The increase of cGMP by atrial natriuretic factor correlates with the distribution of particulate guanylate cyclase

Tremblay, Johanne; Gerzer, R.; Vinay, Patrick; Pang, Stephen C.; Béliveau, Richard; Hamet, Pavel

doi:10.1016/0014-5793(85)81105-4

Cited by 234 publications

(98 citation statements)

References 18 publications

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“…The localization of ANF binding sites also perfectly correlates with that for ANF-induced cGMP production reported by Tremblay et al [20] in a parallel study. Interestingly, ANF-sensitive particulate guanylate cyclase has been documented in all target organs also containing ANF receptor binding sites, strongly suggesting a close association of ANF receptor with guanylate cyclase in the plasma membrane of target cells.…”

Section: Discussionsupporting

confidence: 87%

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Distribution of atrial natriuretic factor receptors in dog kidney fractions

1985

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Specific receptors for atria1 natriuretic factor were studied in purified glomeruli, proximal tubules, thick ascending limbs of Henle's loops and collecting ducts from dog kidney. Glomeruli contain the highest concentration of receptor sites (pK = 9.9, B,,,, = 200 fmol/mg protein), followed by collecting ducts (pK = 9.4, B mai = 150 fmol/mg). Low levels of receptor sites were also detectable in thick ascending limbs of Henle's loops (pK = 9.4, B,,, = 36 fmol/mg) while proximal tubules were completely devoid of specific binding sites. These results indicate that the glomeruli appear to be the primary site of interaction of artrial natriuretic factor in kidney cortex but that it might also act in the medulla on lower nephron tubular function. Atria1 natriuretic factor Vasoactive peptide Peptide receptor Glomerular function Tubular function (Dog kidney)

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Section: Discussionsupporting

confidence: 87%

“…We have documented the distribution of ANF receptors in glomeruli and tubules purified from dog kidney. The results perfectly correlate with a parallel study on ANFinduced cGMP production in the same preparations [20] as well as with the autoradiographic localization of the in vivo uptake of "'I-ANF in rat kidney [21].…”

Section: Introductionsupporting

confidence: 84%

Distribution of atrial natriuretic factor receptors in dog kidney fractions

1985

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“…How then does NEP inhibition lead to modification of the cardio-pulmonary response to hypoxia without elevation of plasma ANP? ANP activity is associated with an increase in guanosine 3':5'-cyclic monophosphate (cyclic GMP) (Tremblay et al, 1985). In the study by Klinger et al (1993b), SCH 42495 reduced pulmonary and renal NEP activity by 50% but as in our study, plasma ANP was significantly decreased.…”

Section: Discussionsupporting

confidence: 43%

Neutral endopeptidase (NEP) inhibition in rats with established pulmonary hypertension secondary to chronic hypoxia

Thompson

Sheedy

Morice

1994

British J Pharmacology

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1Atrial natriuretic peptide (ANP) causes vasorelaxation in the pulmonary vasculature. ANP levels are elevated in conditions characterized by pulmonary hypertension and it has been hypothesized that ANP may be autoregulatory in the pulmonary circulation. 2 One route of ANP metabolism in vivo is by the action of the enzyme neutral endopeptidase (NEP). We have studied the effects of the NEP inhibitor, SCH 42495, in rats with established pulmonary hypertension secondary to chronic hypoxia. 3 Rats (n = 32) were divided into 4 groups. Normoxic controls were kept in air for 10 days (NClO) and all other animals were placed in a normobaric hypoxic chamber (Fi 02 10%). Chronic hypoxic controls were studied at 10 days (CHC10). After 10 days hypoxia the two remaining groups received oral treatment for a further 10 days, consisting of either SCH 42495 (30 mg kg-', twice daily CHT20) or methyl cellulose vehicle (0.4%, twice daily, CHV20). 4 Animals were anaesthetized and blood collected for measurement of plasma ANP. Hearts were dissected and ventricles weighed and the histology of the pulmonary vasculature examined. 5 CHClO rats had significant right ventricular hypertrophy (0.53 ± 0.08) and pulmonary vascular remodelling (29.0 0.01%) and had gained significantly less body weight (33.2 ± 5.5 g) than NC1O rats (0.31 ± 0.04, 10.9 0.01%, and 59.2 ± 11.9 g respectively). CHC1O rats had significantly elevated plasma ANP levels (58.4 ± 9.9 pM) compared with NClO rats (23.9 ± 32 pM). Treatment with SCH 42495 caused a significant reduction in pulmonary vascular remodelling (25.0 ± 0.01%) and right ventricular hypertrophy (0.52 ± 0.09) in CHT20 rats compared with CHV20 controls (33.0 ± 0.02% and 0.61 ± 0.09 respectively). Pulmonary vascular remodelling was also significantly lower in CHT20 rats than CHC1O animals. 6 Thus, short term inhibition of NEP causes regression of established pulmonary vascular remodelling and may be a useful therapeutic strategy in pulmonary hypertension.

