Interrelated effects of aldosterone and plasma potassium on potassium excretion

Young, David B.; Paulsen, A. W.

doi:10.1152/ajprenal.1983.244.1.f28

Cited by 25 publications

(28 citation statements)

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“…To do so, the effect of an acute intracellular acid load on intracellular pH (pHi) recovery was monitored in ICs and PCs. Cells were acidified by the NH 4 Cl prepulse technique, and the initial rate of intracellular pH recovery in the absence of Na + was measured. This pH recovery reflects the activity of proton pumps.…”

Section: Resultsmentioning

confidence: 99%

“…$$ P < 0.01 vs. TK −/− in the absence of inhibitor. The nadir pH i achieved after washout of the NH 4 Cl prepulse was identical in each group, 6.62 ± 0.05 for TK +/+ (n = 8); 6.70 ± 0.11 for TK −/− (n = 9); 6.72 ± 0.05 for TK −/− + Sch28080 (n = 4) and 6.68 ± 0.09 for TK −/− + ouabain (n = 4). Values are means ± SE and were not significantly different (one-way ANOVA).…”

Section: Resultsmentioning

confidence: 99%

“…Therefore, we tested the ability of TK −/− mice to cope with a chronic acid load. TK +/+ and TK −/− mice were administrated 280 mM NH 4 Cl in the drinking water. Although this challenge induced a significant reduction in blood pH and [HCO 3 − ] in both genotypes, metabolic acidosis was significantly less severe in TK −/− mice (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…This absorption occurs through the intercalated cells (ICs) and depends on an apical electroneutral H + ,K + -ATPase (3). This system and, hence, potassium balance, is under the tight control of the mineralocorticoid hormone aldosterone, which activates and fine-tunes K + secretion by the collecting duct (4,5). Despite the fact that aldosterone is the key regulator of renal K + excretion and K + balance, this regulation is not sufficient to ensure the stability of plasma [K + ].…”

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confidence: 99%

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Tissue kallikrein permits early renal adaptation to potassium load

Moghrabi

Houillier

Picard

et al. 2010

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

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Tissue kallikrein (TK) is a serine protease synthetized in renal tubular cells located upstream from the collecting duct where renal potassium balance is regulated. Because secretion of TK is promoted by K + intake, we hypothesized that this enzyme might regulate plasma K + concentration ([K + ]). We showed in wild-type mice that renal K + and TK excretion increase in parallel after a single meal, representing an acute K + load, whereas aldosterone secretion is not modified. Using aldosterone synthase-deficient mice, we confirmed that the control of TK secretion is aldosterone-independent. Mice with TK gene disruption ( TK −/− ) were used to assess the impact of the enzyme on plasma [K + ]. A single large feeding did not lead to any significant change in plasma [K + ] in TK +/+ , whereas TK −/− mice became hyperkalemic. We next examined the impact of TK disruption on K + transport in isolated cortical collecting ducts (CCDs) microperfused in vitro. We found that CCDs isolated from TK −/− mice exhibit net transepithelial K + absorption because of abnormal activation of the colonic H + ,K + -ATPase in the intercalated cells. Finally, in CCDs isolated from TK −/− mice and microperfused in vitro, the addition of TK to the perfusate but not to the peritubular bath caused a 70% inhibition of H + ,K + -ATPase activity. In conclusion, we have identified the serine protease TK as a unique kalliuretic factor that protects against hyperkalemia after a dietary K + load.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Tissue kallikrein permits early renal adaptation to potassium load

Moghrabi

Houillier

Picard

et al. 2010

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

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“…Thus, the maintenance of K ϩ homeostasis has been traditionally understood on the basis of the concept of negative feedback control. However, Rabinowitz (21,22) challenged this traditional view when he pointed out that plasma K ϩ and aldosterone can stimulate renal K ϩ excretion only at levels above their normal ranges (3,25,31,32). In his studies in the sheep (24), meal intake over 1 h produced a pronounced kaliuresis, which occurred in the absence of a change in plasma aldosterone concentration and with only a very small (0.5 meq/l) increase in plasma [K ϩ ].…”

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confidence: 99%

Gut sensing of dietary K⁺ intake increases renal K⁺ excretion

Kim

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Dietary K+ intake may increase renal K+ excretion via increasing plasma [K+] and/or activating a mechanism independent of plasma [K+]. We evaluated these mechanisms during normal dietary K+ intake. After an overnight fast, [K+] and renal K+ excretion were measured in rats fed either 0% K+ or the normal 1% K+ diet. In a third group, rats were fed with the 0% K+ diet, and KCl was infused to match plasma [K+] profile to that of the 1% K+ diet group. The 1% K+ feeding significantly increased renal K+ excretion, associated with slight increases in plasma [K+], whereas the 0% K+ diet decreased K+ excretion, associated with decreases in plasma [K+]. In the KCl-infused 0% K+ diet group, renal K+ excretion was significantly less than that of the 1% K+ group, despite matched plasma [K+] profiles. We also examined whether dietary K+ alters plasma profiles of gut peptides, such as guanylin, uroguanylin, glucagon-like peptide 1, and glucose-dependent insulinotropic polypeptide, pituitary peptides, such as AVP, α-MSH, and γ-MSH, or aldosterone. Our data do not support a role for these hormones in the stimulation of renal K+ excretion during normal K+ intake. In conclusion, postprandial increases in renal K+ excretion cannot be fully accounted for by changes in plasma [K+] and that gut sensing of dietary K+ is an important component of the regulation of renal K+ excretion. Our studies on gut and pituitary peptide hormones suggest that there may be previously unknown humoral factors that stimulate renal K+ excretion during dietary K+ intake.

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