Specific Receptor-Mediated Inhibition by Synthetic Atrial Natriuretic Factor of Hormone-Stimulated Steroidogenesis in Cultured Bovine Adrenal Cells.

Lean, D. R.; Gutkowska, Jolanta; Nguyen, Thang Trung; Cantin, M.; Genest, Jacques

doi:10.1210/endo-115-4-1636

Cited by 296 publications

(16 citation statements)

References 19 publications

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“…Investigations performed during the last two years have shown that ANF is a powerful antagonist of the effect of All on arterial contraction [13], secretion of aldosterone [9] and cortisol [ 12] and glomerular contraction [5]. The finding that intraventricular injection of ANF inhibits the dipsogenic effect of All [21] and the presence of All receptors in cerebral microvessels [35] and circumventricular organs [34,37] suggests that ANF may inhibit some of the central ner vous system effects of All as well.…”

Section: Discussionmentioning

confidence: 99%

Radioautographic Localization of <sup>125</sup>I-Atrial Natriuretic Factor Binding Sites in the Brain

et al. 1986

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Rats were injected through the carotid artery (cephalad direction) with 18.9 µCi of either ¹²⁵I-Arg 101-Tyr 126 atrial natriuretic factor alone or together with an excess of unlabeled hormone. At 2 min after injection, all rats were fixed in vivo by perfusion and serial sections of the whole brain were processed for light microscope radioautography. The radioautographic reaction produced by ¹²⁵I-atrial natriuretic factor alone was localized in all circumventricular organs (except the subcommissural organ), the smooth muscle cells and endothelial cells of arteries, arterioles, veins, venules, the endothelial cells of intraparenchymal capillaries and the epithelial cells of the choroid plexus. In rats which received ¹²⁵I-atrial natriuretic factor plus an excess of unlabeled hormone, the radioautographic reaction was reduced by 70–90%. Binding sites are thus localized in regions of the brain, some of them involved in the central monitoring of blood pressure and osmolarity. In addition, the presence of binding sites in the cerebral vasculature and in the epithelium of the choroid plexus suggests that circulating ANF may play a role in the control of cerebral blood flow and in the production of vertebrospinal fluid.

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Section: Discussionmentioning

confidence: 99%

Radioautographic Localization of <sup>125</sup>I-Atrial Natriuretic Factor Binding Sites in the Brain

et al. 1986

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“…As well as its recognised functions of natriuresis, diuresis and vasorelaxation, ANF has been reported to inhibit several physiological systems [60], including inhibition of renin release from juxtaglomerular cells [61], inhibition of ANGII, inhibition of ACTH, inhibition of PGE 1 and inhibition of forskolin-stimulated steroidogenesis in cultured bovine adrenal glomerulosa cells [62], inhibition of ANGII, ACTH and K + -stimulated aldosterone secretion from the adrenal gland, inhibition of arginine vasopressin secretion and inhibition of endothelin expression and secretion from cultured bovine endothelial cells [63]. Collectively these results suggested a potentially important new function for the natriuretic peptide receptors to mediate, in part, the interactions of ANF and other endogenously released agents.…”

Section: Inhibitory Actions Of Atrial Natriuretic Factormentioning

confidence: 99%

Cytokine-Stimulated Nitric Oxide Production in the Human Renal Proximal Tubule and Its Modulation by Natriuretic Peptides: A Novel Immunomodulatory Mechanism?

Chatterjee

Hawksworth²,

McLay³

1999

Nephron Exp Nephrol

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Although the importance of the human kidney in a variety of disease states is well recognised, the exact mechanisms involved remain unclear. Animal disease models suggest that while high local concentrations of nitric oxide (NO) may play a key role in the initiation and progression of renal disease, low levels may also be essential for normal renal function and cell protection, possibly explaining the variable reports of both beneficial and detrimental responses of renal disease models following NO inhibition. NO has both physiological and pathological roles and clearly a balance between these two primary roles is likely to prevail leading to the conclusion that partial rather than total inhibition of NO production may be beneficial. Despite increasing evidence for the role of NO from animal disease models, little is known of the role of NO and potential modulators within the human kidney. In this review we describe three series of studies during which we examined the ability of primary cultures of human proximal tubular cells to produce NO in response to inflammatory cytokines and the possible role of potential modulators such as the natriuretic peptides. Following challenge with the combination of inflammatory cytokines IL-1β, TNF-α, and IFN-γ, such cultures exhibit a time-dependent increase in inducible NO synthetase induction and corresponding NO production, an effect which was inhibited by L-NMMA. In the second series of studies we demonstrated that increasing concentrations of atrial natriuretic factor (ANF) or C_(4–23)ANF could stimulate a time- and concentration-dependent increase in nitric oxide production which was again abolished by L-NMMA. These results suggested that ANF acting at the natriuretic peptide receptor C could stimulate nitric oxide production in human proximal tubular cells. In the final series of studies we demonstrated that pro-inflammatory cytokine-induced nitric oxide production could be inhibited by ANF, brain natriuretic peptide, C-type natriuretic peptide or C_(4–23)ANF. The actions of the natriuretic peptides and C_(4–23)ANF was to return pro-inflammatory nitric oxide production to those observed when human proximal tubular cells were incubated with ANF alone indicating that this inhibition was mediated via the natriuretic peptide receptor C. The function of NO in the kidney is unclear but undoubtedly it has both beneficial and detrimental actions which in health remain in balance. However, when the kidney is subjected to an immune challenge, high cytotoxic levels of NO are produced locally and appear to be responsible for local damage, unfortunately total inhibition of NO production during such disease states does not always result in benefit. Clearly total abolition of an NO response removes important integral protective actions such as vasodilation. In the ideal situation, treatment of disease processes related to NO excess would involve the inhibition of these high local levels while still protecting vital dependent mechanisms. We believe that th...

