Alpha and beta adrenergic agonists stimulate water absorption in the rat proximal tubule

Weinman, Edward J.; Sansom, Steven C.; Knight, Thomas F.; Senekjian, H. O.

doi:10.1007/bf01872270

Cited by 41 publications

(25 citation statements)

References 26 publications

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“…6B. PSD-95 expression had no effect on whole cell cAMP accumulation, changing neither the maximal level of cAMP accumulation nor the EC 50 . Whole cell cAMP accumulation produced by the mutant ␤ 1 AR (V477A), also was not significantly different from that produced by the wild-type ␤1 adrenergic receptor.…”

Section: Psd-95 Decreases ␤ 1 -Adrenergic Receptor Internalization Whmentioning

confidence: 87%

“…For example, in the kidney proximal tubule, ␤ 2 AR is known to regulate Na ϩ /H ϩ exchange in a manner opposite that of other G␣ scoupled receptors (49,50), and this unusual regulation is explained at least in part by the ability of ␤ 2 AR to couple to NHERF (36). In cardiac myocytes, ␤ 1 AR and ␤ 2 AR are expressed at comparable levels and induce similar rises in cellular cyclic AMP levels when stimulated, yet they exhibit differential effects on regulation of cellular calcium levels and cell contractility (51,52).…”

Section: Discussionmentioning

confidence: 99%

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β1-Adrenergic Receptor Association with PSD-95

Tang

Miller

et al. 2000

Journal of Biological Chemistry

153

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The ␤ 1 -adrenergic receptor (␤ 1 AR) is the most abundant subtype of ␤-adrenergic receptor in the mammalian brain and is known to potently regulate synaptic plasticity. To search for potential neuronal ␤ 1 AR-interacting proteins, we screened a rat brain cDNA library using the ␤ 1 AR carboxyl terminus (␤ 1 AR-CT) as bait in the yeast two-hybrid system. These screens identified PSD-95, a multiple PDZ domain-containing scaffolding protein, as a specific binding partner of the ␤ 1 AR-CT. This interaction was confirmed by in vitro fusion protein pull-down and blot overlay experiments, which demonstrated that the ␤ 1 AR-CT binds specifically to the third PDZ domain of PSD-95. Furthermore, the full-length ␤ 1 AR associates with PSD-95 in cells, as determined by co-immunoprecipitation experiments and immunofluorescence co-localization studies. The interaction between ␤ 1 AR and PSD-95 is mediated by the last few amino acids of the ␤ 1 AR, and mutation of the ␤-Adrenergic receptors (␤ 1 AR, ␤ 2 AR, and ␤ 3 AR) 1 are heptahelical G-protein-coupled receptors that mediate physiological responses to the hormone epinephrine and the neurotransmitter norepinephrine. ␤ 1 AR and ␤ 3 AR exhibit high affinity for both epinephrine and norepinephrine, whereas ␤ 2 AR binds with high affinity only to epinephrine. The tissue distributions of the three receptors are distinct: ␤ 2 AR is highly expressed in many tissues, ␤ 3 AR is expressed at high levels only in adipose tissue, and ␤ 1 AR is expressed at high levels in the heart and brain and lower levels elsewhere (1). In the brain, ␤ 1 AR exhibits a predominantly neuronal expression pattern, whereas ␤ 2 AR is expressed mainly in glial cells (2-4). ␤ 1 AR is thus considered to be the "synaptic" ␤-adrenergic receptor, because electrophysiological experiments with specific antagonists demonstrate that ␤-adrenergic modulation of hippocampal neuronal activity exhibits a ␤ 1 AR-like pharmacological profile (5-7).Noradrenergic stimulation of synaptic ␤ 1 -adrenergic receptors is known to potently regulate memory formation and synaptic plasticity. Emotionally charged events often lead to the creation of vivid memories (8), and the formation of such emotional memories is due in large part to a surge in noradrenaline release and consequent stimulation of brain ␤-adrenergic receptors (8 -13). The powerful effects of ␤-adrenergic stimulation on memory formation correlate well with electrophysiological experiments demonstrating profound effects of ␤-adrenergic stimulation on the development of long term potentiation (LTP), an enhancement of synaptic responses that underlies some forms of memory (14). In both the hippocampus (15)(16)(17)(18)(19)(20)(21)(22) and the amygdala (23-25), two brain regions known to play key roles in the formation of emotional memories, LTP is markedly enhanced by ␤-adrenergic stimulation. This ␤-adrenergic modulation of LTP is mediated exclusively by ␤ 1 -adrenergic receptors, because hippocampal slices prepared from mice lacking ␤ 1 -adrenergic receptors do not exhibit ...

