Ignet

Gene Information

Gene symbol: NPR1

Gene name: natriuretic peptide receptor A/guanylate cyclase A (atrionatriuretic peptide receptor A)

HGNC ID: 7943

Synonyms: GUCY2A, ANPa

Related Genes

#	Gene Symbol	Number of hits
1	GJA4	1 hits
2	MAPK1	1 hits
3	MAPK14	1 hits
4	NOS2A	1 hits
5	NOS3	1 hits
6	NPPA	1 hits
7	NPPC	1 hits
8	NPR2	1 hits
9	NPR3	1 hits
10	PANK1	1 hits
11	SCAND1	1 hits
12	SGK1	1 hits
13	VDR	1 hits

Related Sentences

#	PMID	Sentence
1	10768826	Natriuretic peptides (ANP, BNP and CNP) comprise a family of structurally related peptides, which are derived from three different genes and which share a 17-amino acid internal ring.
2	10768826	Besides their peripheral involvement in diuresis and blood pressure regulation these peptides, their bioactive fragments and their corresponding receptors (natriuretic peptide receptors NPR-A, NPR-B and NPR-C) are found throughout the central nervous system (CNS): NPR-A and NPR-C are found on neurons and astrocytes, while NPR-B is located mainly on neurons and partially colocalizes with NPR-A.
3	10768826	In the CNS of man and rodents NPR-A is found mainly in cortex and hippocampus, whereas NPR-B is present in the amygdala and several brainstem regulatory sites.
4	10768826	Natriuretic peptides are specifically involved in the regulation of the hypothalamo-pituitary-adrenocortical (HPA) system: in man and rodents ANP inhibits the HPA system at all regulatory levels, while CNP stimulates the release of cortisol.
5	10768826	Complementarily, the anatomic structure of natriuretic peptide systems within the CNS supports an important role for these in normal and pathologic emotional behaviour (e.g. anxiety and panic): in rodents ANP was found to reduce anxiety levels, whereas CNP induced the opposite effect.
6	10768826	Moreover, panic anxiety and concomitant ACTH and cortisol secretion elicited by stimulation with the panicogen cholecystokinin-tetrapeptide were also attenuated by ANP infusions in patients as well as in healthy volunteers.
7	10768826	Natriuretic peptides (ANP, BNP and CNP) comprise a family of structurally related peptides, which are derived from three different genes and which share a 17-amino acid internal ring.
8	10768826	Besides their peripheral involvement in diuresis and blood pressure regulation these peptides, their bioactive fragments and their corresponding receptors (natriuretic peptide receptors NPR-A, NPR-B and NPR-C) are found throughout the central nervous system (CNS): NPR-A and NPR-C are found on neurons and astrocytes, while NPR-B is located mainly on neurons and partially colocalizes with NPR-A.
9	10768826	In the CNS of man and rodents NPR-A is found mainly in cortex and hippocampus, whereas NPR-B is present in the amygdala and several brainstem regulatory sites.
10	10768826	Natriuretic peptides are specifically involved in the regulation of the hypothalamo-pituitary-adrenocortical (HPA) system: in man and rodents ANP inhibits the HPA system at all regulatory levels, while CNP stimulates the release of cortisol.
11	10768826	Complementarily, the anatomic structure of natriuretic peptide systems within the CNS supports an important role for these in normal and pathologic emotional behaviour (e.g. anxiety and panic): in rodents ANP was found to reduce anxiety levels, whereas CNP induced the opposite effect.
12	10768826	Moreover, panic anxiety and concomitant ACTH and cortisol secretion elicited by stimulation with the panicogen cholecystokinin-tetrapeptide were also attenuated by ANP infusions in patients as well as in healthy volunteers.
13	12082097	Previously, we showed that increased extracellular tonicity promotes increased type A natriuretic peptide receptor (NPR-A) expression through a p38 MAPKbeta pathway in inner medullary collecting duct cells.
14	12082097	The endothelial and inducible nitric-oxide synthase (eNOS and iNOS respectively) genes are also expressed in this nephron segment and are thought to play a role in regulating urinary sodium concentration.
15	12082097	We sought to determine whether changes in tonicity might regulate NOS gene expression, and if so, whether these latter changes might be linked mechanistically to the increase in NPR-A gene expression.
