Atrial natriuretic factor is unlikely to be involved in the reduced aldosterone production in the Brattleboro rat

Laulin, Jean‐Paul; Brudieux, R

doi:10.1016/0167-0115(90)90002-e

Cited by 8 publications

(6 citation statements)

References 31 publications

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“…However, firstly, when the present stim ulated plasma levels of ANF are compared with basal values, measured under the same experimental conditions which we have pre viously reported (42.6 ± 5.5 pg/ml) in adult Long-Evans rats [20], it appears that they have been increased approximately 2.5-and 9-fold, respectively, after volume expansion Effects of intravenous injections of 0.01. 0 .…”

Section: Discussionmentioning

confidence: 99%

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Age-Related Changes in Secretion and Metabolic Effects of Atrial Natriuretic Factor in Rats

Rakotondrazafy¹,

Davicco²,

Barlet³

et al. 1996

Gerontology

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The effects of aging on the secretion of and renal sensitivity to atrial natriuretic factor (ANF) were studied concomitantly in both senescent (25- to 34-month-old) and in adult (7- to 13-month-old) female and male Long-Evans rats. The plasma concentrations of ANF, measured in response to either a mild stimulation induced by a hypertonic volume expansion (i.e., 20 min after the onset of a continuous infusion during 15 min of a 2.5% NaCl solution; n = 18 old and 23 adult rats) or an intense stimulation produced by morphine injection (i.e., 30 min after an intraperitoneal injection of 5 mg morphine/100 g body weight; n = 11 old and 12 adult rats), were significantly lower (approximately -34 and -80%, respectively) in old as compared with adult animals. Acute intravenous injection of exogenous rat ANF (0.10 and 0.40μg/l00g body weight) induced similar natriuretic, diuretic, and kaliuretic effects in aged (n = 18) and in adult (n = 23) rats. The present data suggest that the significantly reduced (about -20%) natriuretic and kaliuretic responses of the aged rat, observed 20 min after the onset of hypertonic volume expansion, could be partly due to a primary defect in cardiac production and/or release of ANF rather than to a reduction of renal responsivity to ANF.

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Section: Discussionmentioning

confidence: 99%

“…The ANF pro duction was measured in response to a mild stimulation by a hypertonic volume expan sion and to intense stimulation by morphine injection [19,20], The renal effects were mea sured following three different bolus doses of rat ANF.…”

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confidence: 99%

Age-Related Changes in Secretion and Metabolic Effects of Atrial Natriuretic Factor in Rats

Rakotondrazafy¹,

Davicco²,

Barlet³

et al. 1996

Gerontology

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“…However, using hypophysectomized animals, our results indicated that, although AVP and ACTH interacted to enhance aldosterone secretion (21,26), the two hormones together were not able to restore it to normal control values, indicating that other pituitary factors were also required to ensure steroid secretion. In addition, several experiments conducted with Brattleboro rats indicate that aldosterone secretion is decreased in these animals, clearly indicating that the vasopressin from hypothalamo-pituitary complex is directly involved in the regulation of the aldosterone secretion (33)(34)(35)(36)(37). However, as AVP can stimulate ACTH release (4,38), its role on adrenal function may be considered as indirect.…”

Section: Adrenalsteroid Secretionmentioning

confidence: 99%

“…In humans, Oelkers et al (39) showed that AVP increased both aldosterone and cortisol secretion, but an indirect influence of ACTH was suggested by the authors. However, several experiments conducted with Brattleboro rats indicate that aldosterone secretion is decreased in these animals, clearly indicating that the vasopressin from hypothalamo-pituitary complex is directly involved in the regulation of the aldosterone secretion (33,35,37), independently of its action onACTH secretion (34 -37).…”

