Antagonistic actions of renal dopamine and 5‐ hydroxytryptamine: increase in Na+, K+‐ATPase activity in renal proximal tubules via activation of 5‐HT1A receptors

Soares‐da‐Silva, Patrício; Pinto-do-Ó, Perpétua; Bertorello, Alejandro M.

doi:10.1111/j.1476-5381.1996.tb16716.x

Cited by 22 publications

(12 citation statements)

References 25 publications

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“…Hence, for the purpose of this investigation, it seems most important to obtain a satisfactory MAO-A inhibition. It has been reported that 5-hydroxytryptamine (5-HT) is formed endogenously in proximal tubular cells [16] and exerts antinatriuretic effects via 5-HT 1A receptors by increasing the activity of Na + ,K + -ATPase [28]. In contrast to COMT, MAO also metabolizes 5-HT.…”

Section: Discussionmentioning

confidence: 99%

The role of dopamine-metabolizing enzymes in the regulation of renal sodium excretion in the rat

Odlind

Reenilä

Männistö

et al. 2001

Pfl�gers Archiv European Journal of Physiology

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The intrarenal natriuretic hormone dopamine (DA) is metabolized by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). We have previously shown that inhibition of COMT by entacapone results in a potent D1-like receptor-mediated natriuretic response. The present study was performed using anaesthetized rats to compare the importance of MAO and COMT in DA-mediated natriuresis by use of the MAO inhibitor phenelzine. Urinary sodium and DA excretion remained unchanged after MAO inhibition, while excretion of the main metabolite dihydroxyphenylacetic acid (DOPAC) decreased by 55%. The response was unaltered if 5-hydroxytryptamine receptors (5-HT1A) were blocked during MAO inhibition. We also investigated the specific renal activities of MAO and COMT in rat renal cortex during DA-influenced natriuresis. Specific COMT activity in the renal cortex was reduced by 13% after isotonic sodium loading (5% of body mass) whereas renal MAO-A and MAO-B activities remained unaltered. Furthermore, preliminary data obtained from spontaneously hypertensive rats, whose basal urinary DA excretion is higher than that of normotensive Wistar-Kyoto rats, show a tendency for renal COMT activity to be lower. It is concluded that MAOinhibition by phenelzine does not alter sodium excretion. Furthermore, specific renal cortical COMT activity is reduced during partly D1-like receptor-mediated natriuresis, whereas MAO activity remains unchanged. The results suggest that MAO is less important than COMT in regulating DA-mediated natriuresis in the rat kidney.

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Section: Discussionmentioning

confidence: 99%

The role of dopamine-metabolizing enzymes in the regulation of renal sodium excretion in the rat

Odlind

Reenilä

Männistö

et al. 2001

Pfl�gers Archiv European Journal of Physiology

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“…Since the energy for tubular sodium reabsorption is supplied by the Na + ,K + ‐ATPase, it might then be suggested that stimulation of tubular sodium absorption by serotonin would involve activation of the Na + ,K + ‐ATPase. Indeed, Soares da Silva et al . (1996b) demonstrated that stimulation of serotonin receptors with the specific agonist 8‐hydroxy‐2‐(di‐n‐propylamino) tetraline (8‐OH‐DPAT) induced an augmentation of Na + ,K + ‐ATPase activity.…”

Section: Introductionmentioning

confidence: 99%

“…It has been suggested that the interplay between the antagonistic actions of the natriuretic dopamine and the anti‐natriuretic serotonin plays a major role in renal sodium and water excretion (Soares da Silva et al ., 1996b; Vieira‐Coelho et al ., 1997). Both amines modulate urinary sodium excretion without affecting renal haemodynamics (Itskowitz et al ., 1988; Li Kam Wa et al ., 1996; Siragy et al ., 1989).…”

Section: Introductionmentioning

confidence: 99%

Hormonal‐dependent recruitment of Na⁺,K⁺‐ATPase to the plasmalemma is mediated by PKC_β and modulated by [Na⁺]_i