16	12082097	Increased extracellular tonicity effected a time-dependent reduction in eNOS and iNOS protein levels, eNOS mRNA levels, and eNOS gene promoter activity over the first 8 h of the incubation.
17	12082097	The decrease in eNOS expression was signaled in large part through a p38 MAPK-dependent mechanism.
18	12082097	Reduction in eNOS expression together with the concomitant decline in intracellular cyclic GMP levels appears to account for a significant portion of the p38 MAPK-dependent osmotic stimulation of NPR-A gene expression noted previously.
19	12082097	Previously, we showed that increased extracellular tonicity promotes increased type A natriuretic peptide receptor (NPR-A) expression through a p38 MAPKbeta pathway in inner medullary collecting duct cells.
20	12082097	The endothelial and inducible nitric-oxide synthase (eNOS and iNOS respectively) genes are also expressed in this nephron segment and are thought to play a role in regulating urinary sodium concentration.
21	12082097	We sought to determine whether changes in tonicity might regulate NOS gene expression, and if so, whether these latter changes might be linked mechanistically to the increase in NPR-A gene expression.
22	12082097	Increased extracellular tonicity effected a time-dependent reduction in eNOS and iNOS protein levels, eNOS mRNA levels, and eNOS gene promoter activity over the first 8 h of the incubation.
23	12082097	The decrease in eNOS expression was signaled in large part through a p38 MAPK-dependent mechanism.
24	12082097	Reduction in eNOS expression together with the concomitant decline in intracellular cyclic GMP levels appears to account for a significant portion of the p38 MAPK-dependent osmotic stimulation of NPR-A gene expression noted previously.
25	12082097	Previously, we showed that increased extracellular tonicity promotes increased type A natriuretic peptide receptor (NPR-A) expression through a p38 MAPKbeta pathway in inner medullary collecting duct cells.
26	12082097	The endothelial and inducible nitric-oxide synthase (eNOS and iNOS respectively) genes are also expressed in this nephron segment and are thought to play a role in regulating urinary sodium concentration.
27	12082097	We sought to determine whether changes in tonicity might regulate NOS gene expression, and if so, whether these latter changes might be linked mechanistically to the increase in NPR-A gene expression.
28	12082097	Increased extracellular tonicity effected a time-dependent reduction in eNOS and iNOS protein levels, eNOS mRNA levels, and eNOS gene promoter activity over the first 8 h of the incubation.
29	12082097	The decrease in eNOS expression was signaled in large part through a p38 MAPK-dependent mechanism.
30	12082097	Reduction in eNOS expression together with the concomitant decline in intracellular cyclic GMP levels appears to account for a significant portion of the p38 MAPK-dependent osmotic stimulation of NPR-A gene expression noted previously.
31	12623978	Endothelin inhibits NPR-A and stimulates eNOS gene expression in rat IMCD cells.
32	12623978	We have shown in previous studies that high extracellular tonicity is associated with increased expression of the type A natriuretic peptide receptor (NPR-A) and reduced expression of the endothelial NO synthase (eNOS) gene in cultured rat inner-medullary collecting duct cells.
33	12623978	We asked whether endothelin might play a role in the control of basal or osmotically regulated NPR-A or eNOS gene expression in these cells.
34	12623978	Although exogenous endothelin had little or no effect on basal expression of eNOS mRNA or protein or NPR-A gene expression, both the type A (BQ610) and type B (IRL1038) endothelin receptor antagonists proved capable of reducing eNOS mRNA and protein expression, and increasing levels of the NPR-A mRNA.
35	12623978	Increased extracellular tonicity reduced endothelin mRNA accumulation in these cells (approximately 15% of control levels); however, exogenous endothelin failed to normalize osmotically increased NPR-A activity or expression, or osmotically suppressed eNOS expression.
36	12623978	Endothelin inhibits NPR-A and stimulates eNOS gene expression in rat IMCD cells.
37	12623978	We have shown in previous studies that high extracellular tonicity is associated with increased expression of the type A natriuretic peptide receptor (NPR-A) and reduced expression of the endothelial NO synthase (eNOS) gene in cultured rat inner-medullary collecting duct cells.
38	12623978	We asked whether endothelin might play a role in the control of basal or osmotically regulated NPR-A or eNOS gene expression in these cells.
