Time course of renal sodium transport in the pregnant rat

Three continuous lines of amphibian epithelial cells form epithelia with a high transepithelial resistance (greater than 4,000 omega . cm2) in culture. The cell lines are TB-M and TB-6c, derived from the urinary bladder of Bufo marinus, and A6, derived from the kidney of Xenopus laevis. Short-circuit current is equivalent to net mucosa-to-serosa sodium transport in two cell lines and slightly exceeds sodium transport in epithelia formed by TB-6c cells. None of the cell lines has an adenylate cyclase response or a transport or permeability response to vasopressin. Water permeability is low in all three cell lines and is not affected by adenosine 3',5–-cyclic monophosphate (cAMP). In the three lines of cells, cAMP and aldosterone each increases short-circuit current with a time course similar to that seen in naturally occurring epithelia. In contrast to the toad urinary bladder and epithelia of line TB-M in which the aldosterone stimulation of short-circuit current is associated with a fall in transepithelial resistance, there is no change in resistance across epithelia of lines TB-6c and A6. There is also a striking difference in the sensitivity of the three lines to inhibition of short-circuit current by amiloride.

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Aldosterone regulation of Na+ transport and Na+-K+-ATPase in A6 cells: role of growth conditions

AJP Cell Physiology ◽

10.1152/ajpcell.1987.252.5.c468 ◽

1987 ◽

Vol 252 (5) ◽

pp. C468-C476 ◽

Cited By ~ 34

Author(s):

M. P. Paccolat ◽

K. Geering ◽

H. P. Gaeggeler ◽

B. C. Rossier

Keyword(s):

Latent Period ◽

Sodium Transport ◽

Time Course ◽

De Novo ◽

Short Circuit ◽

Relative Rate ◽

Beta Subunits ◽

Base Line ◽

De Novo Synthesis ◽

Fourfold Increase

The effects of aldosterone on transepithelial sodium transport (measured by the short-circuit current (SCC) and on Na+-K+-adenosine triphosphatase (ATPase) biogenesis have been studied in A6 kidney cells grown on collagen-coated filters in two different media. In medium A, base-line SCCA was close to zero but transmural electrical resistance (RA) was high. Aldosterone (100 nM, t24h) drastically increased SCCA and RA, but only after a 4-h latent period. In medium B, base-line SCCB and RB were significantly higher than in medium A. Aldosterone significantly enhanced SCCB and to a lesser extent RB after a much shorter latent period (approximately 45 min) than in medium A. In medium A, aldosterone elicited a fourfold increase in the relative rate of synthesis of alpha- and beta-subunits of Na+-K+-ATPase. A twofold increase was already observed within the observed latent period. This time course suggests that de novo synthesis of sodium pumps might be one of the critical factors underlying the increase in sodium transport in this growth medium. In medium B, aldosterone elicited a two- to fourfold increase in the relative rate of synthesis of the alpha- and beta-subunits of Na+-K+-ATPase that paralleled SCCB. Thus de novo synthesis of Na+-K+-ATPase is clearly not a prerequisite for the early mineralocorticoid response (t90 min - t180 min), but still could be part of the late mineralocorticoid response (t3 h - t24 h). In both media, the immunochemical cellular pool of Na+-K+-ATPase was apparently not modulated by aldosterone for up to 48 h of incubation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Sodium transport and the cellular sodium transport pool of colonic epithelium: effects of sodium loading, aldosterone and lithium

Journal of Endocrinology ◽

10.1677/joe.0.1120247 ◽

1987 ◽

Vol 112 (2) ◽

pp. 247-252 ◽

Cited By ~ 3

Author(s):

C. J. Edmonds ◽

J. Mackenzie

Keyword(s):

