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857 results on '"Giebisch, G"'

9. Role of luminal anion and pH in distal tubule potassium secretion

Author

Amorim, J.B.O., Bailey, M.A., Musa-Aziz, R., Giebisch, G., and Malnic, G.

Subjects
Secretion -- Physiological aspects, Potassium -- Physiological aspects, Biological transport -- Physiological aspects, Kidney tubules -- Physiological aspects, Biological sciences
Abstract

Potassium secretory flux ([J.sub.K]) by the distal nephron is regulated by systemic and luminal factors. In the present investigation, [J.sub.K] was measured with a double-barreled [K.sup.+] electrode during paired microperfusion of superficial segments of the rat distal nephron. We used control solutions (100 mM NaCl, pH 7.0) and experimental solutions in which [Cl.sup.-] had been replaced with a less permeant anion and/or pH had been increased to 8.0. [J.sub.K] increased when [Cl.sup.-] was replaced by either acetate (~37%), sulfate (~32%), or bicarbonate (~62%), and also when the pH of the control perfusate was increased (~26%). The majority (80%) of acetate-stimulated [J.sub.K] was [Ba.sup.2+] sensitive, but furosemide (1 mM) further reduced secretion (~10% of total), suggesting that [K.sup.+]-[Cl.sup.-] cotransport was operative. Progressive reduction in luminal [Cl.sup.-] concentration from 100 to 20 to 2 mM caused increments in [J.sub.K] that were abolished by inhibitors of [K.sup.+]-[Cl.sup.-] cortransport, i.e., furosemide and [(dihydroindenyl)oxy]alkanoic acid. Increasing the pH of the luminal perfusion fluid also increased [J.sub.K] even in the presence of [Ba.sup.2+], suggesting that this effect cannot be accounted for only by [K.sup.+] channel modulation of [K.sup.+] secretion in the distal nephron of the rat. Collectively, these data suggest a role for [K.sup.+]-[Cl.sup.-] cotransport in distal nephron [K.sup.+] secretion. distal tubule; collecting duct; potassium secretion; postassium-chloride cotransport

Published
2003

14. Bicarbonate transport along the loop of Henle: effects of adrenal steroids

Author

Unwin, R., Capasso, G., and Giebisch, G.

Subjects
Kidney tubules -- Research, Bicarbonates -- Research, Biological transport -- Analysis, Adrenocortical hormones -- Physiological aspects, Biological sciences
Abstract

Tubule microperfusion experiments indicate the stimulation of bicarbonate transport (J(HCO3)) in the loop of Henle (LOH) in proximal tubules of rats by adrenal steroid hormones such as glyco- and mineralocorticoids. Adrenalectomized rats exhibit in 40% reduction in J(HCO3) along LOH, as indicated by microcalorimetric studies and fluid resorption by (14C)insulin. Administration of dexamethasone alone or along with aldosterone enhances J(HCO3).

Published
1995

28. Genetic defects in renal phosphate handling

Author

Lifton, R, Somlo, S, Giebisch, G, Seldin, D, Lifton, R ( R ), Somlo, S ( S ), Giebisch, G ( G ), Seldin, D ( D ), Wagner, C A, Hernando, N, Forster, I C, Biber, J, Murer, H, Lifton, R, Somlo, S, Giebisch, G, Seldin, D, Lifton, R ( R ), Somlo, S ( S ), Giebisch, G ( G ), Seldin, D ( D ), Wagner, C A, Hernando, N, Forster, I C, Biber, J, and Murer, H

Abstract

Genetic Diseases of the Kidney identifies and analyzes genetic abnormalities causing renal diseases in human subjects. Although in a sense the genome contains all the instructions required for the formation of a phenotype, the information is encoded in an extremely complicated fashion. In primary genetic diseases, the genetic instruction specifies a phenotype clearly linked with a discreet lesion confined to the kidney. However, the genetic disturbance may be imbedded in a complicated physiologic ensemble, so that the nexus between the genetic disturbance and the phenotype may be obscured; in consequence, the causal sequence is extremely difficult to unravel. In many instances the renal disease is one component of a complicated systemic hereditary disease, either monogenic or polygenic. Indeed, renal disease may arise as the sum of minor inputs from many different, seemingly unrelated genes, so that the genetic contributions may be difficult to identify. Confounding the problem further are environmental influences, originating either in the chromosomal environment from modifier genes, or in the extra-chromosomal environmental from intrauterine or postnatal influences. These considerations have determined both the organization of the text as well as the detailed description of the genetic disorders and the physiologic derangements that emerge.

Published
2008

50. Bicarbonate transport along the loop of Henle: molecular mechanisms and regulation

Author

Giovambattista Capasso, Unwin, R., Rizzo, M., Pica, A., Giebisch, G., Capasso, Giovambattista, Unwin, R, Rizzo, M, Pica, A, and Giebisch, G.

Subjects
H, Sodium-Hydrogen Exchangers, urogenital system, RT-PCR, Biological Transport, Hypertrophy, Hydrogen-Ion Concentration, +, exchanger, Absorption, Bicarbonate, Bicarbonates, Proton-Translocating ATPases, Loop of Henle, Animals, Na, Acid-base
Abstract

The loop of Henle (LOH) is an important site of renal tubule acidification. A combination of several techniques, including in vivo microperfusion, perfusion in vitro of the S3 segment of the proximal tubule and of the thick ascending limb (TAL) of Henle's loop, as well as quantitative PCR performed on isolated TAL, has permitted the definition of key transporters and their role in modulating bicarbonate reabsorption in physiological and pathophysiological conditions. Na(+)-H+ exchange is the most important transport mechanism responsible for bicarbonate reabsorption, although a small but significant contribution of H(+)-ATPase-mediated bicarbonate reabsorption can also be identified. NHE3 is the main of several NHE isoforms expressed in the TAL and in the S3 segment of the proximal tubule. Special properties of the Na(+)-H+ exchanger in the TAL are its relative insensitivity to changes in cell pH (pHi) and the tight coupling between apical and basolateral Na(+)-H+ exchange. Several hormones, including anti-diuretic hormone (ADH), angiotensin II (AII), and gluco- and mineralocorticoids regulate Na(+)-H+ exchange. Loop diuretics such as furosemide stimulate bicarbonate transport along the LOH. Systemic acid-base disturbances also modulate bicarbonate transport: acidosis increases bicarbonate reabsorption, while metabolic alkalosis has the opposite effect. Neither hypokalemic alkalosis nor respiratory alkalosis or respiratory acidosis alter bicarbonate transport along the LOH. A significant role of HCO3 backflux, most likely through the paracellular pathway of the TAL, can also be observed. Changes in extracellular osmolality also affect bicarbonate reabsorption: hypertonicity inhibits, whereas hypotonicity stimulates transport. Transport activation is also observed as an adaptive response to glomerular hyperfiltration.

Published
2002

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