The atrial natriuretic factor: Its physiology and biochemistry

Genest, Jacques; Cantin, M.; Anand‐Srivastava, Madhu B.; Cusson, Jean R.; Léan, André De; García, Raúl; Gutkowska, Jolanta; Hamet, Pavel; Küchel, Otto; Larochelle, Pierre; Nemer, Mona; Schiffrin, Ernesto L.; Schiller, Peter W.; Thibault, Gaétan; Tremblay, Johanne

doi:10.1007/bfb0027530

Cited by 104 publications

(29 citation statements)

References 488 publications

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“…Circulating ANP acts directly via specific receptors in the kidney to promote sodium and water excretion (Genest et al 1988), and the peptide also suppresses aldosterone secretion and causes vasodilatation in selected vascular beds (Murad, 1986). While the cellular mechanisms involved in these responses are not fully understood, recent demonstrations that the ANP receptor exhibits guanylate cyclase activity (Chinkers, Garbers, Chang, Lowe, Chin, Goeddel & Schulz, 1989) and that ANP stimulates cGMP formation (Hamet, Tremblay, Pang, Garcia, Thibault, Gutkowska, Cantin & Genest, 1984) suggest that this cyclic nucleotide may be a key mediator of the peptide's actions.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms underlying chemoreceptor inhibition induced by atrial natriuretic peptide in rabbit carotid body.

Wang

Chen

et al. 1993

The Journal of Physiology

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SUMMARY1. Previous studies in our laboratory revealed the presence of atrial natriuretic peptide (ANP) in preneural chemosensory type I cells of the cat carotid body, and demonstrated that submicromolar concentrations of the peptide inhibited carotid sinus nerve (CSN) activity evoked by hypoxia. In the present study, we have evaluated the role of the cyclic nucleotide second messenger, cyclic G-MP (cGMP), and the involvement of type I cells in rabbit chemosensory inhibition.2. Submicromolar concentrations of the potent ANP analogue, APIII, greatly elevated both the content and release of cGMP from the carotid body. Denervation experiments confirmed earlier immunocytochemical studies which suggested that APIII-induced cGMP production occurs almost exclusively in type I cells; these experiments also indicate that both the sympathetic and sensory innervation to the carotid body exert a trophic influence on the metabolism of this second messenger.3. Submicromolar concentrations of APIII inhibited the CSN activity evoked by hypoxia (79-8 + 3-2 % (mean + S.E.M.) inhibition with 100 nM APIII) and nicotine (74-5 + 3-6 % inhibition with 100 nM APIII), but did not affect basal CSN activity established in 100% 02-equilibrated superfusion solutions.4. The biologically inactive analogue of ANP, C-ANP, failed to produce CSN inhibition; however, the inhibitory effects of APIII were mimicked by cell-permeant analogues of cGMP (dibutyryl-cGMP and 8-bromo-cGMP, 2 mM), which likewise did not alter basal CSN activity. Because we found that unmodified cGMP was an ineffective inhibitor of CSN activity, our data suggest that APIII inhibition is mediated intracellularly by cGMP produced within the type I cells.5. APIII does not inhibit the CSN activity produced by 20 mm K+ (in zero Ca2+ media), which very probably results from direct depolarization of the sensory nerve terminals.6. Catecholamine release from the carotid body evoked by hypoxia is likewise not altered by APIII (100 nM).7. The data are consistent with the notion that APIII and analogues of cGMP alter the release of excitatory and/or inhibitory transmitters from chemosensory type I cells in the carotid body. MS 9953W.-J. WANG AND OTHERS

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Section: Introductionmentioning

confidence: 99%

Mechanisms underlying chemoreceptor inhibition induced by atrial natriuretic peptide in rabbit carotid body.

Wang

Chen

et al. 1993

The Journal of Physiology

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“…As is the case with ANP itself, the effect was largely limited to an increase in sodi um excretion; however, high doses also produced a slight kaliuresis. Since these changes mimick the action of ANP [21], we presume that the natriuretic effect was due almost solely to the ability of ET-3 to release ANP. This concept is supported by the fact that the increase in plas ma ANP following volume expansion was similar to the one we obtained with this dose of ET-3, which brought about a similar natriuretic effect [22],…”

Section: Discussionmentioning

confidence: 99%

Possible Role of Endothelin Acting within the Hypothalamus to Induce the Release of Atrial Natriuretic Peptide and Natriuresis