39	12623978	Although exogenous endothelin had little or no effect on basal expression of eNOS mRNA or protein or NPR-A gene expression, both the type A (BQ610) and type B (IRL1038) endothelin receptor antagonists proved capable of reducing eNOS mRNA and protein expression, and increasing levels of the NPR-A mRNA.
40	12623978	Increased extracellular tonicity reduced endothelin mRNA accumulation in these cells (approximately 15% of control levels); however, exogenous endothelin failed to normalize osmotically increased NPR-A activity or expression, or osmotically suppressed eNOS expression.
41	12623978	Endothelin inhibits NPR-A and stimulates eNOS gene expression in rat IMCD cells.
42	12623978	We have shown in previous studies that high extracellular tonicity is associated with increased expression of the type A natriuretic peptide receptor (NPR-A) and reduced expression of the endothelial NO synthase (eNOS) gene in cultured rat inner-medullary collecting duct cells.
43	12623978	We asked whether endothelin might play a role in the control of basal or osmotically regulated NPR-A or eNOS gene expression in these cells.
44	12623978	Although exogenous endothelin had little or no effect on basal expression of eNOS mRNA or protein or NPR-A gene expression, both the type A (BQ610) and type B (IRL1038) endothelin receptor antagonists proved capable of reducing eNOS mRNA and protein expression, and increasing levels of the NPR-A mRNA.
45	12623978	Increased extracellular tonicity reduced endothelin mRNA accumulation in these cells (approximately 15% of control levels); however, exogenous endothelin failed to normalize osmotically increased NPR-A activity or expression, or osmotically suppressed eNOS expression.
46	12623978	Endothelin inhibits NPR-A and stimulates eNOS gene expression in rat IMCD cells.
47	12623978	We have shown in previous studies that high extracellular tonicity is associated with increased expression of the type A natriuretic peptide receptor (NPR-A) and reduced expression of the endothelial NO synthase (eNOS) gene in cultured rat inner-medullary collecting duct cells.
48	12623978	We asked whether endothelin might play a role in the control of basal or osmotically regulated NPR-A or eNOS gene expression in these cells.
49	12623978	Although exogenous endothelin had little or no effect on basal expression of eNOS mRNA or protein or NPR-A gene expression, both the type A (BQ610) and type B (IRL1038) endothelin receptor antagonists proved capable of reducing eNOS mRNA and protein expression, and increasing levels of the NPR-A mRNA.
50	12623978	Increased extracellular tonicity reduced endothelin mRNA accumulation in these cells (approximately 15% of control levels); however, exogenous endothelin failed to normalize osmotically increased NPR-A activity or expression, or osmotically suppressed eNOS expression.
51	12623978	Endothelin inhibits NPR-A and stimulates eNOS gene expression in rat IMCD cells.
52	12623978	We have shown in previous studies that high extracellular tonicity is associated with increased expression of the type A natriuretic peptide receptor (NPR-A) and reduced expression of the endothelial NO synthase (eNOS) gene in cultured rat inner-medullary collecting duct cells.
53	12623978	We asked whether endothelin might play a role in the control of basal or osmotically regulated NPR-A or eNOS gene expression in these cells.
54	12623978	Although exogenous endothelin had little or no effect on basal expression of eNOS mRNA or protein or NPR-A gene expression, both the type A (BQ610) and type B (IRL1038) endothelin receptor antagonists proved capable of reducing eNOS mRNA and protein expression, and increasing levels of the NPR-A mRNA.
55	12623978	Increased extracellular tonicity reduced endothelin mRNA accumulation in these cells (approximately 15% of control levels); however, exogenous endothelin failed to normalize osmotically increased NPR-A activity or expression, or osmotically suppressed eNOS expression.
56	15007040	Sgk1 mediates osmotic induction of NPR-A gene in rat inner medullary collecting duct cells.
57	15007040	We have shown previously that increased extracellular osmolality stimulates expression and promoter activity of the type A natriuretic peptide receptor (NPR-A) gene in rat inner medullary collecting duct (IMCD) cells through a mechanism that involves activation of p38 mitogen-activated protein kinase (MAPK).
58	15007040	The Sgk1 induction was almost completely inhibited by the p38 MAPK inhibitor SB203580, indicating that NaCl activates Sgk1 through the p38 MAPK pathway.
