Dopamine-dependent inhibition of jejunal Na+-K+-ATPase during high-salt diet in young but not in adult rats

1998 ◽  
Vol 275 (6) ◽  
pp. G1317-G1323 ◽  
Author(s):  
M. Augusta Vieira-Coelho ◽  
Vera A. Lucas Teixeira ◽  
Yigael Finkel ◽  
Patricio Soares-Da-Silva ◽  
Alejandro M. Bertorello
Keyword(s):  
Atpase Activity ◽  
Cellular Level ◽  
High Salt ◽  
Catecholamine Level ◽  
Adult Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
Endogenous Dopamine ◽  
Dependent Inhibition ◽  
Old Rats

During high-salt diet endogenous dopamine (DA) reduces jejunal sodium transport in young but not in adult rats. This study was designed to evaluate whether this effect is mediated, at the cellular level, by inhibition of Na+-K+-ATPase activity. Enzyme activity was determined in isolated jejunal cells by the rate of [γ-32P]ATP hydrolysis. Cells were obtained from weanling and adult rats fed either with high- or normal-salt diet. In 20-day-old but not in 40-day-old rats Na+-K+-ATPase activity was significantly reduced during high-salt diet. This inhibition was abolished by a blocker of DA synthesis. The decreased activity was associated with a decreased α1-subunit at the plasma membrane. During high-salt diet there was an increase in DA content in jejunal cells from 20-day-old rats, associated with a parallel decrease in 5-hydroxytryptamine, compared with normal-salt diet. In 40-day-old rats, however, the catecholamine level remained unchanged during high-salt diet. Incubation of isolated jejunal cells with DA resulted in a dose-dependent inhibition of Na+-K+-ATPase activity in 20- but not in 40-day-old rats. We conclude that during high-salt diet, jejunal Na+-K+-ATPase in 20-day-old rats is inhibited, and this effect is likely to be mediated by locally formed DA.

Endogenous dopamine modulates jejunal sodium absorption during high-salt diet in young but not in adult rats

1994 ◽  
Vol 107 (3) ◽  
pp. 675-679 ◽  
Author(s):  
Yigael Finkel ◽  
Ann Christine Eklöf ◽  
Lena Granquist ◽  
Patricio Soares-da-Silva ◽  
Alejandro M Bertorello
Keyword(s):  
High Salt ◽  
Sodium Absorption ◽  
Adult Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
Endogenous Dopamine

High-salt diet upregulates activity and mRNA of renal Na(+)-K(+)-ATPase in Dahl salt-sensitive rats

1993 ◽  
Vol 264 (3) ◽  
pp. F448-F452 ◽  
Author(s):  
A. Nishi ◽  
G. Celsi ◽  
A. Aperia
Keyword(s):  
Atpase Activity ◽  
Proximal Tubule ◽  
Hormonal Regulation ◽  
High Salt ◽  
Dopa Decarboxylase ◽  
Primary Defect ◽  
High Salt Diet ◽  
Salt Diet ◽  
Tubular Cells ◽  
Proximal Tubule Segments

We examined the effect of a high-salt (HS) diet on the regulation of renal cortical Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) in young Dahl salt-sensitive (DS) and salt-resistant (DR) rats. The activity of Na(+)-K(+)-ATPase, determined in permeabilized proximal tubule segments, was similar in DS and DR rats on normal salt (NS) diet. HS diet resulted in a twofold increase in proximal tubule Na(+)-K(+)-ATPase activity in DS rats but not in DR rats. The mRNA abundance, which was also similar in DS and DR rats on NS diet, increased after 2 days on HS diet in both innervated and denervated kidneys from DS rats but had no effect in DR rats. The activity of Na(+)-K(+)-ATPase and the content of alpha 1- and beta-protein in cortical homogenate were similar in DS and DR rats on both NS and HS diets. Treatment with benserazide, an inhibitor of dopa decarboxylase, upregulated proximal tubule Na(+)-K(+)-ATPase activity and increased Na(+)-K(+)-ATPase mRNA in DR rats on HS diet. Taken together, these data indicate that there is a primary defect in the dynamic hormonal regulation of Na(+)-K(+)-ATPase activity in intact tubular cells, which might stimulate Na(+)-K(+)-ATPase transcription.

scholarly journals High Salt Diet During Pregnancy Alters Kidney Renin Granules In The Adult Rats Offspring.

