Ambient C1- ions modify rat mesangial cell contraction by modulating cell inositol trisphosphate and Ca2+ via enhanced prostaglandin E2.

Okuda, Takatoshi; Kojima, Itaru; Ogata, Etsuro; Kurokawa, Kiyoshi

doi:10.1172/jci114373

Cited by 39 publications

(19 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Specifically, the capacity of the different agonists to stimulate arachidonic acid release and thereby elicit increased prostaglandin release, which is in turn subject to modulation by the prevailing chloride concentration, is a distinct possibility. Thus, in mesangial cells, low chloride increases release of prostaglandin E2 (Okuda et al, 1989) whereas, high chloride stimulates thromboxane (Wilcox et al, 1985).…”

Section: Discussionmentioning

confidence: 96%

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Quilley

Lin

McGiff

1993

British J Pharmacology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 96%

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Quilley

Lin

McGiff

1993

British J Pharmacology

View full text Add to dashboard Cite

“…Alternatively, prostaglandins may affect signaling by the extracellular mesangial (Goormatigh) cells (38). Finally, although epithelial cells of more distal nephron structures produce predominantly PGE2 (39), the profile of cyclooxygenase products produced by macula densa cells is unknown.…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 is associated with the macula densa of rat kidney and increases with salt restriction.

et al. 1994

View full text Add to dashboard Cite

The kidney is a rich source of prostaglandins. These eicosanoids, formed by cyclooxygenase-dependent metabolism of arachidonic acid, are important physiologic mediators of renal glomerular hemodynamics and tubular sodium and water reabsorption. Two separate isoforms of cyclooxygenase (COX) have now been identified: constitutive COX-1, encoded by a 2.8-kb mRNA, and mitogen-activated COX-2, encoded by a 4.0-4.5-kb mRNA. COX-2 expression increases during development and inflammation, but, except for brain, constitutive expression is low. It has been generally accepted that physiologic renal production of prostaglandins is mediated by COX-1. However, in the absence of inflammation, low levels of COX-2 mRNA are also detectable in the kidney. To examine the role of COX-2 in the kidney and determine its intrarenal localization, we used a 1.3-kb cDNA probe specific for the 3' untranslated region of rat COX-2 and COX-2-specific antiserum. The COX-2-specffic cDNA probe hybridized with a 4.4-kb transcript in total RNA from adult rat kidney. Immunoblots of microsomes isolated from kidney cortex and papilla indicated immunoreactive COX-2 in both locations. In situ hybridization and immunohistochemistry indicated that renal cortical COX-2 expression was localized to the macula densa of the juxtaglomerular apparatus and to adjacent epithelial cells of the cortical thick ascending limb of Henle. In addition, COX-2 immunoreactivity was detected in interstitial cells in the papilla. No COX-2 message or immunoreactive protein was detected in arterioles, glomeruli, or cortical or medullary collecting ducts.When animals were chronically sodium restricted, the level of COX-2 in the region of the macula densa increased threefold (from 0.86±0.08 to 2.52±0.43/mm2) and the total area of the COX-2 immunoreactive cells in cortex increased from 34 tm2/nmm2 of cortex to 226 ,um2/mm2 of cortex. The

show abstract

“…However, it is unclear how furosemide causes an increase in cAMP that could explain its effect on membrane potential and renin release. Alternatively, a decreased intracellular Cl Ϫ concentration caused by inhibition of NKCC1-dependent chloride transport might either inhibit voltage-dependent calcium channels (27) directly or indirectly by driving HCO 3 Ϫ out of the cell via the Cl Ϫ /HCO 3 Ϫ exchanger (33). Thus a resulting reduction in cytosolic Ca in granular cells may be another pathway through which loop diuretics stimulate renin release (12).…”

Section: Discussionmentioning

confidence: 99%

Contribution of the basolateral isoform of the Na-K-2Cl⁻cotransporter (NKCC1/BSC2) to renin secretion

Castrop

Lorenz²,

Hansen³

et al. 2005

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

Acute administration of loop diuretics like furosemide leads to a stimulation of renin secretion, an effect thought to result from inhibition of Na-K-2Cl cotransporter (NKCC2)-mediated salt transport at the luminal surface of the macula densa (MD). However, loop diuretics also inhibit NKCC1, the second isoform of the Na-K-2Cl cotransporter, with similar potency. In the present study, we examined the influence of furosemide on renin secretion in NKCC1-deficient mice to distinguish between effects of the loop diuretic involving NKCC2 and, by implication, the MD pathway, and effects that might occur via inhibition of NKCC1. Baseline plasma renin concentration (PRC) was 1,212 ± 211 in NKCC1+/+ ( n = 13) and 3,851 ± 579 ng ANG I·ml−1·h−1 in NKCC1−/− mice ( n = 14; P = 0.00024). Acute administration of furosemide (50 mg/kg i.p.) increased PRC significantly to 9,324 ± 1,018 ng ANG I·ml−1·h−1 in NKCC1+/+ ( n = 13; P < 0.0001 compared with basal) and to 14,188 ± 2,274 ng ANG I·ml−1·h−1 in NKCC1−/− mice [ n = 14; P = 0.0002 compared with basal; P = 0.034 compared with wild-type (WT) plus furosemide]. Renin mRNA expression was about threefold higher in NKCC1−/− compared with WT mice. There was considerable recruitment of granular cells to upstream regions of afferent arterioles in NKCC1−/− mice. Patch-clamp studies in single juxtaglomerular granular (JG) cells from WT mice showed an ∼10% increase in membrane capacitance during incubation with furosemide (10−4 M), indicating a direct effect of the loop diuretic on renin secretion. No effect of furosemide on membrane capacitance was observed in JG cells from NKCC1-deficient mice. Furosemide (10−3 M) significantly stimulated renin release from primary cultures of JG cells from WT mice, whereas no response was observed in NKCC1−/− mice. Our data suggest that a functional NKCC1 suppresses basal renin release, at least in part, through a direct effect on JG cells.

show abstract

Ambient C1- ions modify rat mesangial cell contraction by modulating cell inositol trisphosphate and Ca2+ via enhanced prostaglandin E2.

Cited by 39 publications

References 29 publications

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Cyclooxygenase-2 is associated with the macula densa of rat kidney and increases with salt restriction.

Contribution of the basolateral isoform of the Na-K-2Cl⁻cotransporter (NKCC1/BSC2) to renin secretion

Contact Info

Product

Resources

About

Ambient C1- ions modify rat mesangial cell contraction by modulating cell inositol trisphosphate and Ca2+ via enhanced prostaglandin E2.

Cited by 39 publications

References 29 publications

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Cyclooxygenase-2 is associated with the macula densa of rat kidney and increases with salt restriction.

Contribution of the basolateral isoform of the Na-K-2Cl−cotransporter (NKCC1/BSC2) to renin secretion

Contact Info

Product

Resources

About

Contribution of the basolateral isoform of the Na-K-2Cl⁻cotransporter (NKCC1/BSC2) to renin secretion