Epithelial Cells ◽

Sodium Transport ◽

Time Course ◽

Electrical Potential ◽

Electrical Potential Difference ◽

Active Sodium ◽

Prolonged Infusion ◽

Sodium Loading ◽

Sodium Flux

ABSTRACT The cellular sodium transport pool and sodium transepithelial fluxes were investigated in vivo in rat distal colon in relation to sodium loading by intravenous infusion (3·5 h), and to short (4 h) and prolonged (72 h) i.v. administration of aldosterone. Considerable natriuresis and increase in body sodium content were produced by the sodium load but there was no significant effect on the transcellular sodium flux (active absorption from lumen to plasma) or on the sodium transport pool. Both short and prolonged aldosteronism produced similar increases in the transport pool and in the transcellular sodium flux, but the transepithelial electrical potential difference (p.d.) was significantly greater in rats given the prolonged infusion. Addition of amiloride to the solution in the lumen of the colon almost completely abolished the p.d., the transport pool and the transcellular sodium flux of the rats receiving prolonged infusion, but had much less effect in those given the short infusion. The time-course of recovery of p.d. following prolonged aldosteronism was similar to that described for the turnover rate of rat colonic epithelial cells. Lithium within the lumen had no significant effect in untreated rats but after prolonged aldosterone infusion lithium reduced the p.d. and the transcellular sodium flux although the transport pool was not reduced. These findings are consistent with the hypothesis that aldosteronism renders the apical membranes of the epithelial cells permeable to lithium and that intracellular accumulation of lithium depresses active sodium transfer. The observations are interpreted in terms of an epithelial model in which aldosterone induces amiloride-sensitive pathways (diffusion channels permeable to sodium and lithium) in the apical membrane which totally replace the amiloride-insensitive pathways when aldosteronism is prolonged; the resulting expansion of the sodium transport pool is the stimulus for increased active sodium transport across the basolateral membranes. J. Endocr. (1987) 112, 247–252

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A modulatory role of endogenous opioids on prolactin secretion at the end of pregnancy in the rat

Journal of Endocrinology ◽

10.1677/joe.0.1400097 ◽

1994 ◽

Vol 140 (1) ◽

pp. 97-102 ◽

Cited By ~ 17

Author(s):

M Soaje ◽

R P Deis

Keyword(s):

Time Course ◽

Prolactin Secretion ◽

Endogenous Opioids ◽

Opioid Antagonist ◽

Serum Prolactin ◽

Serum Progesterone ◽

Pregnant Rats ◽

Pregnant Rat ◽

Ru 486 ◽

Prolactin Suppression

Abstract It is well known that the fall in serum progesterone concentrations during late pregnancy induces prolactin secretion in rats. On day 19 of pregnancy, administration of 10 mg of the antiprogesterone RU-486/kg induced a small but significant increase in serum prolactin. A lower dose (2 mg/kg) was not effective. Administration of naloxone (2 mg/kg) to pregnant rats on day 19 of pregnancy did not modify circulating prolactin but, after RU-486 treatment, a notable increase in serum prolactin was obtained 30 min after naloxone was given. The lack of effect of naloxone-methobromide in pregnant rats pretreated with RU-486 may indicate that the opioid-induced prolactin suppression acts centrally, most probably at the hypothalamic level. During day 21 of pregnancy, the time-course of prolactin secretion, measured at 0900, 1400, 1900 and 2200 h, was inversely correlated with circulating progesterone levels. At 0900 h, serum prolactin was very low with high serum progesterone concentrations but a significant increase in serum prolactin occurred at 2200 h; this was coincident with a significant decrease in the steroid. The stimulatory effect of naloxone on prolactin secretion was clearly dependent on the circulating progesterone level. Thus, at 1900 h of day 21, naloxone induced a significant increase in serum prolactin but, at 2200 h, the opioid antagonist dramatically enhanced the circulating level of prolactin. The serum prolactin increase induced by naloxone at 1900 h was prevented by the s.c. administration of 5 mg progesterone given 7 h earlier. Similarly, the large increase in serum prolactin levels at 1800 h on day 19 of pregnancy, after administration of RU-486 plus naloxone, was completely abolished by treatment with CB154. The lack of effect of RU-486 and naloxone on serum prolactin levels in virgin rats on the day of pro-oestrus demonstrates that the effect of naloxone on prolactin in pregnant rat is peculiar to the end of pregnancy. In conclusion, the attenuation of the central inhibitory action of progesterone facilitates the release of prolactin which is dramatically enhanced by naloxone treatment. These results provide an important new insight into the existence of a neuromodulatory regulation of prolactin secretion by the opioid system showing a paradoxical opioid-induced prolactin suppression at the end of pregnancy. Journal of Endocrinology (1994) 140, 97–102

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Kinetics of sodium and lithium movements across the blood-brain barrier of an insect

Journal of Experimental Biology ◽

10.1242/jeb.74.1.239 ◽

1978 ◽

Vol 74 (1) ◽

pp. 239-251

Author(s):

P. K. Schofield ◽

J. E. Treherne

Keyword(s):

Blood Brain Barrier ◽

Sodium Transport ◽

Time Course ◽

Brain Barrier ◽

Sodium Ions ◽

Sodium Depletion ◽

Lithium Ions ◽

Initial Exposure ◽

Ion Species ◽

Kinetics Of

The electrical responses of axons were used to monitor the time-course of a change in the concentration of an ion species in the fluid bathing the axons in connectives of isolated cockroach nerve cords. Initial exposure of the connectives to sodium-deficient Ringer resulted in a depletion of extra-axonal sodium which was much slower than the restoration observed on return of the sodium Ringer. It is suggested that this asymmetry could result from a sodium reservoir which delays the initial decline. Subsequent net inward and outward movements of sodium ions were rapid and symmetrical. Unlike sodium ions, lithium ions were apparently unable to reach the axon surfaces following sodium depletion. In view of the similar properties of sodium and lithium ions in many biological systems it is therefore unlikely that the sodium movements were passive. Instead, the results support the idea of net sodium transport by the perineurial and/or glial elements.