59	15007040	Transient transfection of a mouse Sgk1 expression vector along with a -1590 NPR-A luciferase reporter resulted in an approximately 3-fold increment in reporter activity, which was significantly reduced by cotransfection with a kinase-dead Sgk1 mutant.
60	15007040	Neither Sgk1 nor the kinase-dead mutant had any effect on endothelial nitric oxide synthase (eNOS) promoter activity, and the Sgk1 mutant and 8-bromo-cyclic guanosine monophosphate were, to some degree, additive in reducing osmotically stimulated NPR-A promoter activity.
61	15007040	Collectively, these data imply that Sgk1 operates over an eNOS-independent, p38 MAPK-dependent pathway in mediating osmotic induction of the NPR-A gene promoter.
62	15007040	Sgk1 mediates osmotic induction of NPR-A gene in rat inner medullary collecting duct cells.
63	15007040	We have shown previously that increased extracellular osmolality stimulates expression and promoter activity of the type A natriuretic peptide receptor (NPR-A) gene in rat inner medullary collecting duct (IMCD) cells through a mechanism that involves activation of p38 mitogen-activated protein kinase (MAPK).
64	15007040	The Sgk1 induction was almost completely inhibited by the p38 MAPK inhibitor SB203580, indicating that NaCl activates Sgk1 through the p38 MAPK pathway.
65	15007040	Transient transfection of a mouse Sgk1 expression vector along with a -1590 NPR-A luciferase reporter resulted in an approximately 3-fold increment in reporter activity, which was significantly reduced by cotransfection with a kinase-dead Sgk1 mutant.
66	15007040	Neither Sgk1 nor the kinase-dead mutant had any effect on endothelial nitric oxide synthase (eNOS) promoter activity, and the Sgk1 mutant and 8-bromo-cyclic guanosine monophosphate were, to some degree, additive in reducing osmotically stimulated NPR-A promoter activity.
67	15007040	Collectively, these data imply that Sgk1 operates over an eNOS-independent, p38 MAPK-dependent pathway in mediating osmotic induction of the NPR-A gene promoter.
68	15007040	Sgk1 mediates osmotic induction of NPR-A gene in rat inner medullary collecting duct cells.
69	15007040	We have shown previously that increased extracellular osmolality stimulates expression and promoter activity of the type A natriuretic peptide receptor (NPR-A) gene in rat inner medullary collecting duct (IMCD) cells through a mechanism that involves activation of p38 mitogen-activated protein kinase (MAPK).
70	15007040	The Sgk1 induction was almost completely inhibited by the p38 MAPK inhibitor SB203580, indicating that NaCl activates Sgk1 through the p38 MAPK pathway.
71	15007040	Transient transfection of a mouse Sgk1 expression vector along with a -1590 NPR-A luciferase reporter resulted in an approximately 3-fold increment in reporter activity, which was significantly reduced by cotransfection with a kinase-dead Sgk1 mutant.
72	15007040	Neither Sgk1 nor the kinase-dead mutant had any effect on endothelial nitric oxide synthase (eNOS) promoter activity, and the Sgk1 mutant and 8-bromo-cyclic guanosine monophosphate were, to some degree, additive in reducing osmotically stimulated NPR-A promoter activity.
73	15007040	Collectively, these data imply that Sgk1 operates over an eNOS-independent, p38 MAPK-dependent pathway in mediating osmotic induction of the NPR-A gene promoter.
74	15007040	Sgk1 mediates osmotic induction of NPR-A gene in rat inner medullary collecting duct cells.
75	15007040	We have shown previously that increased extracellular osmolality stimulates expression and promoter activity of the type A natriuretic peptide receptor (NPR-A) gene in rat inner medullary collecting duct (IMCD) cells through a mechanism that involves activation of p38 mitogen-activated protein kinase (MAPK).
76	15007040	The Sgk1 induction was almost completely inhibited by the p38 MAPK inhibitor SB203580, indicating that NaCl activates Sgk1 through the p38 MAPK pathway.
77	15007040	Transient transfection of a mouse Sgk1 expression vector along with a -1590 NPR-A luciferase reporter resulted in an approximately 3-fold increment in reporter activity, which was significantly reduced by cotransfection with a kinase-dead Sgk1 mutant.