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Nauilo Lima Costa ◽  
Débora Rothstein Ramos ◽  
Karen Lucasechi Lopes ◽  
Luzia Naoko Shinohara Furukawa ◽  
Joel Claudio Heimann
Keyword(s):  
High Salt ◽  
Adult Rats ◽  
High Salt Diet ◽  
Salt Diet

scholarly journals Inhibition of Na-K-ATPase in thick ascending limbs by NO depends on O2− and is diminished by a high-salt diet

2004 ◽  
Vol 287 (2) ◽  
pp. F224-F230 ◽  
Author(s):  
Marisela Varela ◽  
Marcela Herrera ◽  
Jeffrey L. Garvin
Keyword(s):  
Atpase Activity ◽  
Cultured Cells ◽  
Atp Hydrolysis ◽  
Tap Water ◽  
Normal Diet ◽  
High Salt ◽  
Thick Ascending Limb ◽  
High Salt Diet ◽  
Effect Change ◽  
Salt Diet

A high-salt diet enhances nitric oxide (NO)-induced inhibition of transport in the thick ascending limb (THAL). Long exposures to NO inhibit Na-K-ATPase in cultured cells. We hypothesized that NO inhibits THAL Na-K-ATPase after long exposures and a high-salt diet would augment this effect. Rats drank either tap water or 1% NaCl for 7–10 days. Na-K-ATPase activity was assessed by measuring ouabain-sensitive ATP hydrolysis by THAL suspensions. After 2 h, spermine NONOate (SPM; 5 μM) reduced Na-K-ATPase activity from 0.44 ± 0.03 to 0.30 ± 0.04 nmol Pi·μg protein−1·min−1 in THALs from rats on a normal diet ( P < 0.03). Nitroglycerin also reduced Na-K-ATPase activity ( P < 0.04). After 20 min, SPM had no effect (change −0.07 ± 0.05 nmol Pi·μg protein−1·min−1). When rats were fed high salt, SPM did not inhibit Na-K-ATPase after 120 min. To investigate whether ONOO− formed by NO reacting with O2− was involved, we measured O2− production. THALs from rats on normal and high salt produced 35.8 ± 0.3 and 23.7 ± 0.8 nmol O2−·min−1·mg protein−1, respectively ( P < 0.01). Because O2− production differed, we studied the effects of the O2− scavenger tempol. In the presence of 50 μM tempol, SPM did not inhibit Na-K-ATPase after 120 min (0.50 ± 0.05 vs. 0.52 ± 0.07 nmol Pi·μg protein−1·min−1). Propyl gallate, another O2− scavenger, also prevented SPM-induced inhibition of Na-K-ATPase activity. SPM inhibited pump activity in tubules from rats on high salt when O2− levels were increased with xanthine oxidase and hypoxanthine. We concluded that NO inhibits Na-K-ATPase after long exposures when rats are on a normal diet and this inhibition depends on O2−. NO donors do not inhibit Na-K-ATPase in THALs from rats on high salt due to decreased O2− production.

scholarly journals ENaC activity in the cortical collecting duct of HKα1 H+,K+-ATPase knockout mice is uncoupled from Na+ intake

2017 ◽  
Vol 312 (6) ◽  
pp. F1073-F1080 ◽  
Author(s):  
Elena Mironova ◽  
I. Jeanette Lynch ◽  
Jonathan M. Berman ◽  
Michelle L Gumz ◽  
James D. Stockand ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Knockout Mice ◽  
Purinergic Signaling ◽  
Collecting Duct ◽  
High Salt ◽  
Cortical Collecting Duct ◽  
High Salt Diet ◽  
Salt Diet

