Dietary NaCl and KCl do not regulate renal density of the thiazide diuretic receptor

Fanestil, Darrell D.; Vaughn, Duke A.; Blakely, Patricia

doi:10.1152/ajpregu.1997.273.4.r1241

Cited by 7 publications

(7 citation statements)

References 12 publications

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“…Ingestion of excess MgCl 2 resulted in increased P Mg ϩϩ, in increased renal TZR density, and in increased urinary excretion of Mg, calcium, and chloride (Table 4). These data demonstrating an effect of a dietary element (magnesium) on renal TZR density contrast with prior reports from this laboratory in which we failed to alter renal TZR density by varying the ingestion of sodium chloride or potassium chloride (12). These combined reports demonstrate the exquisite selectivity of the renal TZR response to dietary Mg.…”

Section: Discussioncontrasting

confidence: 98%

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Dietary Magnesium, Not Calcium, Regulates Renal Thiazide Receptor

Fanestil

Hyde

Blakely

et al. 1999

Journal of the American Society of Nephrology

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Abstract. This study reports for the first time a relationship between dietary Mg and the renal thiazide-sensitive Na-Cl cotransporter (TZR, measured by saturation binding with 3H-metolazone). Ion-selective electrodes measured plasma ionized magnesium (PMg+ +), calcium (PCa + +), and potassium (PK +). Restricting dietary Mg for 1 wk decreased PMg + + 18%, TZR 25%, and renal excretion of magnesium (UMg) and calcium (UCa) more than 50% without changing PCa + +, PK +, or plasma aldosterone. A low Mg diet for 1 d significantly decreased PMg + +, TZR, UMg and UCa. Return of dietary Mg after 5 d of Mg restriction restored PMg + + and TZR toward normal. In the control, Mg-deficient, and Mg-repleting animals, TZR correlated with PMg + + (r = 0.86) and with UMg (r = 0.87) but not UCa (r = 0.09). Increasing oral intake of Mg for 1 wk increased PMg + + 14%, TZR 32%, UMg 74%, and UCa more than fourfold without changing PCa + + or PK +. In contrast, increasing dietary Ca content from 0.02% to 1.91% did not change TZR, but increased UCa fivefold without changing PCa + +. Hormonal mediators (if any) involved in the relationship between dietary Mg and TZR remain to be elucidated, as does the relationship between TZR and tubular reabsorption of Mg.

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Section: Discussioncontrasting

confidence: 98%

“…Concurrently, we reported from our laboratory that several dietary manipulations failed to cause significant changes in the renal density of TZR. Renal TZR density did not change in response to large changes in the dietary intake of NaCl or KCl (12). Metabolic acid-base disturbances produced only transient or modest changes in renal TZR density (13).…”

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confidence: 85%

Dietary Magnesium, Not Calcium, Regulates Renal Thiazide Receptor

Fanestil

Hyde

Blakely

et al. 1999

Journal of the American Society of Nephrology

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“…In rats, dietary NaCl restriction has been reported to increase thiazide-sensitive Na ϩ -Cl Ϫ transport by threefold (79) and to increase NCC protein expression twofold (145). Dietary NaCl restriction, however, was not shown to increase the number of [ 3 H]metolazone binding sites in kidney cortex (82) or to increase NCC message expression (192). In the rabbit, dietary NaCl loading, which suppresses aldosterone secretion, increases the fractional volume of DCT cells and increases basolateral cell membrane amplification (134) and Na ϩ -K ϩ -ATPase activity (166).…”

Section: Regulation Of Na ϩ and CL ϫ Transportmentioning

confidence: 91%

Mammalian Distal Tubule: Physiology, Pathophysiology, and Molecular Anatomy

Reilly¹,

Ellison²

2000

Physiological Reviews

315

283

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The distal tubule of the mammalian kidney, defined as the region between the macula densa and the collecting duct, is morphologically and functionally heterogeneous. This heterogeneity has stymied attempts to define functional properties of individual cell types and has led to controversy concerning mechanisms and regulation of ion transport. Recently, molecular techniques have been used to identify and localize ion transport pathways along the distal tubule and to identify human diseases that result from abnormal distal tubule function. Results of these studies have clarified the roles of individual distal cell types. They suggest that the basic molecular architecture of the distal nephron is surprisingly similar in mammalian species investigated to date. The results have also reemphasized the role played by the distal tubule in regulating urinary potassium excretion. They have clarified how both peptide and steroid hormones, including aldosterone and estrogen, regulate ion transport by distal convoluted tubule cells. Furthermore, they highlight the central role that the distal tubule plays in systemic calcium homeostasis. Disorders of distal nephron function, such as Gitelman's syndrome, nephrolithiasis, and adaptation to diuretic drug administration, emphasize the importance of this relatively short nephron segment to human physiology. This review integrates molecular and functional results to provide a contemporary picture of distal tubule function in mammals.

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“…Feeding rats a low-K ϩ diet did not change binding of the thiazide-like diuretic [ 3 H]metolazone, which is an indirect mea-sure of NCC density (84). However, it did decrease NCC mRNA expression (8) and total protein abundance (79).…”

Section: Low K ϩ Mediates Phosphorylation Of Nccmentioning

confidence: 99%

Regulation of the Renal NaCl Cotransporter and Its Role in Potassium Homeostasis

Hoorn

Gritter

Cuevas³

et al. 2020

Physiological Reviews

119

137

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Daily dietary potassium (K+) intake may be as large as the extracellular K+ pool. To avoid acute hyperkalemia, rapid removal of K+ from the extracellular space is essential. This is achieved by translocating K+ into cells and increasing urinary K+ excretion. Emerging data now indicate that the renal thiazide-sensitive NaCl cotransporter (NCC) is critically involved in this homeostatic kaliuretic response. This suggests that the early distal convoluted tubule (DCT) is a K+ sensor that can modify sodium (Na+) delivery to downstream segments to promote or limit K+ secretion. K+ sensing is mediated by the basolateral K+ channels Kir4.1/5.1, a capacity that the DCT likely shares with other nephron segments. Thus, next to K+-induced aldosterone secretion, K+ sensing by renal epithelial cells represents a second feedback mechanism to control K+ balance. NCC’s role in K+ homeostasis has both physiological and pathophysiological implications. During hypovolemia, NCC activation by the renin-angiotensin system stimulates Na+ reabsorption while preventing K+ secretion. Conversely, NCC inactivation by high dietary K+ intake maximizes kaliuresis and limits Na+ retention, despite high aldosterone levels. NCC activation by a low-K+ diet contributes to salt-sensitive hypertension. K+-induced natriuresis through NCC offers a novel explanation for the antihypertensive effects of a high-K+ diet. A possible role for K+ in chronic kidney disease is also emerging, as epidemiological data reveal associations between higher urinary K+ excretion and improved renal outcomes. This comprehensive review will embed these novel insights on NCC regulation into existing concepts of K+ homeostasis in health and disease.

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Dietary NaCl and KCl do not regulate renal density of the thiazide diuretic receptor

Cited by 7 publications

References 12 publications

Dietary Magnesium, Not Calcium, Regulates Renal Thiazide Receptor

Dietary Magnesium, Not Calcium, Regulates Renal Thiazide Receptor

Mammalian Distal Tubule: Physiology, Pathophysiology, and Molecular Anatomy

Regulation of the Renal NaCl Cotransporter and Its Role in Potassium Homeostasis

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