Angiotensin II Enhances the Expression of Giα in A10 Cells (Smooth Muscle): Relationship with Adenylyl Cyclase Activity

Palaparti, Anuradha; Ge, Chang; Anand‐Srivastava, Madhu B.

doi:10.1006/abbi.1999.1153

Cited by 29 publications

(32 citation statements)

References 58 publications

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“…2A shows that peptides 1, 2, 3, and 4 of the cytoplasmic domain of the NPR-C receptor at 10 Ϫ7 M inhibited adenylyl cyclase activity by 40, 30, 35, and 36%, respectively, in rat heart particulate fractions. In addition, ANP-(99 -126), C-ANP-(4 -23), R37A, and angiotensin II, as reported earlier (3,26,30,36), also inhibited the enzyme activity by about 20 -25%. However, peptides X, Y, and Z did not inhibit adenylyl cyclase activity.…”

Section: Effect Of Different Fragments Of the Cytoplasmic Domain Of Nsupporting

confidence: 55%

Cytoplasmic Domain of Natriuretic Peptide Receptor C Constitutes Gi Activator Sequences That Inhibit Adenylyl Cyclase Activity

Pagano

Anand‐Srivastava

2001

Journal of Biological Chemistry

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We have recently demonstrated that a 37-amino acid peptide corresponding to the cytoplasmic domain of the natriuretic peptide receptor C (NPR-C) inhibited adenylyl cyclase activity via pertussis toxin (PT)-sensitive G i protein.In the present studies, we have used seven different peptide fragments of the cytoplasmic domain of the NPR-C receptor with complete, partial, or no G i activator sequence to examine their effects on adenylyl cyclase activity. The peptides used were KKYRITIER-RNH (peptide 1), RRNHQEESNIGK (peptide 2), HREL-REDSIRSH (peptide 3), RRNHQEESNIGKHRELR (peptide 4), QEESNIGK (peptide X), ITIERRNH (peptide Y), and ITIYKKRRNHRE (peptide Z). Peptides 1, 3, and 4 have complete G i activator sequences, whereas peptides 2 and Y have partial G i activator sequences with truncated carboxyl or amino terminus, respectively. Peptide X has no structural specificity, whereas peptide Z is the scrambled peptide control for peptide 1. Peptides 1, 3, and 4 inhibited adenylyl cyclase activity in a concentration-dependent manner with apparent K i between 0.1 and 1 nM; however, peptide 2 inhibited adenylyl cyclase activity with a higher K i of about 10 nM, and peptides X, Y, and Z were unable to inhibit adenylyl cyclase activity. The maximal inhibitions observed were between 30 and 40%. The inhibition of adenylyl cyclase activity by peptides 1-4 was absolutely dependent on the presence of guanine nucleotides and was completely attenuated by PT treatment. In addition, the stimulatory effects of isoproterenol, glucagon, and forskolin on adenylyl cyclase activity were inhibited to different degrees by these peptides. These results suggest that the small peptide fragments of the cytoplasmic domain of the NPR-C receptor containing 12 or 17 amino acids were sufficient to inhibit adenylyl cyclase activity through a PT-sensitive G i protein. The peptides having complete structural specificity of G i activator sequences at both amino and carboxyl termini were more potent to inhibit adenylyl cyclase activity as compared with the peptides having a truncated carboxyl terminus, whereas the truncation of the amino-terminal motif completely attenuates adenylyl cyclase inhibition.

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Section: Effect Of Different Fragments Of the Cytoplasmic Domain Of Nsupporting

confidence: 55%

Cytoplasmic Domain of Natriuretic Peptide Receptor C Constitutes Gi Activator Sequences That Inhibit Adenylyl Cyclase Activity

Pagano

Anand‐Srivastava

2001

Journal of Biological Chemistry

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“…In one study, ANG II administration downregulated G s ␣ protein in preglomerular arterioles in spontaneous hypertensive rats and upregulated the protein in control Wistar-Kyoto rats (45). However, other studies have found no interactions between ANG II and G s ␣ protein levels in the vascular system (1,11,34). The present study indicates that an interaction between ANG II and G s ␣ protein may exist in the kidney.…”

Section: Discussionmentioning

confidence: 42%

“…stimulates the expression of the inhibitory G proteins G i ␣-2 and G i ␣-3 (1,11,34,35,45), suggesting a role for these proteins in ureteral obstruction given that inhibitory G i ␣-2 protein is colocalized with the G s ␣ protein in the basolateral membrane of collecting duct principal cells (43).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II regulates V2 receptor and pAQP2 during ureteral obstruction

Jensen¹,

Bae²,

Fenton³

et al. 2009

American Journal of Physiology-Renal Physiology

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Release of bilateral ureteral obstruction (BUO) is associated with nephrogenic diabetes insipidus (NDI) and a reduced abundance of the vasopressin-regulated aquaporins. To evaluate the role of the vasopressin type 2 receptor (V2R), we determined V2R abundance in kidneys from rats subjected to 24-h BUO or 24-h unilateral ureteral obstruction (UUO) followed by 48-h release. Because angiotensin II type 1 (AT1) receptor blockade attenuates postobstructive polyuria and aquaporin-2 (AQP2) downregulation, we examined the effect of AT1 receptor blockade on AQP2 phosphorylated at serine 256 (pS256-AQP2) and V2 receptor complex abundance in kidney inner medulla (IM). Furthermore, cAMP generation in sodium fluoride- and forskolin-stimulated inner medullary membrane fractions was studied after release of BUO. V2R was significantly reduced to 12% of sham levels in IM and to 52% of sham levels in cortex and outer stripe of outer medulla (OSOM) from BUO rats. In UUO rats, V2R abundance in the obstructed kidney IM decreased to 35% of sham levels, whereas it was comparable to sham levels in the nonobstructed kidney IM. No significant change was observed in cortex and OSOM. AT1 receptor blockade attenuated V2R, pS256-AQP2, and G(s)alpha protein downregulation in IM and partially reversed the obstruction-induced inhibition of sodium fluoride- and forskolin-stimulated cAMP generation in inner medullary membrane fractions from BUO rats. In conclusion, V2R downregulation plays a pivotal role in development of NDI after release of BUO. In addition, we have shown that angiotensin II regulates the V2 receptor complex and pS256-AQP2 in postobstructive kidney IM, probably by stimulating cAMP generation.

