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- Brismar, Hjalmar, et al.
(författare)
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beta-Adrenoceptor agonist sensitizes the dopamine-1 receptor in renal tubular cells
- 2002
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772 .- 1365-201X. ; 175:4, s. 333-340
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Tidskriftsartikel (refereegranskat)abstract
- The renal effects of dopamine are mainly mediated via the dopamine-1 receptor (D1 receptor). This receptor is recruited from intracellular compartments to the plasma membrane by dopamine and atrial natriuretic peptide (ANP), via adenylyl cyclase activation. We have studied whether isoproterenol, a beta -adrenoceptor (beta -AR) agonist that may interact with dopamine in the regulation of rat renal Na+, K+ -adenosine triphosphatase (ATPase) activity, can recruit D1 receptors to the plasma membrane. The spatial regulation of D1 receptors was examined using confocal microscopy techniques in LLCPK cells and the functional interaction between dopamine and isoproterenol was examined by studying their effects on Na+, K+ -ATPase activity in microdissected single proximal tubular segments from rat. Isoproterenol was found to translocate the D1 receptors from the interior of the cell towards the plasma membrane. The recruitment of dopamine 1 receptors was found to be cyclic adenosine phosphate (cAMP) dependent, while protein kinase C (PKC) activation was not involved. The functional studies on Na+, K+ -ATPase activity showed that the effect of isoproterenol was abolished by a D1-like receptor antagonist (SCH 23390), and mediated via protein kinase A (PKA) and PKC dependent pathways. The results provide an explanation for the interaction between G protein-coupled receptors. The effects of isoproterenol on Na+, K+ -ATPase activity can be explained by a heterologous recruitment of D1 receptors to the plasma membrane.
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- Brismar, Hjalmar, et al.
(författare)
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Mechanisms by which intrarenal dopamine and ANP interact to regulate sodium metabolism
- 2000
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Ingår i: Clinical and experimental hypertension (1993, Print). - 1064-1963 .- 1525-6006. ; 22:3, s. 303-307
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Tidskriftsartikel (refereegranskat)abstract
- Maintenance of a normal blood pressure requires a precise and fine-tuned regulation of salt metabolism. This is accomplished by a bidirectional regulation of renal tubular sodium transporters by natriuretic and antinatriuretic hormones. Dopamine, produced in the renal proximal tubular cells, plays an important role in this interactive system. Dopamine inhibits the activity of Na+,K(+)ATPase as well as of many important sodium influx pathways in the nephron. These effects of dopamine are particularly pronounced in situation of sodium loading. There is an abundance of evidence suggesting that the natriuretic effects of ANP are to a large extent mediated via renal dopamine 1 like receptors. The renal tubular dopamine 1 like receptors are, under basal conditions, mainly located intracellularly. ANP and its second messenger, cGMP, cause a rapid translocation of the dopamine 1 like receptors to the plasma membrane. This phenomenon may explain how ANP and dopamine act in concert to regulate sodium metabolism Regulation of sodium metabolism and blood pressure is critically dependent on a normal function of the renal dopamine system. Hence, abnormalities in the interaction between dopamine and ANP may predispose to hypertension.
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- Brismar, Hjalmar, et al.
(författare)
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The role of endocytosis in renal dopamine D1 receptor signaling
- 2006
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Ingår i: Pflügers Archiv. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 451:6, s. 793-802
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Tidskriftsartikel (refereegranskat)abstract
- Desensitization of G-protein-coupled receptors (GPCR) includes receptor endocytosis. This phenomenon is suggested, at least for some receptors, to be associated with receptor resensitization. Here, we examined the role of receptor endocytosis for two different GPCR, the dopamine-1 (D1) receptor and the beta 1-adrenoceptor (beta(1)-AR) in renal tissue. The functional role of receptor endocytosis was examined on Na+, K+-ATPase activity in microdissected proximal tubules from rat kidney. The spatial regulation of endogenous D1 receptors and beta(1)-AR was examined by confocal microscopy techniques in LLCPK cells. Phenylarsine oxide (PAO) an endocytosis inhibitor, attenuated isoproterenol-induced decrease in Na+, K+-ATPase activity but had no such effect on dopamine-induced decrease in Na+, K+-ATPase activity. We have previously shown that isoproterenol sensitizes the renal dopamine system, by recruiting silent D1 receptors from the interior of the cell towards the plasma membrane. This effect was attenuated by PAO as well as by cytochalasin D while these substances had no effect on dopamine-induced D1 receptor recruitment. The beta(1)-AR was localized to the plasma membrane in control cells. Isoproterenol induced a rapid internalization of the beta(1)-AR; which was prevented by PAO. The results suggest that endocytosis of beta(1)-AR in renal proximal tubular cells is an important step in signal generation, while endocytosis of proximal tubular D1 receptor is not.
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- Crambert, S, et al.
(författare)
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Prolactin and dopamine 1-like receptor interaction in renal proximal tubular cells
- 2010
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Ingår i: American journal of physiology. Renal physiology. - : American Physiological Society. - 1522-1466 .- 1931-857X. ; 299:1, s. F49-F54
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Tidskriftsartikel (refereegranskat)abstract
- Prolactin is a natriuretic hormone and acts by inhibiting the activity of renal tubular Na+-K+-ATPase activity. These effects require an intact renal dopamine system. Here, we have studied by which mechanism prolactin and dopamine interact in Sprague-Dawley rat renal tissue. Na+-K+-ATPase activity was measured as ouabain-sensitive ATP hydrolysis in microdissected renal proximal tubular segments. Intracellular signaling pathways were studied by a variety of different techniques, including Western blotting using phosphospecific antibodies, immunoprecipitation, and biotinylation assays. We found that dopamine and prolactin regulated Na+-K+-ATPase activity via similar signaling pathways, including protein kinase A, protein kinase C, and phosphoinositide 3-kinase activation. The cross talk between prolactin and dopamine 1-like receptors was explained by a heterologous recruitment of dopamine 1-like receptors to the plasma membrane in renal proximal tubular cells. Prolactin had no effect on Na+-K+-ATPase activity in spontaneously hypertensive rats, a rat strain with a blunted response to dopamine. These results further emphasize the central role of the renal dopamine system in the interactive regulation of renal tubular salt balance.
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