Proximal tubule Na+-K+-ATPase activity is inhibited during high-salt diet: evidence for DA-mediated effect

Bertorello, A. M.; Hökfelt, T; Goldstein, M. B.; Aperia, Anita

doi:10.1152/ajprenal.1988.254.6.f795

Cited by 84 publications

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“…The basal activity of Na ϩ ,K ϩ -ATPase was not different between rats on either NS or HS intake, and although this finding agrees with 1 report, 31 it differs from other published reports in which the authors found a decrease in basal Na ϩ ,K ϩ -ATPase activity in rats placed on an HS intake. 32 However, it should be noted that Bertorello et al 32 observed a decrease in basal Na ϩ ,K ϩ -ATPase activity in rats after 10 days of HS intake, whereas in the present study, we conducted our measurements after 24 hour of HS intake. It is likely that the exposure to HS intake needs to be of longer duration before changes in basal Na ϩ ,K ϩ -ATPase activity in rats can be observed.…”

Section: Discussionmentioning

confidence: 58%

Aging, High Salt Intake, and Renal Dopaminergic Activity in Fischer 344 Rats

et al. 1999

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Abstract-The present study examined renal dopaminergic activity and its response to high salt (HS) intake in adult (6-month-old) and old (24-month-old) Fischer 344 rats. Daily urinary excretion of L-3,4-dihydroxyphenylalanine (L-DOPA), dopamine, and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid was similar in adult and old rats; by contrast, daily urinary excretion of norepinephrine in old rats was almost twice that in adult animals. HS intake (1% NaCl) over a period of 24 hours resulted in a 2-fold increase in the urinary excretion of dopamine, DOPAC, and norepinephrine in adult animals but not in old animals. Norepinephrine and L-DOPA plasma levels did not change during HS intake and were similar in both groups of rats. The natriuretic response to an HS intake in old rats (from 4.7Ϯ0.4 to 10.) was less than in adult rats (from 5.2Ϯ0.4 to 13.5Ϯ2.5 nmol ⅐ kg. A diuretic response to HS intake was observed in adult rats (from 20.9Ϯ2.3 to 37.6Ϯ2.8 mL ⅐ kg Ϫ1 ⅐ d Ϫ1 ) but not in old rats (from 37.7Ϯ5.7 to 42.3Ϯ6.0 mL ⅐ kg). Dopamine levels and dopamine/L-DOPA ratios in the renal cortex of old rats were greater than in adult rats. HS intake increased both dopamine levels and dopamine/L-DOPA ratios in the renal cortex of adult rats but not in old rats. Aromatic L-amino acid decarboxylase activity was higher in old rats than in adult rats; HS intake increased L-amino acid decarboxylase activity (nmol ⅐ mg protein Ϫ1 ⅐ l5 min Ϫ1 ) in adult rats (from 67Ϯ1 to 93Ϯ1) but not in old rats (from 86Ϯ2 to 87Ϯ2). Dopamine inhibited Na ϩ ,K ϩ -ATPase activity in proximal tubules obtained from adult rats, but it failed to exert such an inhibitory effect in old rats. It is concluded that renal dopaminergic tonus in old rats is higher than in adult rats but fails to respond to HS intake as observed in adult rats. This may be due in part to the inability of dopamine to inhibit Na ϩ ,K ϩ -ATPase activity in old rats. (Hypertension. 1999;34:666-672.)

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Section: Discussionmentioning

confidence: 58%

Aging, High Salt Intake, and Renal Dopaminergic Activity in Fischer 344 Rats

et al. 1999

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“…The results presented here show that a substantial amount of newly-formed dopamine is deaminated to DOPAC; this occurs largely in the renal cortex where saturation of deamination of dopamine could be observed, but also to some extent in the medulla and this difference may be related to the limited production of dopamine in the rat renal medulla. Alternatively, it could be hypothesized that in the rat renal medulla the specific activity of MAO may exceed that in the renal cortex, as has been found to occur in the kidney of the cat (Caramona & Soares-daSilva, 1990 In recent years, several lines of evidence have suggested that dopamine may exert considerable effects within the kidney and contribute actively in the maintenance of blood pressure at levels considered as acceptable (Lee, 1982;Yoshimura & Takahashi, 1988;Bertorello et al, 1988). The activation of -I type D1 dopamine receptors in the renal vasculature produced vasodilatation resulting in increased renal blood flow and glomerular filtration rate (Felder et al, 1988).…”