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Section: Psd-95 Decreases ␤ 1 -Adrenergic Receptor Internalization Whmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

β1-Adrenergic Receptor Association with PSD-95

Tang

Miller

et al. 2000

Journal of Biological Chemistry

153

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“…Proximal tubular cells express α-and -adrenergic receptors, and these substances may be involved in epithelial transport [64]. Isoproterenol, a -adrenergic substance, induces proliferation in cultured proximal tubular cells from two species [65].…”

Section: Adrenergic Substancesmentioning

confidence: 99%

Vasoactive Factors and Tubulointerstitial Injury

Wolf

1999

Kidney Blood Press Res

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Morphological changes of the tubulointerstitial architecture are a major determinant in the progression of chronic renal disease. The evolution of the tubulointerstitial lesion includes early tubular hypertrophy, recruitment of inflammatory cells into the tubulointerstitial space, and proliferation of interstitial fibroblasts resulting in the irreversible changes of tubular atrophy and tubulointerstitial fibrosis. Many of these diverse effects are mediated by autocrine or paracrine release of growth factors, cytokines, and chemokines. Proteinuria, reduction in functional renal mass per se, alterations in tubular fluid reabsorption, and well as hemodynamic changes in the injured kidney may all stimulate local release of such growth factors. A more recent conception is that vasoactive substances, traditionally viewed to be only involved in the regulation of vascular tone, could actually mediate many of these functions of the more 'classical’ growth factors and cytokines. In this regard, one of the most intensively studied vasoactive substances is angiotensin II which has been linked to the progression of renal disease by a host of mechanisms, including the induction of tubular hypertrophy and proliferation of interstitial fibroblasts. There is also increasing evidence that other vasoconstrictive factors such as endothelins and eicosanoids are involved in pathophysiological changes leading eventually to tubulointerstitial fibrosis. On the other hand, natriuretic peptides may exert antifibrogenic properties. Although interference with the renin angiotensin system is currently the only treatment being effective in attenuating the loss of function in patients with chronic renal insufficiency, it is likely that future studies will also investigate the role of other vasoactive substances in the progression of human chronic renal disease.

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“…Besides all these evidences for renal catecholamine production, it is known that the monoamines can affect different nephron segments due to the presence of receptors like DA receptors, α-and β-adrenoceptors [7][8][9]. In addition, mammalian kidney also possesses monoamine oxidase (MAO) and catechol-O-methyl transferase (COMTE) [10], the enzymes responsible for monoamine degradation.…”

Section: Introductionmentioning

confidence: 99%

Catecholamine Production Along the Nephron

Marco

Vio²,

Santos³

et al. 2007

Cell Physiol Biochem

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The present work proposes an extra neural site of catecholamine production along the nephron. LLC-PK₁, MDCK, and mIMCD-3 (proximal and distal tubules and inner medullary collecting duct, respectively) presented the following amine concentrations in the cell homogenates: Norepinephrine = 275±34, 56±16 and 255±21; Epinephrine = 161±20, 83±17 and 53±7; and Dopamine = 63±15, 39±6 and 36±7 pg/mg cell protein (Means ± SEM), respectively. The culture medium showed Norepinephrine = 168±25, 22±3 and 135±8; Epinephrine = 32±6, 152±17 and 39±5; and Dopamine = 27±9, 241±34 and 26±5 pg/mg cell protein, respectively. The synthesis enzymes as tyrosine hydroxylase, dopa decarboxylase and dopamine β-hydroxylase were detected by Western blotting. Biopterin, the enzymatic cofactor of tyrosine hydroxylase, was quantified in the intracellular and medium of mIMCD-3 cells (17±4 and 24±3 nmol/mg cell protein, respectively) and in the medium of MDCK cells (19±4 nmol/mg cell protein). The data confirmed that the proximal tubule is an important source of dopa decarboxilase and Dopamine and epithelial cell along the nephron express the biochemical pathway for catecholamine production.

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Alpha and beta adrenergic agonists stimulate water absorption in the rat proximal tubule

Cited by 41 publications

References 26 publications

β1-Adrenergic Receptor Association with PSD-95

β1-Adrenergic Receptor Association with PSD-95

Vasoactive Factors and Tubulointerstitial Injury

Catecholamine Production Along the Nephron

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