Control of sodium and potassium transport in the cortical collecting duct of the rat. Effects of bradykinin, vasopressin, and deoxycorticosterone.

Tomita, Kimio; Pisano, John J.; Knepper, Mark A.

doi:10.1172/jci111935

Cited by 279 publications

(186 citation statements)

References 33 publications

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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

show abstract

“…Accordingly, we have shown that TK activates the epithelial Na + channel ENaC by cleaving its gamma subunit (34). In CCDs isolated from rats microperfused in vitro, Tomita et al (35) showed that basolateral bradykinin inhibits net Na + absorption by affecting an electroneutral, amiloride-resistant, thiazide-sensitive NaCl transporter that remained unidentified until our recent report (35). In this study, we observed that CCDs from TK −/− mice actually absorb sodium via an electroneutral process.…”

Section: Discussionmentioning

confidence: 50%

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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“…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%