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“…ANP acts on its specific receptors, which are distributed preferentially in the renal and pulmonary vasculature [11], to activate particulate guanylyl cyclase to form 3Ј,5Ј-cyclic guanosine monophosphate (cGMP), resulting in vasodilation [12]. Further, ANP inhibits renin release from the juxtaglomerular apparatus [13], which in turn inhibits sodium and water retention derived from the angiotensinaldosterone system.…”

Section: Discussionmentioning

confidence: 99%

Atrial natriuretic peptide infusion for a neonate undergoing repair of congenital diaphragmatic hernia

Tajima¹,

Iranami

Ogawa

et al. 2002

Journal of Anesthesia

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3 ml·kg Ϫ1 ·h Ϫ1 of crystalloid solution and 0.8 ml·kg Ϫ1 ·h Ϫ1 fresh frozen plasma solution), her urinary output showed only a trace amount through the urinary catheter. Analysis of arterial blood gases sampled from the left radial artery found pH 7.368, PaO 2 73.7 mmHg, PaCO 2 31.0 mmHg, and base excess Ϫ6.3 mmol·l Ϫ1 (FiO 2 0.3, inspiratory pressure 22 cmH 2 O, positive endexpinatory pressure (PEEP) 4 cmH 2 O, and ventilatory frequency 40 bpm). On echocardiographic examination, she had PDA and PFO with left to right shunt, and her left venticular function was slightly depressed. On the first day of life, she was scheduled for surgical repair of CDH. The preoperative physical examination revealed wet mucous membrane, normal skin turgor, and normal anterior fontanel. The serum urea nitrogen and creatinine levels were 20 mg·dl Ϫ1 and 0.8 mg·dl Ϫ1 , respectively. The other preoperative laboratory data were within normal limits. Anuria persisted for 12 h before surgery, despite intravenous administration of dopamine (3 µg·kg Ϫ1 ·min Ϫ1 ) and furosemide (0.3 mg·kg Ϫ1 ).Anesthesia was induced and maintained with fentanyl (10 µg·kg Ϫ1 ) and isoflurane (0.5%-1.0%) in an air-oxygen mixture (FiO 2 0.4-1.0, pressure-controlled mode 20 cmH 2 O, PEEP 2 cmH 2 O, and respiratory frequency 40 bpm). Pancuronium (0.1 mg·kg Ϫ1 ) was given as a supplement. After the induction, catheters were inserted into the right radial artery and the internal jugular vein for continuous measurement of arterial and central venous pressures. The intraoperative heart rate was within the range of 170-180 bpm, and arterial and central venous blood pressure were within the ranges of 75/50-60/40 mmHg and 5-6 mmHg, respectively. The serum Na ϩ and K ϩ concentrations were 134.4 and 3.5 mEq·l Ϫ1 , respectively. After crystalloid solution (6.3 ml·kg Ϫ1 ·h Ϫ1 ) and an additional 20 ml of 5% albumin were infused for 1.5 h, the anuria persisted. Despite little blood loss, the hematocrit decreased from 46.4% to 38.2%. The heart rate and blood pressure were stable. The mucous membrane was moist. Skin turgor

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Specific Receptor-Mediated Inhibition by Synthetic Atrial Natriuretic Factor of Hormone-Stimulated Steroidogenesis in Cultured Bovine Adrenal Cells.

Cited by 296 publications

References 19 publications

Radioautographic Localization of <sup>125</sup>I-Atrial Natriuretic Factor Binding Sites in the Brain

Radioautographic Localization of <sup>125</sup>I-Atrial Natriuretic Factor Binding Sites in the Brain

Cytokine-Stimulated Nitric Oxide Production in the Human Renal Proximal Tubule and Its Modulation by Natriuretic Peptides: A Novel Immunomodulatory Mechanism?

Atrial natriuretic peptide infusion for a neonate undergoing repair of congenital diaphragmatic hernia

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