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“…These actions of ANP are brought about via the activation of membrane-bound protein, natriuretic peptide receptor type A (NPR-A), or guanylyl cyclase A. [2][3][4] NPR-A is a 130-KDa transmembrane protein containing an ANP-binding motif at its extracellular NH 2 terminus and GC activity at its COOH-terminal intracellular domain. 5 Activation of NPR-A leads to the conversion of GTP to the intracellular second messenger cGMP, which is involved in most of the biological responses associated with natriuretic peptides.…”

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Characterization of a cGMP-Response Element in the Guanylyl Cyclase/Natriuretic Peptide Receptor A Gene Promoter

et al. 2004

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Abstract-Previous studies have shown that atrial natriuretic peptide (ANP) can inhibit transcription of its receptor, guanylyl cyclase A, by a mechanism dependent on cGMP and have suggested the presence of a putative cGMP-response element (cGMP-RE) in the Npr1 gene promoter. To localize and characterize the putative cis-acting element, we have subcloned a 1520-bp fragment of the rat Npr1 promoter in an expression vector containing the luciferase reporter gene. Several fragments, generated by exonuclease III-directed deletions, were transiently transfected into cells to measure their promoter activity. Deletion from Ϫ1520 to Ϫ1396 of a 1520-bp-long Npr1 promoter led to a 5-fold increase in luciferase activity. Subsequent deletion to the position Ϫ1307 resulted in a decrease of luciferase activity by 90%. Preincubation of cells with 100 nM of ANP or 100 M 8-bromo-cGMP inhibited luciferase activity of the 1520-bp and 1396-bp-long fragments, but not the activity of the 1307-bp fragment, suggesting that the cGMP-RE is localized between positions Ϫ1396 and Ϫ1307. The cGMP regulatory region was narrowed by gel shift assays and footprinting to position Ϫ1372 to Ϫ1354 from the transcription start site of Npr1 and indicated its interaction with transcriptional factor(s). Cross-competition experiments with mutated oligonucleotides led to the definition of a consensus sequence (Ϫ1372 AaAtRKaNTTCaAcAKTY Ϫ1354) for the novel cGMP-RE, which is conserved in the human (75% identity) and mouse (95% identity) Npr1 promoters. Key Words: cyclic GMP Ⅲ natriuretic peptides Ⅲ receptors, atrial natriuretic factor A trial natriuretic peptide (ANP) is a cardiac hormone with potent effects in the kidney, vasculature, and nervous system. It has vasorelaxant activity in vascular smooth muscle and promotes urinary sodium and water excretion by the kidney (for review, see Reference 1 ). These actions of ANP are brought about via the activation of membrane-bound protein, natriuretic peptide receptor type A (NPR-A), or guanylyl cyclase A. 2-4 NPR-A is a 130-KDa transmembrane protein containing an ANP-binding motif at its extracellular NH 2 terminus and GC activity at its COOH-terminal intracellular domain. 5 Activation of NPR-A leads to the conversion of GTP to the intracellular second messenger cGMP, which is involved in most of the biological responses associated with natriuretic peptides. 2-5 Increased cGMP yields receptor desensitization, resulting in a decrease of ANP-stimulated cGMP synthesis. 6 Receptor preoccupancy appears to be a mechanism of apparent receptor desensitization 7 but transfection experiments with NPR-A cDNA have revealed that early desensitization by ANP pretreatment can be due to dephosphorylation of NPR-A protein. 8 Besides, a previous study demonstrated that NPR-A activity, as well as its mRNA levels, is diminished in a time-and concentration-dependent manner by ANP or by a cell-permeable cGMP analog, 8-bromo-cGMP. 9 Those results suggest transcriptional regulation via a putative cGMPresponse element (cGMP-RE) in the p...

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The increase of cGMP by atrial natriuretic factor correlates with the distribution of particulate guanylate cyclase

Cited by 234 publications

References 18 publications

Distribution of atrial natriuretic factor receptors in dog kidney fractions

Distribution of atrial natriuretic factor receptors in dog kidney fractions

Neutral endopeptidase (NEP) inhibition in rats with established pulmonary hypertension secondary to chronic hypoxia

Characterization of a cGMP-Response Element in the Guanylyl Cyclase/Natriuretic Peptide Receptor A Gene Promoter

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