78	15007040	Neither Sgk1 nor the kinase-dead mutant had any effect on endothelial nitric oxide synthase (eNOS) promoter activity, and the Sgk1 mutant and 8-bromo-cyclic guanosine monophosphate were, to some degree, additive in reducing osmotically stimulated NPR-A promoter activity.
79	15007040	Collectively, these data imply that Sgk1 operates over an eNOS-independent, p38 MAPK-dependent pathway in mediating osmotic induction of the NPR-A gene promoter.
80	15007040	Sgk1 mediates osmotic induction of NPR-A gene in rat inner medullary collecting duct cells.
81	15007040	We have shown previously that increased extracellular osmolality stimulates expression and promoter activity of the type A natriuretic peptide receptor (NPR-A) gene in rat inner medullary collecting duct (IMCD) cells through a mechanism that involves activation of p38 mitogen-activated protein kinase (MAPK).
82	15007040	The Sgk1 induction was almost completely inhibited by the p38 MAPK inhibitor SB203580, indicating that NaCl activates Sgk1 through the p38 MAPK pathway.
83	15007040	Transient transfection of a mouse Sgk1 expression vector along with a -1590 NPR-A luciferase reporter resulted in an approximately 3-fold increment in reporter activity, which was significantly reduced by cotransfection with a kinase-dead Sgk1 mutant.
84	15007040	Neither Sgk1 nor the kinase-dead mutant had any effect on endothelial nitric oxide synthase (eNOS) promoter activity, and the Sgk1 mutant and 8-bromo-cyclic guanosine monophosphate were, to some degree, additive in reducing osmotically stimulated NPR-A promoter activity.
85	15007040	Collectively, these data imply that Sgk1 operates over an eNOS-independent, p38 MAPK-dependent pathway in mediating osmotic induction of the NPR-A gene promoter.
86	15126246	Water deprivation increased the B(max) of glomerular binding sites for ANP(1-28) and C-type natriuretic peptide (CNP)(1-22) without modifying their affinity, an effect that was prevented in the presence of C-atrial natriuretic factor (C-ANF), suggesting that natriuretic peptide receptor-C (NPR-C) binding sites might be enhanced.
87	15126246	Our results indicate that ANP(1-28), CNP(1-22), and C-ANF inhibit cAMP synthesis directly stimulated by forskolin or by the physiological agonists histamine and 5-hydroxytryptamine.
88	15126246	In addition, using affinity cross-linking studies we have observed that water deprivation increases the expression of the 67-kDa NPR-C-like protein, and HS-142, which binds to NPR-A and the 77-kDa NPR-C-like but not the 67-kDa protein, reduced ligand internalization without affecting cAMP inhibition by ANP(1-28).
89	15590756	The increase in NPR-A expression was associated with an increase in NPR-A gene promoter activity that was critically dependent on the presence of a functional VD receptor response element located approximately 495 bp upstream from the transcription start site of the gene.
90	15590756	This element was associated with the VD receptor/retinoid X receptor complex in vitro.
91	16109786	The C-type natriuretic (CNP) peptide signals through the type B natriuretic peptide receptor (NPR-B) in vascular smooth muscle cells to activate the particulate guanylyl cyclase activity intrinsic to that receptor and raise cellular cyclic GMP levels.
92	16109786	In the present study, we demonstrate that CNP down-regulates the expression of this receptor leading to a reduction in NPR-B activity.
93	16109786	Pretreatment of rat aortic smooth muscle cells with CNP reduces NPR-B activity, NPR-B protein levels, NPR2 (NPR-B gene) mRNA levels, and NPR2 promoter activity.
94	16109786	Atrial natriuretic peptide, which signals through the type A natriuretic peptide receptor (NPR-A) to increase cyclic GMP levels in these cells, also reduced NPR-B mRNA levels and inhibited NPR-B promoter activity; however, this inhibition was not additive with that produced by CNP, implying that the two ligands traffic over a common signal transduction pathway.
95	16904201	Atrial natriuretic peptide receptor types A (NPR-A) and C (NPR-C) binding properties and functional characteristics in renal glomeruli have been investigated in deoxycorticosterone acetate (DOCA)-treated hypertensive Wistar-Kyoto (WKY) rats and their respective controls.
96	16904201	We found that DOCA administration had no significant effect on the maximum binding capacity or the affinity of renal NPR-A and NPR-C.