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Regulation of protein phosphorylation and sodium transport in toad bladder.

The Journal of General Physiology ◽

10.1085/jgp.65.2.153 ◽

1975 ◽

Vol 65 (2) ◽

pp. 153-177 ◽

Cited By ~ 54

Author(s):

K G Walton ◽

R J DeLorenzo ◽

P F Curran ◽

P Greengard

Keyword(s):

Molecular Weight ◽

Sodium Transport ◽

Time Course ◽

Polyacrylamide Gel Electrophoresis ◽

Apparent Molecular Weight ◽

Specific Protein ◽

Toad Bladder ◽

Active Sodium ◽

Bladder Epithelium ◽

Osmotic Water

It is well established that active sodium-ion transport and water flow across isolated toad bladder are increased by antidiuretic hormone (ADH) and by cAMP. These agents were also observed in previous studies to cause changes in the amount of radioactive phosphate in a specific protein in the toad bladder. This protein, found by SDS-polyacrylamide gel electrophoresis of toad bladder epithelial preparations, had an apparent molecular weight of 49,000 daltons. In the present study, a correlation was found between the ability of a variety of substances to affect the amount of radioactive phosphate in this 40,000-dalton protein and their ability to alter the rate of sodium transport. Thus several agents (ADH, cAMP, theophylline, adenine, prostaglandin E1, and Mn Cl-2) caused a decrease in the amount of radioactive phosphate in the 49,000-dalton protein and also stimulated active sodium transport across the bladder. Conversely, ZnCl-2 produced an increase in the amount of radioactive phosphate in this protein and an inhibition of sodium transport. With each of these agents, the time-course of change in phosphorylation of this protein was, in general, similar to that for sodium transport. A second phosphoprotein, with an apparent molecular weight of about 42,000 daltons, showed changes in parallel with, but less extensive than, those observed in the 49,000 dalton protein. There was no consistent relationship between changes in level of phosphorylation of either in the 49,000- or 42,000- dalton protein and changes in osmotic water permeability. The results are compatible with the possibility that regulation by ADH and by cAMP of sodium transport in the toad bladder epithelium may be mediated through regulation of the amount of phosphate in a specific protein.

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PROGESTERONE AND 20α-HYDROXYSTEROID-DEHYDROGENASE REGULATION IN THE CORPUS LUTEUM OF THE PREGNANT RAT

Acta Endocrinologica ◽

10.1530/acta.0.0900176 ◽

1979 ◽

Vol 90 (1) ◽

pp. 176-184 ◽

Cited By ~ 4

Author(s):

K. Loewit ◽

N. Zambelis

Keyword(s):

Wistar Rats ◽

Time Course ◽

Hydroxysteroid Dehydrogenase ◽

Mechanisms Of Action ◽

Corpora Lutea ◽

Pregnant Rat ◽

Female Wistar Rats ◽

Series Of Experiments ◽

Complex Regulation

ABSTRACT Female Wistar rats were mated and passively immunized against bovine luteinizing hormone (bLH) between days 7–12 of gestation. In a first series of experiments the effect of simultaneous progesterone treatment on the histochemically detectable activity of 20α-hydroxysteroiddehydrogenase (20α-OHSD) in the corpora lutea of pregnancy was evaluated. In other experiments the exact time course was established between the first histologically demonstrable signs of termination of pregnancy and the appearance of 20α-OHSD activity in corpora lutea of pregnancy. It was found that progesterone substitution not only prevented the deleterious effects of the anti-bLH-serum on gestation but also the re-appearance of 20α-OHSD activity in the corpora lutea of pregnancy up to day 12 of pregnancy. Moreover in animals injected with anti-bLH-serum from day 7 on and sacrificed on days 8–2, signs of foetal destruction clearly preceded the pathological re-appearance of 20α-OHSD activity by 2–3 days. These results support previous findings on a direct or indirect role of progesterone in the complex regulation of 20α-OHSD activity. Possible mechanisms of action are discussed.

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Epithelial organization and hormone sensitivity of toad urinary bladder cells in culture

AJP Renal Physiology ◽

10.1152/ajprenal.1981.241.2.f129 ◽

1981 ◽

Vol 241 (2) ◽

pp. F129-F138 ◽

Cited By ~ 1

Author(s):

J. P. Johnson ◽

R. E. Steele ◽

F. M. Perkins ◽

J. B. Wade ◽

A. S. Preston ◽

...

