Increased renal atrial natriuretic peptide synthesis in rats with deoxycorticosterone acetate-salt treatment

Lee, Y. J.; Shin, Shyi–Jang; Tan, Mian‐Shin; Hsieh, Tusty‐Jiuan; Tsai, Juei-Hsiung

doi:10.1152/ajprenal.1996.271.4.f779

Cited by 21 publications

(30 citation statements)

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“…This method has proved to be reliable for comparing the changes of a gene product in relatively low abundance. Our previous reports demonstrated that renal ANP mRNA is significantly enhanced and the elevation of urinary ANP excretion correlated well with urinary sodium excretion in diabetic rats (Shin et al 1997) and deoxycorticosterone acetate (DOCA)-treated rats (Lee et al 1996). These findings support the proposal that renal-synthesized natriuretic peptide may be related to the change in water-electrolyte balance (Greenwald et al 1991).…”

Section: Discussionsupporting

confidence: 68%

“…To determine the relative changes in tissue CNP mRNA expression, the yield of CNP PCR products was normalized to the amount of -actin cDNA amplified from the tissue samples. This method has been used in several studies (Lee et al 1996, Shin et al 1997. Experiments were designed to determine the accuracy of the semi-quantitative RT-PCR.…”

Section: Resultsmentioning

confidence: 99%

“…Using RT-PCR followed by Southern blot analysis, we compared the relative amount of CNP mRNA expression in the renal tissues, a method used in our previous reports (Lee et al 1996, Shin et al 1997. This method has proved to be reliable for comparing the changes of a gene product in relatively low abundance.…”

Section: Discussionmentioning

confidence: 99%

“…Radioimmunoassay CNP-like immunoreactivities (ir-CNP) from samples of plasma and urine were determined by a radioimmunoassay (RIA, Peninsula Laboratories, Inc., Belmont, CA, USA) after extraction as previously described (Lee et al 1996). Briefly, 2 ml plasma or 5 ml urine were passed through Sep-Pack C 18 cartridges (Waters Associates, Milford, MA, USA) and eluted with 5 ml 60% acetonitrile (ACN) containing 0·1% trifluoracetic acid (TFA).…”

Section: Nc (N=8)mentioning

confidence: 99%

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Increased C-type natriuretic peptide mRNA expression in the kidney of diabetic rats

Shin

Wen²,

Yj³

et al. 1998

Journal of Endocrinology

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To investigate the responsiveness of renal-synthesized C-type natriuretic peptide (CNP) to changes in water and electrolyte balance, we measured renal CNP mRNA levels, plasma CNP concentrations and urinary CNP excretion rates in streptozotocin-induced diabetic rats eating a normal (0·26% NaCl) or low (0·04% NaCl) salt diet. Using reverse transcription-PCR followed by Southern blot analysis, we found that renal cortical and medullary CNP mRNA levels were markedly enhanced in diabetic rats from the 14th day and remained enhanced with an accompanying elevation of urinary CNP excretion rates for the entire 60-day study period. All increases of renal CNP mRNA and urinary CNP excretion rates in diabetic rats were attenuated in low salt diet-treated diabetic rats as well as insulin-treated diabetic rats. These results demonstrate that renal CNP synthesis is enhanced in diabetic rats and the increase of renal CNP mRNA is ameliorated by salt restriction and insulin treatment. These results imply that renal-synthesized CNP is responsive to the alteration of water and electrolyte homeostasis in diabetic rats.

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Section: Discussionsupporting

confidence: 68%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Nc (N=8)mentioning

confidence: 99%

See 2 more Smart Citations

Increased C-type natriuretic peptide mRNA expression in the kidney of diabetic rats

Shin

Wen²,

Yj³

et al. 1998

Journal of Endocrinology

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“…Urine was collected for the final 2 hours for measurement of volume, sodium, cyclic GMP (cyclic GMP RIA kit; PerkinElmer), and immunoreactive urodilatin (urodilatin RIA kit; Phoenix Pharmaceuticals Inc.). More than 99% of natriuretic peptide immunoreactivity in the urine reflects urodilatin (66). The inner medullas of paired kidneys were isolated for the measurements of Sgk1, NPR-A, urodilatin, αENaC, β-tubulin, and GAPDH mRNAs and/or proteins.…”

Section: Figure 11mentioning

confidence: 99%

Tonicity-dependent induction of Sgk1 expression has a potential role in dehydration-induced natriuresis in rodents

