Gut sensing of dietary K⁺ intake increases renal K⁺excretion.
ABSTRACT 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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ABSTRACT: Guanylin peptides (GPs) family includes guanylin (GN), uroguanylin (UGN), lymphoguanylin, and recently discovered renoguanylin. This growing family is proposed to be intestinal natriuretic peptides. After ingestion of a salty meal, GN and UGN are secreted into the intestinal lumen, where they inhibit sodium absorption and induce anion and water secretion. At the same conditions, those hormones stimulate renal electrolyte excretion by inducing natriuresis, kaliuresis, and diuresis and therefore prevent hypernatremia and hypervolemia after salty meals. In the intestine, a well-known receptor for GPs is guanylate cyclase C (GC-C) whose activation increases intracellular concentration of cGMP. However, in the kidney of GC-C-deficient mice, effects of GPs are unaltered, which could be by new cGMP-independent signaling pathway (G-protein-coupled receptor). This is not unusual as atrial natriuretic peptide also activates two different types of receptors: guanylate cylcase A and clearance receptor which is also G-protein coupled receptor. Physiological role of GPs in other organs (liver, pancreas, lung, sweat glands, and male reproductive system) needs to be discovered. However, it is known that they are involved in pathological conditions like cystic fibrosis, asthma, intestinal tumors, kidney and heart failure, obesity, and metabolic syndrome.ISRN Nephrology. 04/2013; 2013.
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ABSTRACT: The discovery of the renal outer medullary K+ channel (ROMK, K(ir)1.1), the founding member of the inward-rectifying K+ channel (K(ir)) family, by Ho and Hebert in 1993 revolutionized our understanding of potassium channel biology and renal potassium handling. Because of the central role that ROMK plays in the regulation of salt and potassium homeostasis, considerable efforts have been invested in understanding the underlying molecular mechanisms. Here we provide a comprehensive guide to ROMK, spanning from the physiology in the kidney to the organization and regulation by intracellular factors to the structural basis of its function at the atomic level.AJP Renal Physiology 06/2009; 297(4):F849-63. · 4.42 Impact Factor
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ABSTRACT: The kidneys maintain extracellular K(+) homeostasis by altering K(+) excretion to match K(+) intake. Because this can occur without changes in plasma K(+) concentrations ([K(+)]), how the kidneys sense K(+) intake is unclear. We tested the hypothesis that the pituitary plays a critical role in signaling K(+) intake to the kidneys. If this hypothesis is true, hypophysectomy would impair kidney responses to altered K(+) intake. Hypophysectomized (Hypox) and sham-operated control rats (n = 8 each) were compared for their abilities to adjust K(+) excretion during a transition from normal to reduced (to 1/3 of normal) K(+) intake, followed by a reversal to normal K(+) intake. Food was provided only at night, and renal K(+) excretion was determined both for absorptive (night or feeding) and postabsorptive (day or non-feeding) periods. In normal rats, both absorptive and postabsorptive renal K(+) excretion were changed in parallel to the changes in K(+) intake, indicating a rapid adaptation of normal kidneys to altered K(+) intake. In Hypox rats, whereas absorptive renal K(+) excretion was changed in response to changes in K(+) intake, postabsorptive K(+) excretion was not responsive (P<0.001), indicating impaired renal responses to altered K(+) intake. In addition, Hypox rats, compared to control rats, showed K(+) intolerance (increases in plasma [K(+)]) upon feeding (i.e., K(+) intake) at night (P<0.01), indicating impairment of acute renal responses to K(+) intake. These data support that the pituitary plays a key role in the signaling of K(+) intake to the kidneys (and kidney responses to altered K(+) intake).AJP Regulatory Integrative and Comparative Physiology 04/2013; · 3.28 Impact Factor