Stimulatory effects of atrial natriuretic factor on phosphoinositide hydrolysis in cultured bovine aortic smooth muscle cells

Hirata, Masato; Chang, Chung Ho; Murad, Ferid

doi:10.1016/0167-4889(89)90060-8

Cited by 166 publications

(94 citation statements)

References 34 publications

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“…Firstly, we investigated whether simultaneous application of natriuretic peptides with different adenylyl cyclase activators led to a modified cyclic AMP response. ANP, BNP and CNP (all at 1 JIM) failed to alter significantly either basal-, forskolin-(10 fM), isoprenaline-(100 jM) or NECA-(10 I4M) Effects of natriuretic peptides on phosphoinositide turnover Since ANP has been observed to stimulate phosphoinositide turnover in vascular smooth muscle cells (Resink et al, 1988;Hirata et al, 1989) and in inner medullary collecting tubule cells (Berl et al, 1991), we investigated whether this response might also be elicited in the guinea-pig cerebellum. All three natriuretic peptides, in the presence of 5 Time (min) cerebellar slices, without any contemporary change in cyclic AMP accumulation or phosphoinositide turnover.…”

Section: Effects Of Natriuretic Peptides On Cyclic Amp Generationmentioning

confidence: 99%

“…Thus, a decrease in adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels has been observed either through an inhibition of adenylyl cyclase activity (Pandey et al, 1985;Resink et al, 1988;Anand-Srivastava et al, 1990;Tseng et al, 1990) or through activation of cyclic GMP-stimulated phosphodiesterases (MacFarland et al, 1991). Activation of phosphoinositide turnover has been reported in vascular smooth muscle cells (Resink et al, 1988;Hirata et al, 1989) and in inner medullary collecting tubule cells (Berl et al, 1991 Ltd, 1994 Results Tissue preparation and cyclic nucleotides accumulation Preparation and incubation of slices were essentially the same as described previously (Hernandez et al, 1993 …”

Section: Introductionmentioning

confidence: 99%

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Natriuretic peptide‐induced cyclic GMP accumulation in adult guinea‐pig cerebellar slices

Hernández

Alexander

Kendall

1994

British J Pharmacology

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Section: Effects Of Natriuretic Peptides On Cyclic Amp Generationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Natriuretic peptide‐induced cyclic GMP accumulation in adult guinea‐pig cerebellar slices

Hernández

Alexander

Kendall

1994

British J Pharmacology

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“…8,9 The 77-kDa protein is implicated in ligand internalization as a clearance receptor, 10 whereas 67-kDa protein is coupled to adenylyl cyclase inhibition through inhibitory guanine nucleotide regulatory protein Gi 7,11 or to activation of phospholipase C (PLC). 12 However, we showed that NPR-C activation by C-ANP [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] and resultant decrease in cAMP levels contribute to the activation of phosphatidyl inositol turnover signaling and suggested a cross-talk between NPR-C-mediated adenylyl cyclase inhibition and PLC signaling pathways. 13 The activity of adenylyl cyclase is regulated by 2 guanine nucleotide regulatory proteins (G proteins): Gs (stimulatory) and Gi (inhibitory).…”

mentioning

confidence: 99%

“…NPR-A and NPR-B are membrane guanylyl cyclase receptors, whereas NPR-C does not possess guanylyl cyclase activity. Two different subtypes of NPR-C with molecular mass of 67 and 77 kDa have been identified with a broad range of ligands, including ANP, brain natriuretic peptide, C-type natriuretic peptide, and C-ANP [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] [des(Gln, 18 Ser, 19 Gly, 20 Leu, 21 ; however, C-ANP 4-23 is specific for NPR-C and has no affinity for NPR-A or NPR-B. 8,9 The 77-kDa protein is implicated in ligand internalization as a clearance receptor, 10 whereas 67-kDa protein is coupled to adenylyl cyclase inhibition through inhibitory guanine nucleotide regulatory protein Gi 7,11 or to activation of phospholipase C (PLC).…”

mentioning

confidence: 99%

Natriuretic Peptide Receptor-C Attenuates Hypertension in Spontaneously Hypertensive Rats