97	16904201	Our results indicate that the cAMP production by NPR-C is not altered in DOCA-induced hypertension, since ANP(1-28), CNP(1-22) and C-ANP, which specifically bind to NPR-C, show a similar inhibitory effect on cAMP production stimulated by the physiological agonist histamine in glomeruli from DOCA-treated rats and controls.
98	16904201	Finally, we have found that DOCA-induced hypertension does not modify NPR-A or NPR-C expression in rat glomerular membranes.
99	16904201	These findings indicate that NPR-A and NPR-C binding properties and NPR-C-mediated inhibition of cAMP generation remain unaltered in DOCA-treated rats.
100	16904201	Atrial natriuretic peptide receptor types A (NPR-A) and C (NPR-C) binding properties and functional characteristics in renal glomeruli have been investigated in deoxycorticosterone acetate (DOCA)-treated hypertensive Wistar-Kyoto (WKY) rats and their respective controls.
101	16904201	We found that DOCA administration had no significant effect on the maximum binding capacity or the affinity of renal NPR-A and NPR-C.
102	16904201	Our results indicate that the cAMP production by NPR-C is not altered in DOCA-induced hypertension, since ANP(1-28), CNP(1-22) and C-ANP, which specifically bind to NPR-C, show a similar inhibitory effect on cAMP production stimulated by the physiological agonist histamine in glomeruli from DOCA-treated rats and controls.
103	16904201	Finally, we have found that DOCA-induced hypertension does not modify NPR-A or NPR-C expression in rat glomerular membranes.
104	16904201	These findings indicate that NPR-A and NPR-C binding properties and NPR-C-mediated inhibition of cAMP generation remain unaltered in DOCA-treated rats.
105	16904201	Atrial natriuretic peptide receptor types A (NPR-A) and C (NPR-C) binding properties and functional characteristics in renal glomeruli have been investigated in deoxycorticosterone acetate (DOCA)-treated hypertensive Wistar-Kyoto (WKY) rats and their respective controls.
106	16904201	We found that DOCA administration had no significant effect on the maximum binding capacity or the affinity of renal NPR-A and NPR-C.
107	16904201	Our results indicate that the cAMP production by NPR-C is not altered in DOCA-induced hypertension, since ANP(1-28), CNP(1-22) and C-ANP, which specifically bind to NPR-C, show a similar inhibitory effect on cAMP production stimulated by the physiological agonist histamine in glomeruli from DOCA-treated rats and controls.
108	16904201	Finally, we have found that DOCA-induced hypertension does not modify NPR-A or NPR-C expression in rat glomerular membranes.
109	16904201	These findings indicate that NPR-A and NPR-C binding properties and NPR-C-mediated inhibition of cAMP generation remain unaltered in DOCA-treated rats.
110	16904201	Atrial natriuretic peptide receptor types A (NPR-A) and C (NPR-C) binding properties and functional characteristics in renal glomeruli have been investigated in deoxycorticosterone acetate (DOCA)-treated hypertensive Wistar-Kyoto (WKY) rats and their respective controls.
111	16904201	We found that DOCA administration had no significant effect on the maximum binding capacity or the affinity of renal NPR-A and NPR-C.
112	16904201	Our results indicate that the cAMP production by NPR-C is not altered in DOCA-induced hypertension, since ANP(1-28), CNP(1-22) and C-ANP, which specifically bind to NPR-C, show a similar inhibitory effect on cAMP production stimulated by the physiological agonist histamine in glomeruli from DOCA-treated rats and controls.
113	16904201	Finally, we have found that DOCA-induced hypertension does not modify NPR-A or NPR-C expression in rat glomerular membranes.
114	16904201	These findings indicate that NPR-A and NPR-C binding properties and NPR-C-mediated inhibition of cAMP generation remain unaltered in DOCA-treated rats.
115	17033090	Atrial natriuretic peptide (ANP) regulates blood pressure mainly through the occupation of the guanylyl cyclase-coupled receptor NPR-A, which requires ATP interaction for maximal activation.
116	17033090	In the presence of ATP, NPR-A showed higher affinity for ANP(1-28) and lower Bmax.
117	17033090	Atrial natriuretic peptide (ANP) regulates blood pressure mainly through the occupation of the guanylyl cyclase-coupled receptor NPR-A, which requires ATP interaction for maximal activation.
118	17033090	In the presence of ATP, NPR-A showed higher affinity for ANP(1-28) and lower Bmax.