Section: Discussionmentioning

confidence: 97%

Deamination of newly‐formed dopamine in rat renal tissues

Fernandes

Pestana

Soares-da-Silva

1991

British J Pharmacology

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1 The present study has examined the formation of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) in slices of the rat renal cortex and the renal medulla loaded with exogenous L-fl-3,4-dihydroxyphenylalanine (L-DOPA). The effects of pargyline and of two selective inhibitors of monoamine oxidase (MAO) types A and B, respectively Ro 41-1049 and Ro 19-6327, on the deamination of newlysynthesized dopamine in kidney slices incubated with exogenous L-DOPA were also tested. The assay of L-DOPA, dopamine, noradrenaline and DOPAC was performed by means of h.p.l.c. with electrochemical detection. 2 Incubation of renal slices with exogenous L-DOPA resulted in a concentration-dependent accumulation of dopamine and DOPAC; the tissue levels of newly-formed dopamine and DOPAC in slices of the renal medulla were 6-8% of those in cortical slices. 3 Pargyline (0.1 mM) produced a marked decrease (84% reduction) in the formation of DOPAC in kidney slices loaded with 1.0mM L-DOPA; this effect was accompanied by a 17% increase in the accumulation of dopamine. Similar effects were obtained at higher concentrations of pargyline (0.5 and 1.0mM). At 5.0 and 10.0mm pargyline, a marked decrease (46 and 76% reduction) in the accumulation of newlyformed dopamine was observed. 4 The accumulation of dopamine and DOPAC was found to be time-dependent in experiments in which tissues were incubated with 5 and 1IOPM L-DOPA for 5, 10, 20 and 30min. Pargyline (0.1 mM) produced an increase in the accumulation of dopamine at all incubation periods and decreased the formation of DOPAC. 5Ro 41-1049 (50, 100 and 250 nM) was found to produce a concentration-dependent increase of newlyformed dopamine (16-66% increase) and reduced DOPAC formation (44-89% reduction). Ro 19-6327 (50, 100 and 250nM), was found not to affect the accumulation of newly-formed dopamine, but significantly reduced the formation of DOPAC. 6 It is concluded that deamination of newly-formed dopamine in kidney slices loaded with L-DOPA constitutes an important mechanism of amine inactivation. The results presented also suggest that most of the MAO, located inside the compartment where the synthesis of dopamine occurs, is of the A type.

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“…Whereas the local actions of dopamine within proximal tubule cells have been described with some detail in the last few years, the factors that trigger the peripheral dopaminergic response still remained to be identified. A large increase in the content of sodium within the diet is directly related to the natriuretic response, and in vivo experiments have shown that dopamine does not inhibit proximal tubule sodium reabsorption unless there is a sodium load (33)(34)(35)(36). Because the dopaminergic response is initiated by synthesis of dopamine by the proximal tubule cells and the translocation of dopamine receptors from cytosolic storage compartments to the plasma membrane (37), there must be an intracellular mechanism that senses the presence of the sodium load.…”

Section: Discussionmentioning

confidence: 99%

Agonist-dependent Regulation of Renal Na+, K+-ATPase Activity Is Modulated by Intracellular Sodium Concentration

Efendiev

Bertorello

Zandomeni

et al. 2002

Journal of Biological Chemistry

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We tested the hypothesis that the level of intracellular sodium modulates the hormonal regulation of the Na ؉ ,K ؉ -ATPase activity in proximal tubule cells. By using digital imaging fluorescence microscopy of a sodium-sensitive dye, we determined that the sodium ionophore monensin induced a dose-specific increase of intracellular sodium. A correspondence between the elevation of intracellular sodium and the level of dopamine-induced inhibition of Na ؉ ,K ؉ -ATPase activity was determined. At basal intracellular sodium concentration, stimulation of cellular protein kinase C by phorbol 12-myristate 13-acetate (PMA) promoted a significant increase in Na ؉ ,K ؉ -ATPase activity; however, this activation was gradually reduced as the concentration of intracellular sodium was increased to become a significant inhibition at concentrations of intracellular sodium higher than 16 mM. Under these conditions, PMA and dopamine share the same signaling pathway to inhibit the Na ؉ ,K ؉ -ATPase. The effects of PMA and dopamine on the Na ؉ ,K ؉ -ATPase activity and the modulation of these effects by different intracellular sodium concentrations were not modified when extracellular and intracellular calcium were almost eliminated. These results suggest that the level of intracellular sodium modulates whether hormones stimulate, inhibit, or have no effect on the Na ؉ ,K ؉ -ATPase activity leading to a tight control of sodium reabsorption.

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Proximal tubule Na+-K+-ATPase activity is inhibited during high-salt diet: evidence for DA-mediated effect

Cited by 84 publications

References 0 publications

Aging, High Salt Intake, and Renal Dopaminergic Activity in Fischer 344 Rats

Aging, High Salt Intake, and Renal Dopaminergic Activity in Fischer 344 Rats

Deamination of newly‐formed dopamine in rat renal tissues

Agonist-dependent Regulation of Renal Na+, K+-ATPase Activity Is Modulated by Intracellular Sodium Concentration

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