Sarkar

Brochu

et al. 2014

Hypertension

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Abstract-C-Atrial natriuretic peptide (ANP) 4-23 , a ring deleted analog of ANP that specifically interacts with natriuretic peptide receptor-C (NPR-C), has been shown to decrease the enhanced expression of Giα proteins implicated in the pathogenesis of hypertension. In the present study, we investigated whether in vivo treatment of spontaneously hypertensive rats (SHRs) with C-ANP 4-23 could attenuate the development of high blood pressure (BP) and explored the underlying mechanisms responsible for this response. Intraperitoneal injection of C-ANP 4-23 at the concentration of 2 or 10 nmol/kg body weight to prehypertensive SHRs attenuated the development of high BP, and at 8 weeks it was decreased by ≈20 and 50 mm Hg, respectively; however, this treatment did not affect BP in Wistar-Kyoto rats. C-ANP 4-23 treatment of adult SHRs for 2 weeks also attenuated high BP, heart rate, and restored the impaired vasorelaxation toward control levels. In addition, the enhanced levels of superoxide anion (O 2 − ), peroxynitrite, NADPH oxidase activity, and the enhanced expression of Giα proteins, NOX4, p47 phox , nitrotyrosine, and decreased levels of endothelial nitric oxide synthase (eNOS or NOS3) and NO in SHRs were attenuated by C-ANP 4-23 treatment; however, the altered levels of NPR-A/NPR-C were not affected by this treatment. In conclusion, these results indicate that NPR-C activation by C-ANP 4-23 attenuates the development of high BP in SHRs through the inhibition of enhanced levels of Giα proteins and nitroxidative stress and not through eNOS/ cGMP pathway and suggest that NPR-C ligand may have the potential to be used as therapeutic agent in the treatment of Li et al NPR-C and Blood Pressure Regulation 847injection of pertussis toxin in prehypertensive rats (2-week-old SHRs) has been reported to prevent the development of BP,22 suggesting the implication of enhanced expression of Gi proteins in the pathogenesis of hypertension. C-ANP 4-23 that specifically interacts with NPR-C has been reported to decrease the levels of Giα proteins in A10 vascular smooth muscle cell (VSMC) 23 and in VSMC from SHRs. 24 In addition, C-ANP 4-23 was also shown to attenuate the enhanced oxidative stress in VSMC from SHRs 24 that contributes to the enhanced expression of Giα proteins in SHRs.25 Taken together, it may be possible that C-ANP 4-23 treatment of SHRs could also attenuate the high BP in SHRs. The present study was undertaken to investigate the effect of in vivo administration of C-ANP 4-23 on the development of high BP in SHRs. We have provided the first evidence that the treatment of prehypertensive SHRs with C-ANP 4-23 , an activator of NPR-C, attenuates the development of high BP in SHRs through the inhibition of enhanced expression of Gi proteins and oxidative stress.We have provided the first evidence that NPR-C activation by C-ANP 4-23 attenuates high BP through decreasing the enhanced oxidative stress and the augmented levels of Giα proteins. From these results it may be suggested that C-ANP [4][5][6][7][8][9][10][...

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“…10 In addition, other reports have suggested a possible indirect coupling of this receptor to the guanylate cyclase/cyclic GMP system.…”

mentioning

confidence: 99%

Atrial natriuretic factor receptor subtypes in the rat central nervous system.

et al. 1991

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Stimulatory effects of atrial natriuretic factor on phosphoinositide hydrolysis in cultured bovine aortic smooth muscle cells

Cited by 166 publications

References 34 publications

Natriuretic peptide‐induced cyclic GMP accumulation in adult guinea‐pig cerebellar slices

Natriuretic peptide‐induced cyclic GMP accumulation in adult guinea‐pig cerebellar slices

Natriuretic Peptide Receptor-C Attenuates Hypertension in Spontaneously Hypertensive Rats

Atrial natriuretic factor receptor subtypes in the rat central nervous system.

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