Keyword(s):

Urinary Bladder ◽

Cell Line ◽

Cell Lines ◽

Water Permeability ◽

Sodium Transport ◽

Time Course ◽

Cultured Cells ◽

Transepithelial Transport ◽

Seeding Density ◽

Toad Urinary Bladder

Two continuous cell lines (TB-M and TB-6c) derived from epithelial cells of the toad urinary bladder form epithelia in culture that manifest hormone-sensitive transepithelial transport. Development of transepithelial electrical resistance (R) and transport rate (ISC) are dependent on time and density of cells seeded, but steady-state ISC and R are characteristic for each cell line and independent of seeding density. Some responses of intact toad bladder are preserved in culture, whereas others are altered or absent. Neither cell line responds to vasopressin. Analogues of cAMP increase sodium transport and urea permeability in both cell lines but do not affect water permeability. The intramembrane particle aggregates associated with the vasopressin- and cAMP-induced increase in water permeability of the intact bladder could not be detected in the cell lines. Aldosterone increases sodium transport in both cell lines, and the time course and concentration dependence of the response to aldosterone are similar to those of the intact bladder. The relative effect of a series of steroids on ISC reveals corticosterone to be a more potent mineralocorticoid in cultured cells than in the intact bladder.

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Effect of aldosterone on potassium transport in the toad bladder

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.229.1.99 ◽

1975 ◽

Vol 229 (1) ◽

pp. 99-106 ◽

Cited By ~ 7

Author(s):

HJ Rodriguez ◽

WP Wiesmann ◽

S Klahr

Keyword(s):

Latent Period ◽

Sodium Transport ◽

Time Course ◽

Rna Synthesis ◽

Actinomycin D ◽

Potassium Transport ◽

Potassium Uptake ◽

Toad Bladder ◽

Potassium Influx

The effect of aldosterone on potassium uptake by the toad bladder is described. The hormone stimulated the uptake of potassium across the serosal border of the bladder. The increased uptake was the consequence of an increase in the rate of potassium influx. An effect on potassium uptake was characterized by a latent period of approximately 60 min; it was evident for periods as long as 5 h, and it was abolished by addition of actinomycin D. The time course of the aldosterone effect on potassium closely resembled the effect of the hormone on sodium transport. It is suggested that aldosterone influences potassium transport in the toad bladder via DNA-dependent RNA synthesis. In addition, it is suggested that the effect of the hormone on potassium and sodium may be in some way related.

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Adrenergic influences on uterine smooth muscle

Philosophical Transactions of the Royal Society of London Series B Biological Sciences ◽

10.1098/rstb.1973.0016 ◽

1973 ◽

Vol 265 (867) ◽

pp. 135-148 ◽

Cited By ~ 63

Keyword(s):

Cyclic Amp ◽

Time Course ◽

Calcium Content ◽

Bathing Solution ◽

Methoxy Derivative ◽

Membrane Hyperpolarization ◽

Pregnant Rat ◽

Calcium Dependent ◽

Electrogenic Sodium Pump ◽

Tissue Calcium

1. The mechanism of β adrenergic inhibition of pregnant rat myometrium was investigated. 2. Isoproterenol (4 x 10 -7 mol/l) caused membrane hyperpolarization of about 12 mV . The magnitude of this hyperpolarization was unaffected by K-free and Cl-free (isethionate substitution) solutions, and was reduced by about 50 % in the presence of ouabain (10 -3 mol/1) and at 10 °C. Hyperpolarization was calcium -dependent, was partially reduced by 12.5 mmol/1 [Ca 2+ ]0 and was abolished when 2.0 mmol/1 La was added to the bathing solution. 3. Isoproterenol (4 x 10 -7 mol/1) increased tissue cyclic AMP levels with a time course paralleling that of the relaxation both at 37 and at 10 °C. Papaverine (10 -4 mol/1) also showed similar actions. 4. Tissue calcium content as measured by the lanthanum technique increased during a K induced contracture and decreased when isoproterenol (4 x 10 -7 mol/1), papaverine (10 -4 mol/1), or dibutyryl cyclic AMP (10 -3 mol/1) relaxed the K contracture. 5. Another relaxant, D-600, a methoxy derivative of verapamil, (10-5 mol/1) had no effect on membrane polarization, tissue cyclic AMP or tissue calcium content. 6. It is concluded that there is an active component to the β adrenergic hyperpolarization of the rat myometium, although an electrogenic sodium pump is not likely to be involved. Rather an electrogenic calcium pump, possibly activated by cyclic AMP, is consistent with the data obtained. Moreover, a mechanism in which cyclic AMP stimulates calcium extrusion may underlie the adrenergically mediated relaxation in the myometrium .

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