Role of Sodium/Phosphate-Cotransporter in Myocardial Contractile Responses to Inorganic Phosphate

Onwochei, Michael O.

doi:10.1097/00005344-199310000-00018

Cited by 7 publications

(2 citation statements)

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“…RGS11), suggesting that ␣-syntrophin acts as a scaffold for diverse cellular proteins. The Na ϩ /PO 4 Ϫ co-transporter has been previously linked to ␣ 1 -AR function in the heart (36,45,46), and it may prove interesting to examine whether ␣-syntrophin facilitates the co-localization of the Na ϩ /PO 4 Ϫ co-transporter to ␣ 1D -AR. In essence, the ␣ 1D -AR/dystrophin signalosome forms a signaling microdomain to enable efficient functional coupling by maintaining all of the necessary components within close spatial proximity.…”

Section: Discussionmentioning

confidence: 99%

Blood Pressure Is Regulated by an α1D-Adrenergic Receptor/Dystrophin Signalosome

Lyssand

DeFino

Tang

et al. 2008

Journal of Biological Chemistry

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Hypertension is a cardiovascular disease associated with increased plasma catecholamines, overactivation of the sympathetic nervous system, and increased vascular tone and total peripheral resistance. A key regulator of sympathetic nervous system function is the ␣ 1D -adrenergic receptor (AR), which belongs to the adrenergic family of G-protein-coupled receptors (GPCRs). Endogenous catecholamines norepinephrine and epinephrine activate ␣ 1D -ARs on vascular smooth muscle to stimulate vasoconstriction, which increases total peripheral resistance and mean arterial pressure. Indeed, ␣ 1D -AR KO mice display a hypotensive phenotype and are resistant to salt-induced hypertension. Unfortunately, little information exists about how this important GPCR functions because of an inability to obtain functional expression in vitro. Here, we identified the dystrophin proteins, syntrophin, dystrobrevin, and utrophin as essential GPCR-interacting proteins for ␣ 1D -ARs. We found that dystrophins complex with ␣ 1D -AR both in vitro and in vivo to ensure proper functional expression. More importantly, we demonstrate that knock-out of multiple syntrophin isoforms results in the complete loss of ␣ 1D -AR function in mouse aortic smooth muscle cells and abrogation of ␣ 1D -AR-mediated increases in blood pressure. Our findings demonstrate that syntrophin and utrophin associate with ␣ 1D

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Section: Discussionmentioning

confidence: 99%

Blood Pressure Is Regulated by an α1D-Adrenergic Receptor/Dystrophin Signalosome

Lyssand

DeFino

Tang

et al. 2008

Journal of Biological Chemistry

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“…It inhibits herpes virus DNA polymerase (4,7,26,27), influenza virus RNA polymerase (22), and retroviral reverse transcriptase (9,16,25,28). Foscarnet directly inhibits eucaryotic NaPO 4 (17,21,23,29) and NaSO 4 cotransport (1). Foscarnet also alters the number of membrane NaPO 4 cotransporters (19,20).…”

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confidence: 99%

Foscarnet alters antidiuretic hormone-mediated transport

Hoch

Shahmehdi

Louis

et al. 1995

Antimicrob Agents Chemother

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Therapy with foscarnet is associated with acute renal failure. Prior studies have emphasized foscarnet's proximal tubular toxicity, but there have been isolated reports of foscarnet-induced nephrogenic diabetes insipidus. As a phosphate analog, foscarnet is a competitive inhibitor of NaPO 4 cotransport. However, foscarnet's effect on antidiuretic hormone (ADH)-induced transport has not been previously investigated. We studied foscarnet's modulation of transport in the toad urinary bladder. Foscarnet at 10 M to 10 mM did not alter basal water or urea flux. Urea transport induced by a maximal dose of ADH (24 mIU/ml) was inhibited by 0.1 to 5.0 mM foscarnet. In tissues challenged with 0.5 to 1.0 mIU of ADH per ml, 1.0 to 10 mM foscarnet increased water flow but did not alter urea flux. Foscarnet also increased water flow induced by 1.0 to 10 M forskolin. In tissues pretreated with 10 M naproxen, foscarnet did not alter water flow induced by 0.5 to 1.0 mIU of ADH per ml or forskolin. These results indicate that foscarnet stimulates water flow induced by 0.5 to 1.0 mIU of ADH per ml at a site proximal to that of the generation of cyclic AMP and inhibits urea flux induced by a maximal dose of ADH at a separate site. In humans, foscarnet nephrotoxicity is likely not limited to the proximal nephron, but extends to the collecting duct. Patients receiving foscarnet should be closely monitored for disorders of urinary concentration.

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Use of phosphonocarboxylic acids as inhibitors of sodium-phosphate cotransport

Loghman‐Adham

1996

General Pharmacology: The Vascular System

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Role of Sodium/Phosphate-Cotransporter in Myocardial Contractile Responses to Inorganic Phosphate

Cited by 7 publications

References 0 publications

Blood Pressure Is Regulated by an α1D-Adrenergic Receptor/Dystrophin Signalosome

Blood Pressure Is Regulated by an α1D-Adrenergic Receptor/Dystrophin Signalosome

Foscarnet alters antidiuretic hormone-mediated transport

Use of phosphonocarboxylic acids as inhibitors of sodium-phosphate cotransport

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