Kinins inhibit conductive Na+ uptake by rabbit inner medullary collecting duct cells

1990 ◽  
Vol 258 (6) ◽  
pp. F1584-F1591 ◽  
Author(s):  
M. L. Zeidel ◽  
K. Jabs ◽  
D. Kikeri ◽  
P. Silva
Keyword(s):  
Initial Rate ◽  
Collecting Duct ◽  
Physiological Effect ◽  
Na Transport ◽  
Inner Medullary Collecting Duct ◽  
Transport Effects ◽  
Collecting Duct Cells ◽  
Medullary Collecting Duct ◽  
Na Uptake

Kinins promote natriuresis in vivo, at least in part by altering Na+ transport in the collecting duct. Using freshly prepared suspensions of rabbit inner medullary collecting duct (IMCD) cells, we have examined the effects of kinins on Na+ transport using measurements of oxygen consumption (QO2) and isotopic Na+ uptake. Bradykinin (BK) inhibited IMCD cell QO2 by 24.7 +/- 0.9% without significantly reducing QO2 in cells derived from the outer medullary collecting duct. BK and kallidin half-maximally inhibited QO2 at concentrations in the 10(-12)-10-(-11) M range; beta 1-receptor agonists did not alter QO2, and beta 1-receptor antagonism did not reduce the effect of kinins. These observations indicate that the actions of kinins on IMCD cells are mediated by beta 2-receptors or a distinct subclass. Several observations indicate that kinins reduce QO2 by inhibiting Na+ entry: in the absence of Na+, BK did not reduce QO2; BK inhibition of QO2 was not additive with ouabain, amiloride, atrial natriuretic peptide (ANP), or 8-bromoguanosine 3',5'-cyclic monophosphate and was abolished in the presence of the cation ionophore amphotericin B. Measurements of isotopic Na+ uptake demonstrated that BK reduced the initial rate of Na+ entry by 58%; BK inhibited the amiloride-sensitive component of conductive Na+ uptake. Because ANP inhibits conductive Na+ entry in IMCD cells via stimulation of cGMP accumulation, the effect of BK on cGMP levels was determined. Unlike ANP, BK did not increase cGMP levels, indicating that transport effects of kinins in IMCD are not mediated by cGMP. Thus kinins directly inhibit conductive Na+ entry in IMCD cells at concentrations suggestive of a physiological effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Endothelin, a peptide inhibitor of Na(+)-K(+)-ATPase in intact renaltubular epithelial cells

1989 ◽  
Vol 257 (6) ◽  
pp. C1101-C1107 ◽  
Author(s):  
M. L. Zeidel ◽  
H. R. Brady ◽  
B. C. Kone ◽  
S. R. Gullans ◽  
B. M. Brenner
Keyword(s):  
Initial Rate ◽  
Vascular Endothelial Cells ◽  
Collecting Duct ◽  
Vascular Endothelial ◽  
Na Transport ◽  
Intact Cells ◽  
Medullary Collecting Duct ◽  
Endothelin A ◽  
Potent Vasoconstrictor

Endothelin, a potent vasoconstrictor released by vascular endothelial cells, can induce natriuresis in vivo. These studies examined the regulation of Na+ transport by endothelin in suspensions of rabbit proximal tubule (PT) and inner medullary collecting duct (IMCD) cells. Endothelin reduced oxygen consumption (QO2) by 18 +/- 1% in IMCD cells but did not alter QO2 in PT cells. In IMCD cells, endothelin inhibited QO2 half maximally at approximately 5 x 10(-12) M. Several lines of evidence indicate that endothelin reduces QO2 by inhibiting the Na(+)-K(+)-ATPase. 1) Endothelin gave no further inhibition of QO2 after ouabain and blunted the stimulatory effect of amphotericin B on QO2 (+29 +/- 4% in absence of endothelin, 0 +/- 5% in presence of endothelin; n = 6 preparations, P less than 0.001). 2) Endothelin inhibited ouabain-sensitive 86Rb+ uptake by 46.6 +/- 8.6% at 10 s and by 35.4 +/- 5.3% at 30 s without altering uptake at 60 min. 3) Addition of endothelin to IMCD cells induced a net K+ efflux with an initial rate of 32.2 +/- 4.8 nmol.min-1.mg protein-1, consistent with inhibition of the Na(+)-K(+)-ATPase. In contrast to the response observed in intact cells, in permeabilized IMCD cells endothelin did not inhibit ouabain-sensitive ATPase. Several observations indicated that prostaglandin E2 (PGE2) mediates endothelin inhibition of Na(+)-K(+)-ATPase activity. 1) The response to endothelin was blocked by ibuprofen in assays of QO2, net K+ flux, and 86Rb+ uptake. 2) Endothelin and PGE2 gave equivalent, nonadditive inhibition of ouabain-sensitive 86Rb+ uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidification adaptation in cultured inner medullary collecting duct cells

1993 ◽  
Vol 264 (5) ◽  
pp. F765-F769 ◽  
Author(s):  
R. Mankus ◽  
J. H. Schwartz ◽  
E. A. Alexander
Keyword(s):  
Lucifer Yellow ◽  
Collecting Duct ◽  
C Cells ◽  
Inner Medullary Collecting Duct ◽  
Pump Activity ◽  
Collecting Duct Cells ◽  
Medullary Collecting Duct ◽  
New Protein

Chronic acid feeding stimulates the rat inner medullary collecting duct (IMCD) to increase acid secretion in vivo (acidification adaptation), but the mechanism for this phenomenon is unknown. Our purpose was to determine whether IMCD cells undergo adaptation in vitro and to explore the mechanism of this response. Confluent cultured rat IMCD cells were exposed to incubation media supplemented with 10(-7) M deoxycorticosterone acetate, pH 7.0 [acid incubated (AI)] or 7.7 [control (C)], for 48 h, and cell pH (pHi) was determined using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Resting pHi was 7.46 +/- 0.05 for AI and 7.25 +/- 0.04 for C (P < 0.05). N-ethylmaleimide-sensitive pHi recovery after an acute acid pulse was 0.030 +/- 0.002 for AI and 0.020 +/- 0.002 pH U/min for C (P < 0.05). However, when AI and C cells were incubated with 7 x 10(-6) M cycloheximide, the increment in pHi and enhanced proton pump activity was abolished. In addition, exocytic function, as measured by Lucifer yellow release, was increased significantly in AI cells. In summary, incubation of IMCD cells in acid medium stimulates acidification adaptation by a mechanism dependent on new protein synthesis.

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