Chen¹,

Grigsby²,

Law³

et al. 2009

J. Clin. Invest.

199

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In various mammalian species, including humans, water restriction leads to an acute increase in urinary sodium excretion. This process, known as dehydration natriuresis, helps prevent further accentuation of hypernatremia and the accompanying rise in extracellular tonicity. Serum-and glucocorticoid-inducible kinase (Sgk1), which is expressed in the renal medulla, is regulated by extracellular tonicity. However, the mechanism of its regulation and the physiological role of hypertonicity-induced SGK1 gene expression remain unclear. Here, we identified a tonicity-responsive enhancer (TonE) upstream of the rat Sgk1 transcriptional start site. The transcription factor NFAT5 associated with TonE in a tonicity-dependent fashion in cultured rat renal medullary cells, and selective blockade of NFAT5 activity resulted in suppression of the osmotic induction of the Sgk1 promoter. In vivo, water restriction of rats or mice led to increased urine osmolality, increased Sgk1 expression, increased expression of the type A natriuretic peptide receptor (NPR-A), and dehydration natriuresis. In cultured rat renal medullary cells, siRNA-mediated Sgk1 knockdown blocked the osmotic induction of natriuretic peptide receptor 1 (Npr1) gene expression. Furthermore, Npr1 -/-mice were resistant to dehydration natriuresis, which suggests that Sgk1-dependent activation of the NPR-A pathway may contribute to this response. Collectively, these findings define a specific mechanistic pathway for the osmotic regulation of Sgk1 gene expression and suggest that Sgk1 may play an important role in promoting the physiological response of the kidney to elevations in extracellular tonicity. IntroductionPersistent hypertonicity, typically reflecting a high extracellular sodium concentration, stresses mammalian cells due to the ensuing osmotic efflux of water that shrinks the cells and concentrates their contents. Under most conditions, the concentration of extracellular sodium in mammals is controlled primarily through regulation of water metabolism. As extracellular sodium and plasma tonicity rise, the thirst mechanism is activated, and secretion of the neurohypophyseal hormone vasopressin into plasma increases. Vasopressin binds to its cognate receptors in the collecting duct of the kidney, resulting in increased water retention.Following short-term water restriction, several mammals demonstrate an acute increase in urinary sodium excretion that is independent of changes in water metabolism. This response, termed dehydration natriuresis (1-11), plays an important role in preventing further accentuation of hypernatremia and the accompanying rise in extracellular tonicity. A similar natriuresis is seen following infusion of hypertonic saline (12). Investigations to date have suggested a role for central versus peripheral osmoreceptors and blood-borne versus neural effectors in contributing to dehydration-induced natriuresis; however, the precise mechanism(s) underlying this natriuresis remains undefined.

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Ventricular PKC‐ϵ and humoral signaling in DOCA‐Salt rats treated with labedipinedilol‐A

Yeh

Liang

Liou

et al. 2003

Drug Development Research

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Effects of oral antihypertensive monotherapy with labedipinedilol-A, labetalol, atenolol, amlodipine, prazosin (20 mg kg À1 day À1 ), and short-acting nifedipine (3 mg kg À1 day À1) on DOCA-saltinduced translocation of ventricular protein kinase C-E(PKC-E), humoral signaling, and the cardiovascular system were investigated in rats for 4 weeks. The triple blocking activities of labedipinedilol-A (a/badrenoceptor blockade and calcium entry blockade) were compared with single blocking activities of selective drugs. Cytosolic PKC-E immunoreactivity was decreased by labedipinedilol-A, short-acting nifedipine, amlodipine, prazosin, labetalol, atenolol, and losartan. Membranous PKC-E immunoreactivity was significantly decreased by labedipinedilol-A, amlodipine, prazosin, labetalol, and atenolol. Labedipinedilol-A and prazosin more potently decreased membranous than cytosolic PKC-E expression. Labedipinedilol-A, labetalol, and atenolol effectively inhibited DOCA-salt-induced increases in angiotensin II (Ang II). All antihypertensive agents reduced endothelin-1 (ET-1) levels in urine and cardiac weight growth. Treatments with labedipinedilol-A, labetalol, atenolol, and amlodipine normalized DOCA-salt-induced ANP increases. Prazosin did not decrease ANP. Short-acting nifedipine elevated ANP. During long-term antihypertensive therapy in DOCA-salt hypertensive rats, single blockade drugs did not fully inhibit ventricular PKC-E translocation or Ang II, ET-1, and ANP humoral signaling. However, triple blockade labedipinedilol-A therapy had a wide range of a/b-adrenergic receptor and calcium channel inhibitory activities, including diminished reflux tachycardia, inhibition of PKC-E translocation, and reduction of Ang II, ET-1, and ANP formation. Drug Dev.

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Increased renal atrial natriuretic peptide synthesis in rats with deoxycorticosterone acetate-salt treatment

Cited by 21 publications

References 0 publications

Increased C-type natriuretic peptide mRNA expression in the kidney of diabetic rats

Increased C-type natriuretic peptide mRNA expression in the kidney of diabetic rats

Tonicity-dependent induction of Sgk1 expression has a potential role in dehydration-induced natriuresis in rodents

Ventricular PKC‐ϵ and humoral signaling in DOCA‐Salt rats treated with labedipinedilol‐A

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