Antunes‐Rodrigues

Ramalho²,

Reis³

et al. 1993

Neuroendocrinology

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Since endothelin has been localized in neurons in areas involved in water and electrolyte metabolism, areas which also contain atrial natriuretic peptide (ANP) neurons, we determined whether endothelin would release ANP and induce natriuresis. Endothelin-3 (ET-3) in doses ranging from 38 to 760 pmol was microinjected into the third ventricle (3V) of conscious, water-loaded male rats, and the effect on natriuresis and plasma ANP was determined. ET-3 evoked a dose-related natriuresis beginning within 20 min of injection. Even the lowest dose tested (38 pmol) was effective. At a dose of 95 pmol, it produced a rapid increase of plasma ANP within 5 min peaking at 20 min. A slight kaliuresis and antidiuresis was observed at the 2 highest doses of 380 and 760 pmol. The urinary changes following 3V injection of ET-3 were similar to those evoked by ANP, except for the antidiuresis with increased sodium concentration which followed injection of the 2 higher doses. These results suggest that these 2 higher doses also released vasopressin. Alternatively, activation of the sympathetic nervous system by these higher doses may have decreased glomerular filtration rate and been in part responsible for the antidiuresis. The results with 3V injection of ET-3 contrasted sharply with those obtained following intravenous injection of the 95-pmol dose injected intra-ventricularly. This intravenous dose of ANP induced a transient decrease in sodium and potassium excretion and urine volume, maximal at 20 min, and had no effect on plasma ANP concentrations at 5 or 20 min after injection. Previous experiments have shown that the hypothalamic ANP neuronal system plays an essential role in the volume expansion-induced release of ANP and the subsequent natriuresis. We speculate that endothelin released in the brain following volume expansion may activate the ANP neuronal system which is then followed by an increased release of ANP from the atria and possibly from the brain. Further experiments will be necessary to validate this hypothesis.

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“…Although the main forms of ANF in the rat brain are ANF 102-126 and 103-126 [33], structureactivity studies [9,37] suggest that these peptides interact with the same binding sites as ANF 99-126.…”

Section: Discussionmentioning

confidence: 99%

Localization and Characterization of Binding Sites for Circulating and Cerebroventricular Atrial Natriuretic Factor in Rat Choroid Plexus

Konrad¹,

Bianchi²,

Thibault³

et al. 1990

Neuroendocrinology

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In vitro autoradiographic studies showed that high-affinity atrial natriuretic factor (ANF) binding sites are present on rat choroid plexus (Kd = 83.8 pM, B_max = 22.9 fmol/mg protein). Guanylate cyclase-coupled receptors (ANF-Ri) represent 30% and non-guanylate cyclase-coupled ANF receptors (ANF-R2) represent 70% of the total ANF receptors present in this tissue. To provide detailed cellular localization of the binding sites, the technique of electron-microscopic autoradiography was applied using ^l25I-ANF (Ser 99-Tyr 126) as an in vivo ligand. In order to identify possible binding sites at the basolateral and the apical aspects of the choroid plexus, the ligand was injected into the carotid artery or into the lateral cerebral ventricles, respectively. Light-microscopic autoradiography demonstrated that ANF binds specifically to choroid plexus regardless of its route of administration. Electron-microscopic autoradiography showed that silver grains were localized primarily on epithelial cells of the choroid plexus (96–99%) and marginally on endothelial and pial cells. In choroidal epithelial cells, ultrastructural analysis of silver grain distribution revealed that, at 2 min after intracarotid or intracerebroventricular ¹²⁵I-ANF injection, lysosomes were the most distinctly labeled organelle (highest relative specific radioactivity). HPLC Chromatographic analysis disclosed that 96–99% of choroid plexus-bound ANF was already degraded 2 min after injection and that at least 63–66% of the degradation took place at the plasma membrane. These results indicate that ANF binding sites are present on both aspects of choroidal epithelium, and suggest that ANF is very quickly degraded in choroid plexus by membrane-associated as well as lysosome-associated processes.

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The atrial natriuretic factor: Its physiology and biochemistry

Cited by 104 publications

References 488 publications

Mechanisms underlying chemoreceptor inhibition induced by atrial natriuretic peptide in rabbit carotid body.

Mechanisms underlying chemoreceptor inhibition induced by atrial natriuretic peptide in rabbit carotid body.

Possible Role of Endothelin Acting within the Hypothalamus to Induce the Release of Atrial Natriuretic Peptide and Natriuresis

Localization and Characterization of Binding Sites for Circulating and Cerebroventricular Atrial Natriuretic Factor in Rat Choroid Plexus

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