Sodium transport by rat cortical collecting tubule. Effects of vasopressin and desoxycorticosterone.

Reif, Max C.; Troutman, Susan L.; Schafer, James A.

doi:10.1172/jci112433

Cited by 175 publications

(115 citation statements)

References 37 publications

(31 reference statements)

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“…This finding is consistent with previous reports that isolated, perfused rat CCTs do not exhibit electrogenic, amiloride-sensitive Na reabsorption unless the mineralocorticoid levels are raised (Tomita, Pisano, and Knepper, 1985;Reif, Troutman, and Schafer, 1986). The rat colon shows a similar pattern of transepithelial transport.…”

Section: Dependence Of Na Channel Activity On Dietsupporting

confidence: 93%

Regulation of Na channels of the rat cortical collecting tubule by aldosterone.

Pácha

Frindt

Antonian

et al. 1993

The Journal of General Physiology

199

132

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The activity of apical membrane Na channels in the rat cortical collecting tubule was studied during manipulation of the animals' mineralocorticoid status in vivo using a low-Na diet or the diuretic furosemide. Tubules were isolated and split open to expose the luminal membrane surface. Induction of Na channel activity was studied in cell-attached patches of the split tubules. No activity was observed with control animals on a normal diet. Channel activity could be induced by putting the animals on the low-Na diet for at least 48 h. The mean number of open channels per patch (NPo) was maximal after 1 wk on low Na. Channels were also induced within 3 h after injection of furosemide (20 mg/kg body wt per d). NPo was maximal 48 h after the first injection. In both cases, increases in NPo were primarily due to increases in the number of channels per patch (N) at a constant open probability (Po). With salt depletion or furosemide injection NPo is a saturable function of aldosterone concentration with half-maximal activity at ~ 8 nM. When animals were salt repleted after 1-2 wk of salt depletion, both plasma aldosterone and NPo fell markedly within 6 h. NPo continued to decrease over the next 14 h, while plasma aldosterone rebounded partially. Channel activity may be dissociated from aldosterone concentrations under conditions of salt repletion.

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Section: Dependence Of Na Channel Activity On Dietsupporting

confidence: 93%

Regulation of Na channels of the rat cortical collecting tubule by aldosterone.

Pácha

Frindt

Antonian

et al. 1993

The Journal of General Physiology

199

132

View full text Add to dashboard Cite

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“…It is most pronounced in the early ASDN portions (late DCT and early CNT) and progressively decreases along further downstream localized segments (late CNT and CD) (2,6). This morphologically ascertainable gradient is consistent with numerous functional studies showing several-fold higher transepithelial Na ϩ transport rates and ENaC activity in the CNT than in the CD (7)(8)(9)(10)(11). However, the underlying molecular mechanisms for this axial heterogeneity are unclear.…”

supporting

confidence: 86%

Dietary Sodium Intake Regulates the Ubiquitin-Protein Ligase Nedd4-2 in the Renal Collecting System

Loffing‐Cueni¹,

Flores²,

Sauter³

et al. 2006

Journal of the American Society of Nephrology

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The activity of the epithelial sodium (Na ؉ ) channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) needs to be tightly regulated to match urinary Na ؉ excretion with dietary Na ؉ intake. The ubiquitin-protein ligase Nedd4-2, which in vitro interacts with ENaC subunits and reduces ENaC cell surface abundance and activity by ubiquitylation of the channel, may participate in the control of ENaC. This study confirms in vivo by reverse-transcriptase-PCR that Nedd4-2 is expressed throughout the nephron and is detectable by immunoblotting in kidney extracts. By immunohistochemistry, Nedd4-2 was found to be strongly expressed in the ASDN, with low staining intensity in the late distal convoluted tubule and early connecting tubule (where apical ENaC is high) and gradually increasing detection levels toward the collecting duct (CD; where apical ENaC is low). Compared with high-Na ؉ diet (5% Na ؉ ), 2 wk of low-Na ؉ diet (0.01% Na ؉ ) drastically reduces Nedd4-2 immunostaining and increases apical ENaC abundance in ASDN. Reduced Nedd4-2 immunostaining is not dependent on increased apical Na ؉ entry in the CD, because it is similarly observed in mice with intact and with suppressed apical ENaC activity in the CD. Consistent with a role of mineralocorticoid hormones in the long-term regulation of Nedd4-2, 5-d treatment of cultured CD (mpkCCD cl4 ) cells with 1 M aldosterone leads to reduction of Nedd4-2 protein expression. It is concluded that Nedd4-2 abundance is regulated by Na ؉ diet, by a mechanism that likely involves aldosterone. This regulation may contribute to adaptation of apical ENaC activity to altered Na ؉ intake.

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“…Whereas AVP produces a persistent increase in JNa in the rat (39,40), it only transiently stimulates JNa and VT in the rabbit (21,27,41). The biphasic effect of vasopressin action on VT and JNa in the rabbit CCD has been attributed to prostaglandin production in the rabbit CCD (21).…”

Section: Discussionmentioning

confidence: 99%