated turtle bladder (32). Evidence that this mineralocorticoid is necessary for appropriate urinary acidification is also derived from patients with inborn or acquired aldosterone deficiency syndromes (distal renal tubular acidosis type IV) or in animal models with adrenalectomy or pharmacological blockade of the aldosterone pathway (10,(33)(34)(35)(36). In general, it is accepted that sustained effects of mineralocorticoids on acid secretion involve genomic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Nongenomic stimulation of vacuolar H ⁺ -ATPases in intercalated renal tubule cells by aldosterone

Winter

Schulz

Giebisch

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

115

100

View full text Add to dashboard Cite

“…Acidosis in vivo is associated with upregulation of the renin-angiotensin system (6,10,31). Luminal ANG II not only stimulates tNH 3 production but also stimulates tNH 3 secretion into the luminal fluid (20).…”

Section: Discussionmentioning

confidence: 99%

Role of angiotensin II in the enhancement of ammonia production and secretion by the proximal tubule in metabolic acidosis

Nagami¹

2008

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

Nagami GT. Role of angiotensin II in the enhancement of ammonia production and secretion by the proximal tubule in metabolic acidosis. Am J Physiol Renal Physiol 294: F874-F880, 2008. First published February 20, 2008 doi:10.1152/ajprenal.00286.2007.-Acidosis and angiotensin II stimulate ammonia production and transport by the proximal tubule. We examined the modulatory effect of the type 1 angiotensin II receptor blocker losartan on the ability of metabolic acidosis to stimulate ammonia production and secretion by mouse S2 proximal tubule segments. Mice given NH 4Cl for 7 days developed metabolic acidosis (low serum bicarbonate concentration) and increased urinary excretion of ammonia. S2 tubule segments from acidotic mice displayed higher rates of ammonia production and secretion compared with those from control mice. However, when losartan was coadministered in vivo with NH 4Cl, both the acidosisinduced increase in urinary ammonia excretion and the adaptive increase in ammonia production and secretion of microperfused S2 segments were largely blocked. In renal cortical tissue, losartan blocked the acid-induced increase in brush-border membrane NHE3 expression but had no effect on the acid-induced upregulation of phosphate-dependent glutaminase or phosphoenolpyruvate carboxykinase 1 in cortical homogenates. Addition of angiotensin II to the microperfusion solution enhanced ammonia secretion and production rates in tubules from NH 4Cl-treated and control mice in a losartaninhibitable manner. These results demonstrate that a 7-day acid challenge induces an adaptive increase in ammonia production and secretion by the proximal tubule and suggest that during metabolic acidosis, angiotensin II signaling is necessary for adaptive enhancements of ammonia excretion by the kidney and ammonia production and secretion by S2 proximal tubule segments, as mediated, in part, by angiotensin receptor-dependent enhancement of NHE3 expression. ammonia transport; ammoniagenesis; acid-base physiology; losartan; sodium-hydrogen exchanger A MAJOR WAY that the kidneys defend the body against the introduction of excess acid is through the production and excretion of total ammonia (tNH 3 ϭ NH 3 ϩ NH 4 ϩ ) (15,21,29,33,36). The proximal tubule is the major site of this response to acid challenges, increasing its rates of tNH 3 production and secretion and generating new bicarbonate formation (8,26). We previously demonstrated that chronic metabolic acidosis in vivo stimulates tNH 3 production and secretion by mouse S2 proximal tubule segments (24). The increased rates of ammoniagenesis persist even after the tubule is removed from the acidotic animal and assayed in vitro under normal pH conditions. Such adaptive changes result from the induction of key ammoniagenic enzymes (5, 37).In our previous study, short-term (18-h) acid challenges induced an adaptive enhancement in the rate of tNH 3 secretion, but not production in an angiotensin II (ANG II)-dependent manner (22). Giving the acid challenge concurrently with a type 1 ANG II (AT1) r...

show abstract

Acid-base and endocrine effects of aldosterone and angiotensin II inhibition in metabolic acidosis in human patients

Cited by 63 publications

References 20 publications

Association of urine acidification with visceral obesity and the metabolic syndrome

Association of urine acidification with visceral obesity and the metabolic syndrome

Nongenomic stimulation of vacuolar H ⁺ -ATPases in intercalated renal tubule cells by aldosterone

Role of angiotensin II in the enhancement of ammonia production and secretion by the proximal tubule in metabolic acidosis

Contact Info

Product

Resources

About

Acid-base and endocrine effects of aldosterone and angiotensin II inhibition in metabolic acidosis in human patients

Cited by 63 publications

References 20 publications

Association of urine acidification with visceral obesity and the metabolic syndrome

Association of urine acidification with visceral obesity and the metabolic syndrome

Nongenomic stimulation of vacuolar H + -ATPases in intercalated renal tubule cells by aldosterone

Role of angiotensin II in the enhancement of ammonia production and secretion by the proximal tubule in metabolic acidosis

Contact Info

Product

Resources

About

Nongenomic stimulation of vacuolar H ⁺ -ATPases in intercalated renal tubule cells by aldosterone