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“…A complete attenuation of NPR-C-mediated inhibition of adenylyl cyclase with a partial downregulation of NPR-C (ϳ30%) after 6 h of SNAP treatment is in agreement with other studies showing that the inhibition of NPR-C expression by about 50% by NPR-C antisense (39) or by about 35% by pretreatment with C-ANP 4-23 (9) resulted in a complete attenuation of the NPR-C-mediated inhibition of adenylyl cyclase in A10 VSMCs and suggests that a postreceptor modification, such as an alteration in the levels of G i ␣ proteins that couple NPR-C to adenylyl cyclase, may also be responsible for the observed desensitization of adenylyl cyclase inhibition. In this regard, a relationship between the levels of G i ␣ proteins and functions has been reported by several investigators (6,8,9,38).…”

Section: Discussionmentioning

confidence: 77%

Nitric oxide attenuates the expression of natriuretic peptide receptor C and associated adenylyl cyclase signaling in aortic vascular smooth muscle cells: role of MAPK

Arejian

Li²,

Anand‐Srivastava³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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Arejian M, Li Y, Anand-Srivastava MB. Nitric oxide attenuates the expression of natriuretic peptide receptor C and associated adenylyl cyclase signaling in aortic vascular smooth muscle cells: role of MAPK. Am J Physiol Heart Circ Physiol 296: H1859 -H1867, 2009. First published February 27, 2009 doi:10.1152/ajpheart.01108.2008We have earlier shown that the treatment of A10 vascular smooth muscle cells with S-nitroso-N-acetyl-penicillamine (SNAP); nitric oxide donor (NO) for 24 h decreased the expression of natriuretic peptide receptor C (NPR-C) and adenylyl cyclase signaling. The present study was undertaken to examine the implication of different signaling mechanisms in a NO-induced response. The treatment of A10 vascular smooth muscle cells with SNAP decreased the expression of NPR-C and Gi␣ proteins in a time-dependent manner. The expression of Gi␣ proteins was decreased at 6 h, whereas the expression of NPR-C was attenuated at 2 h. The NPR-C-mediated inhibition of adenylyl cyclase was attenuated (ϳ50%) after 2 h of treatment and was completely abolished after 6 h of treatment. The decreased expression of NPR-C and NPR-C-mediated attenuation of adenylyl cyclase after 2 h of treatment was reversed to control levels by PD-98059, a MEK inhibitor. SNAP also modulated the ERK1/2 phosphorylation in a time-dependent manner; an increase was observed up to 2 h, and, thereafter, the ERK1/2 phosphorylation was decreased. On the other hand, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and KT-5823 inhibitor of soluble guanylyl cyclase and protein kinase G, respectively, and Mn(III)tetrakis(4-benzoic acid)porphyrin, a scavenger of peroxynitrite, were unable to restore the SNAPinduced decreased expression of NPR-C protein and increased ERK1/2 phosphorylation to control levels. However, the decreased levels of phosphorylated ERK1/2 and Gi␣ proteins were restored to control levels by 8-bromo-cAMP. These results indicate that a temporal relationship follows between a NO-induced decreased expression of NPR-C and Gi␣ proteins. The decreased expression of NPR-C is mediated through cGMP-independent but MAPK-dependent pathway, whereas NO-induced decreased levels of cAMP may contribute to the decreased activation of MAPK and thereby decreased the expression of Gi␣ proteins. G proteins; mitogen-activated protein kinase NATRIURETIC PEPTIDES (NPs) are a family of three peptide hormones termed atrial NP (ANP), brain NP, and C-type NP, all of which are produced in mammalian hearts, including human hearts (31). ANP regulates a variety of physiological parameters, including blood pressure (7), by interacting with receptors on plasma membrane either to generate second messengers such as cAMP (2, 3) and cGMP (20,48) or to affect ion channels (7). Three types of NP receptors (NPRs) have been cloned; NPR-A (16) and NPR-B (15) subtypes are membranebound guanylate cyclases (130-180 kDa) that mediate the biological actions of NP through a regulation of intracellular cGMP levels (7), whereas NPR-C (4, 17) is a disulfide-bridged homodimer of 67-an...

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Angiotensin II Enhances the Expression of Giα in A10 Cells (Smooth Muscle): Relationship with Adenylyl Cyclase Activity

Cited by 29 publications

References 58 publications

Cytoplasmic Domain of Natriuretic Peptide Receptor C Constitutes Gi Activator Sequences That Inhibit Adenylyl Cyclase Activity

Cytoplasmic Domain of Natriuretic Peptide Receptor C Constitutes Gi Activator Sequences That Inhibit Adenylyl Cyclase Activity

Angiotensin II regulates V2 receptor and pAQP2 during ureteral obstruction

Nitric oxide attenuates the expression of natriuretic peptide receptor C and associated adenylyl cyclase signaling in aortic vascular smooth muscle cells: role of MAPK

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