119	17440494	Introduction of small interfering RNA directed against the vitamin D receptor into the IMCD cells resulted in decreased natriuretic peptide receptor-A gene promoter activity and protein.
120	19165164	However, the expression levels of two transcripts involved in vasodilation (natriuretic peptide receptor A/guanylate cyclase A (NPRA) and endothelial nitric oxide synthase (eNOS)) were positively associated with postprandial ATBF (r = 0.53 and r = 0.55, P < 0.01, respectively).
121	19165164	Although BMI was negatively related to the mRNA content of NPRA and eNOS (r = -0.78 and r = -0.63, P < 0.01, respectively), the strong associations found between postprandial ATBF and the two transcripts were not affected by obesity.
122	19165164	This study demonstrates for the first time that ATBF responsiveness to nutrient intake is related to the transcription of two genes expressed in adipose tissue and directly involved in vasodilatory actions (eNOS and NPRA), suggesting that part of the regulation of ATBF is at a transcriptional level.
123	19165164	However, the expression levels of two transcripts involved in vasodilation (natriuretic peptide receptor A/guanylate cyclase A (NPRA) and endothelial nitric oxide synthase (eNOS)) were positively associated with postprandial ATBF (r = 0.53 and r = 0.55, P < 0.01, respectively).
124	19165164	Although BMI was negatively related to the mRNA content of NPRA and eNOS (r = -0.78 and r = -0.63, P < 0.01, respectively), the strong associations found between postprandial ATBF and the two transcripts were not affected by obesity.
125	19165164	This study demonstrates for the first time that ATBF responsiveness to nutrient intake is related to the transcription of two genes expressed in adipose tissue and directly involved in vasodilatory actions (eNOS and NPRA), suggesting that part of the regulation of ATBF is at a transcriptional level.
126	19165164	However, the expression levels of two transcripts involved in vasodilation (natriuretic peptide receptor A/guanylate cyclase A (NPRA) and endothelial nitric oxide synthase (eNOS)) were positively associated with postprandial ATBF (r = 0.53 and r = 0.55, P < 0.01, respectively).
127	19165164	Although BMI was negatively related to the mRNA content of NPRA and eNOS (r = -0.78 and r = -0.63, P < 0.01, respectively), the strong associations found between postprandial ATBF and the two transcripts were not affected by obesity.
128	19165164	This study demonstrates for the first time that ATBF responsiveness to nutrient intake is related to the transcription of two genes expressed in adipose tissue and directly involved in vasodilatory actions (eNOS and NPRA), suggesting that part of the regulation of ATBF is at a transcriptional level.
129	19436108	In vivo, water restriction of rats or mice led to increased urine osmolality, increased Sgk1 expression, increased expression of the type A natriuretic peptide receptor (NPR-A), and dehydration natriuresis.
130	19436108	In cultured rat renal medullary cells, siRNA-mediated Sgk1 knockdown blocked the osmotic induction of natriuretic peptide receptor 1 (Npr1) gene expression.
131	19436108	In vivo, water restriction of rats or mice led to increased urine osmolality, increased Sgk1 expression, increased expression of the type A natriuretic peptide receptor (NPR-A), and dehydration natriuresis.
132	19436108	In cultured rat renal medullary cells, siRNA-mediated Sgk1 knockdown blocked the osmotic induction of natriuretic peptide receptor 1 (Npr1) gene expression.
133	23352981	The results showed that the protein expression levels of c-Kit and membrane-bound stem cell factor (mSCF) in gastric smooth muscle layers were decreased in STZ-induced diabetic mice.
134	23352981	Pretreatment of the cultured gastric smooth muscle cells (GSMCs) with different concentration of CNP can significantly decrease the mSCF expression level. 8-Bromoguanosine-3',5'-cyclomo-nophosphate (8-Br-cGMP), a membrane permeable cGMP analog, mimicked the effect of CNP but not cANF (a specific NPR-C agonist).
135	23352981	These findings suggest that up-regulation of NPs/NPR-A, B/cGMP and NPs/NPR-C signaling pathways may be involved in diabetes-induced loss of gastric ICC.
136	23741625	Among the top 10 ranked DMRs, we identified several genes, including NPR1, PANK1, SCAND1, and GJA4, which are known to be associated with cardiometabolic traits.