Budu

Efendiev

Cinelli

et al. 2002

British J Pharmacology

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The present study demonstrates that stimulation of hormonal receptors of proximal tubule cells with the serotonin‐agonist 8‐hydroxy‐2‐(di‐n‐propylamino) tetraline (8‐OH‐DPAT) induces an augmentation of Na+,K+‐ATPase activity that results from the recruitment of enzyme molecules to the plasmalemma. Cells expressing the rodent wild‐type Na+,K+‐ATPase α‐subunit had the same basal Na+,K+‐ATPase activity as cells expressing the α‐subunit S11A or S18A mutants, but stimulation of Na+,K+‐ATPase activity was completely abolished in either mutant. 8‐OH‐DPAT treatment of OK cells led to PKCβ‐dependent phosphorylation of the α‐subunit Ser‐11 and Ser‐18 residues, and determination of enzyme activity with the S11A and S18A mutants indicated that both residues are essential for the agonist‐dependent stimulation of Na+,K+‐ATPase activity. When cells were treated with both dopamine and 8‐OH‐DPAT, an activation of Na+,K+‐ATPase was observed at basal intracellular sodium concentration (∼9 mM), and this activation was gradually reduced and became a significant inhibition as the concentration of intracellular sodium gradually increased from 9 to 19 mM. Thus, besides the antagonistic effects of dopamine and 8‐OH‐DPAT, intracellular sodium modulates whether an activation or an inhibition of Na+,K+‐ATPase is produced. British Journal of Pharmacology (2002) 137, 1380–1386. doi:

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“…Tissue DreDaration PCT fragments were prepared as described before (13). Tissue DreDaration PCT fragments were prepared as described before (13).…”

Section: Introductionmentioning

confidence: 99%

Short-Term vs. Sustained Inhibition of Proximal Tubule Na, K-ATPase Activity by Dopamine: Cellular Mechanisms

Pinto-do-O

Chibalin

Katz

et al. 1997

Clinical and Experimental Hypertension

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Dopamine (DA) produces a natriuresis attributed in part to inhibition of Na,K-ATPase activity (NKA) in the proximal tubule (PCT), and impairment in this inhibition has been linked to several forms of hypertension in animals. Here we examined whether the intracellular signaling mechanisms involved are the same in the early and late phases of this phenomenon. DA (1 microM) inhibited NKA similarly after 15 min (by 38%) or 180 min (by 36%) incubation, taken to represent short-term (ST) and sustained (Sd) pump regulation, respectively. Calphostin C, a specific inhibitor of protein kinase C (PKC), completely blocked the ST action of DA on NKA, whereas IP20, a specific inhibitor of protein kinase (PKA), had no effect. In contrast, IP20 completely abolished the Sd (180 min) inhibition by DA, whereas calphostin C had only a partial or variable effect. The DA-1 agonist fenoldopam (which does not activate PKC but increases cAMP) alone failed to inhibit the pump at 180 min (as it does also in the short-term in PCT), suggesting that ST inhibition is required for the Sd effect to occur. Furthermore, PTH1-34, a known ST inhibitor of NKA suppressed the pump at 180 min (by 46%), but unlike in the short-term, this effect was completely prevented by IP20. In contrast, PTH3-34, which does not stimulate adenylyl cyclase or activate PKA, caused only a small (19%) and variable Sd inhibition. In conclusion, short-term inhibition of the PCT pump by dopamine is mediated via PKC, whereas the sustained inhibition requires the PKA pathway in addition to the ongoing PKC-mediated effect.

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Antagonistic actions of renal dopamine and 5‐ hydroxytryptamine: increase in Na⁺, K⁺‐ATPase activity in renal proximal tubules via activation of 5‐HT_1A receptors

Cited by 22 publications

References 25 publications

The role of dopamine-metabolizing enzymes in the regulation of renal sodium excretion in the rat

The role of dopamine-metabolizing enzymes in the regulation of renal sodium excretion in the rat

Hormonal‐dependent recruitment of Na⁺,K⁺‐ATPase to the plasmalemma is mediated by PKC_β and modulated by [Na⁺]_i

Short-Term vs. Sustained Inhibition of Proximal Tubule Na, K-ATPase Activity by Dopamine: Cellular Mechanisms

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Antagonistic actions of renal dopamine and 5‐ hydroxytryptamine: increase in Na+, K+‐ATPase activity in renal proximal tubules via activation of 5‐HT1A receptors

Cited by 22 publications

References 25 publications

The role of dopamine-metabolizing enzymes in the regulation of renal sodium excretion in the rat

The role of dopamine-metabolizing enzymes in the regulation of renal sodium excretion in the rat

Hormonal‐dependent recruitment of Na+,K+‐ATPase to the plasmalemma is mediated by PKCβ and modulated by [Na+]i

Short-Term vs. Sustained Inhibition of Proximal Tubule Na, K-ATPase Activity by Dopamine: Cellular Mechanisms

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Antagonistic actions of renal dopamine and 5‐ hydroxytryptamine: increase in Na⁺, K⁺‐ATPase activity in renal proximal tubules via activation of 5‐HT_1A receptors

Hormonal‐dependent recruitment of Na⁺,K⁺‐ATPase to the plasmalemma is mediated by PKC_β and modulated by [Na⁺]_i