Section: Adrenalsteroid Secretionmentioning

confidence: 99%

Regulation of Adrenocortical Function by Vasopressin

Gallo‐Payet

Guillon

1998

Horm Metab Res

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Accumulating data obtained from various animal species indicate that vasopressin (AVP) participates in the regulation of adrenocortical function. AVP doubled aldosterone and cortisol secretion but did not affect corticosterone secretion. Pharmacological studies indicate that the AVP receptors in the cortex belong to the V1 a subtype. Activation of V1 a receptors induces breakdown of membrane phosphoinositides, with subsequent accumulation of inositol phosphates and diacylglycerol. These effects occur after receptor binding, G-protein activation and coupling to a specific phospholipase C. Inositol trisphosphate, transiently produced, induces a rapid release of Ca2+ from intracellular stores. Diacylglycerol activates protein kinase C, which, together with calcium, is responsible for steroid secretion. The early events of AVP action are mediated by two types of G-proteins. One is coupled to phospholipase C, and insensitive to pertussis toxin (probably Gq/11) and a second one, which is inactivated by pertussis toxin (Gi protein), is involved in the stimulation of calcium influx. This Ca2+ influx pathway is very important, as no steroidogenic effect of AVP could be observed when experiments were performed in a calcium-free medium or in pertussis toxin-treated cells. Besides the pituitary, the adrenal is also a source for AVP production. Indeed, AVP is synthesized and secreted by chromaffin cells either present in the medulla or scattered throughout the cortex with a more prominent concentration in zona glomerulosa. AVP receptors are also present on chromaffin cells. However, in contrast to AVP receptors in the cortex, these mainly belong to the V1 b subtype, although V1 a receptors are also detected. The results summarized in this review conclusively indicate that AVP is one of the regulators of both cortex and medulla, an influence which may be mediated in part via pituitary AVP and in part via local production of AVP.

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“…As the most prevalent female malignant tumor globally, morbidity of breast cancer has been steadily increasing since 1987, and its incidence accounts for approximately 24.5% of all women’s malignancies ( Sung et al, 2021 ). Not a single-gene disorder, breast cancer is a diversified disease classified by histology, immunopathology, mRNA expression profile and miRNA expression features rather than a monogenic disease ( Laulin and Brudieux, 1990 ). As molecular biological research deepens, abnormal signaling pathways of tumor inhibitor genes and oncogenes manifest connection with breast cancer development ( Boo et al, 2016 ; Gilam et al, 2016 ; Nassar et al, 2017 ; Sun et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

ADAMTS9-AS1 Constrains Breast Cancer Cell Invasion and Proliferation via Sequestering miR-301b-3p

Chen

Cheng²,

Zou

et al. 2021

Front. Cell Dev. Biol.

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Objective: For determination of how ADAMTS9-AS1/miR-301b-3p/TGFBR2/JAK STAT signaling axis modulates progression of breast cancer cells.Methods: Target lncRNA was determined by differential analysis of breast cancer expression data and survival analysis. Differentially expressed miRNAs and target mRNAs that had binding sites with target lncRNA were predicted. GSEA software was used to carry out pathway enrichment analysis for mRNAs. Binding of the researched genes were tested with RNA binding protein immunoprecipitation (RIP). How miR-301b-3p bound TGFBR2 mRNA was tested by dual-luciferase method. Transwell, colony formation, EdU approaches were employed for verification of invasion and proliferation of breast cancer cells in each treatment group.Results: Markedly inactivated ADAMTS9-AS1 in breast cancer pertained to patient’s prognosis. MiR-301b-3p was capable of binding TGFBR2/ADAMTS9-AS1. However, overexpression of ADAMTS9-AS1 stimulated miR-301b-3p binding ADAMTS9-AS1 and repressed miR-301b-3p binding TGFBR2 mRNA. ADAMTS9-AS1 interference enhanced cancer proliferation and invasion, facilitated levels of KI67, PCNA, MMP-9 and MMP-2, and activated the JAK STAT signaling pathway. While silencing miR-301b-3p reversed the effect of ADAMTS9-AS1 interference. In addition, TGFBR2 interference or restraining JAK STAT signaling counteracted the effect of ADAMTS9-AS1.Conclusion: ADAMTS9-AS1 could sequester miR-301b-3p to inhibit progression of breast cancer via TGFBR2/JAK STAT pathway. This study supplies a rationale for incremental apprehension of ADAMTS9-AS1 in breast cancer progression.

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Atrial natriuretic factor is unlikely to be involved in the reduced aldosterone production in the Brattleboro rat

Cited by 8 publications

References 31 publications

Age-Related Changes in Secretion and Metabolic Effects of Atrial Natriuretic Factor in Rats

Age-Related Changes in Secretion and Metabolic Effects of Atrial Natriuretic Factor in Rats

Regulation of Adrenocortical Function by Vasopressin

ADAMTS9-AS1 Constrains Breast Cancer Cell Invasion and Proliferation via Sequestering miR-301b-3p

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