Modulation of the epithelial Na+ channel (ENaC) activity in the collecting duct (CD) is an important mechanism for normal Na+ homeostasis. ENaC activity is inversely related to dietary Na+ intake, in part due to inhibitory paracrine purinergic regulation. Evidence suggests that H+,K+-ATPase activity in the CD also influences Na+ excretion. We hypothesized that renal H+,K+-ATPases affect Na+ reabsorption by the CD by modulating ENaC activity. ENaC activity in HKα1 H+,K+-ATPase knockout (HKα1−/−) mice was uncoupled from Na+ intake. ENaC activity on a high-Na+ diet was greater in the HKα1−/− mice than in WT mice. Moreover, dietary Na+ content did not modulate ENaC activity in the HKα1−/− mice as it did in WT mice. Purinergic regulation of ENaC was abnormal in HKα1−/− mice. In contrast to WT mice, where urinary [ATP] was proportional to dietary Na+ intake, urinary [ATP] did not increase in response to a high-Na+ diet in the HKα1−/− mice and was significantly lower than in the WT mice. HKα1−/− mice fed a high-Na+ diet had greater Na+ retention than WT mice and had an impaired dipsogenic response. These results suggest an important role for the HKα1 subunit in the regulation of purinergic signaling in the CD. They are also consistent with HKα1-containing H+,K+-ATPases as important components for the proper regulation of Na+ balance and the dipsogenic response to a high-salt diet. Such observations suggest a previously unrecognized element in Na+ regulation in the CD.

11β-Hydroxysteroid dehydrogenase in developing rat intestine

1996 ◽  
Vol 148 (3) ◽  
pp. 561-566 ◽  
Author(s):  
J Pácha ◽  
I Mikšík
Keyword(s):  
Thyroid Hormones ◽  
Large Intestine ◽  
Distal Colon ◽  
Hydroxysteroid Dehydrogenase ◽  
High Salt ◽  
Adult Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
Weanling Rats ◽  
Intestinal Segments

Abstract The enzyme 11β-hydroxysteroid dehydrogenase (11β-OHSD) prevents the binding of corticosterone to mineralocorticoid receptors by reversible conversion of biologically active corticosterone to inactive 11-dehydrocorticosterone. To clarify the relationship between high plasma concentrations of corticosterone during weaning and high activity of intestinal transport pathways that are induced by aldosterone in immature intestine, we have studied the distribution, developmental pattern and regulation of 11 β-OHSD in intestinal segments that possess mineralocorticoid target epithelium. Dehydrogenase activity was already high in the caecum, and the proximal and distal colon on the second postnatal day and altered little until adulthood. In contrast, the activity in the ileum was low during the first two weeks of life, rose more than 5-fold in the next 20 days to attain a peak in 30-day-old rats, and thereafter declined to the values of adult animals. There was no significant reductase activity (conversion of 11-dehydrocorticosterone to corticosterone) in any intestinal segment of young and adult rats. The regulation of intestinal 11β-OHSD by corticosteroids and thyroid hormones was studied in the ileum and distal colon. In weanling rats, adrenalectomy or a high-salt diet decreased 11β-OHSD activities in both intestinal segments whereas dexamethasone administration prevented this decline in adrenalectomized rats and administration of deoxycorticosterone acetate led to a significant increase of intestinal 11β-OHSD activities in rats kept on a high-salt diet. Dexamethasone administration to intact adult rats also stimulated 11 β-OHSD activity in the ileum and distal colon. The changes in thyroid status of weanling rats did not change the 11β-OHSD activities. We conclude that (1) the developmental patterns of 11β-OHSD activity in the small and large intestine are not identical and this discrepancy may facilitate the maturation effect of glucocorticoids in the small intestine and the stimulatory effect of aldosterone in the large intestine and (2) corticosteroids but not thyroid hormones can modulate 11β-OHSD activity in the developing intestine. Journal of Endocrinology (1996) 148, 561–566

463-P: Deterioration of Atherosclerosis via Dysbiosis in ApoE Null Mice Fed with High-Salt Diet

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 463-P
Author(s):  
TOMONORI KIMURA ◽  
YOSHITAKA HASHIMOTO ◽  
TAKAFUMI SENMARU ◽  
EMI USHIGOME ◽  
MASAHIDE HAMAGUCHI ◽  
...  
Keyword(s):  
High Salt ◽  
High Salt Diet ◽  
Salt Diet
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