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ANG — ATP5O

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Muscella et al., J Neurochem 2000 : These results indicate that the activity of Na+, K ( + ) -ATPase in astrocytes is increased by physiological concentrations of Ang II and that the AT1 receptor subtype mediates the Na+, K ( + ) -ATPase response to Ang II via PKC-delta activation
Caruso-Neves et al., Biochim Biophys Acta 2000 : The Na+-ATPase , insensitive to ouabain, but sensitive to furosemide, is stimulated by Ang- ( 1-7 ) ( 68 % by 10 ( -9 ) M ), in a dose dependent manner
Zhang et al., American journal of physiology. Renal physiology 2001 : Beginning at 10 ( -13 ) M, ANG II increased Na+-K+-ATPase in freshly isolated rat proximal tubules to a maximum stimulation at 10 ( -11 ) M of 1.43 +/- 0.08-fold above control ... These data suggest that the NO/cGMP signaling pathway serves as a negative component in the regulation of Na+-K+-ATPase activity by ANG II
Muscella et al., J Endocrinol 2002 (Breast Neoplasms) : Both Na+/K+ATPase activation and stimulation of proliferation were mediated by binding of Ang II to AT1, as the effects were completely blocked by DuP 753, a specific AT1 antagonist
Hou et al., Am J Physiol Cell Physiol 2002 : In summary, these studies suggest that ANG II causes H ( + ) -ATPase inhibition and an increase of cell sodium due to activation of Na ( + ) /H ( + ) exchange
Zhang et al., Nitric Oxide 2002 : Studies were designed to examine the role of NO-derived oxidants and peroxynitrite on the regulation of Na ( + ), K ( + ) -ATPase activity by angiotensin II (ANG II) freshly isolated rat proximal tubules
Rangel et al., Biochim Biophys Acta 2002 : Recently, our group described an AT(1) mediated direct stimulatory effect of angiotensin II (Ang II) on the Na ( + ) -ATPase activity of proximal tubules basolateral membranes (BLM) [ Am. J. Physiol. 248 ( 1985 ) F621 ] ... Data in the present report suggest the participation of a protein kinase C ( PKC ) in the molecular mechanism of Ang II-mediated stimulation of the Na ( + ) -ATPase activity due to the following observations : ( i ) the stimulation of protein phosphorylation in BLM, induced by Ang II, is mimicked by the PKC activator TPA, and is completely reversed by the specific PKC inhibitor, calphostin C ; ( ii ) the Na ( + ) -ATPase activity is stimulated by Ang II and TPA in the same magnitude, being these effects abolished by the use of the PKC inhibitors, calphostin C and sphingosine ; ( iii ) the Na ( + ) -ATPase activity is activated by catalytic subunit of PKC ( PKC-M ), in a similar and nonadditive manner to Ang II ; and ( iv ) Ang II stimulates the phosphorylation of MARCKS, a specific substrate for PKC
Isenovic et al., Endocrinology 2004 (MAP Kinase Signaling System) : This investigation used primary cultured rat vascular smooth muscle cells to examine angiotensin II (Ang II) regulation of Na ( + ), K ( + ) -ATPase ( Na ( + ) pump ) activity, and Na ( + ) pump alpha ( 1 ) - and beta ( 1 ) -subunit gene transcription
Yingst et al., American journal of physiology. Renal physiology 2004 (Hypertension, Renal) : From these data, we show that ANG II directly stimulates Na-K-ATPase activity at rate limiting concentrations of intracellular sodium ... Thus ANG II rapidly stimulated the activity of Na-K-ATPase in 2 min or less by a mechanism that could involve changes in phosphorylation and conformation of Na-K-ATPase
De Souza et al., Regul Pept 2004 : Ang II and Ang- ( 1-7 ) inhibit the Na+ -ATPase activity in a dose dependent manner ( from 10 ( -11 ) to 10 ( -5 ) M ), with maximal effect obtained at 10 ( -7 ) M for both peptides
Rangel et al., Regul Pept 2005 : In the present paper, we study the involvement of PI-PLCbeta on the stimulatory effect of angiotensin II (Ang II) on the proximal tubule Na+-ATPase activity
Muscella et al., J Cell Physiol 2005 (Breast Neoplasms) : Here, using serum starved MCF-7 cells, we have demonstrated that the effect of Ang II on the Na+/K+ATPase activity was inhibited by a synthetic myristoylated peptide with sequences based on the endogenous PKC-zeta pseudosubstrate region ( zeta-PS ) and by high doses of GF109203X, inhibitor of PKCs
Lara et al., Biochem J 2006 : In this condition, Ang- ( 1-7 ) at 0.1 nM inhibited the Na+-ATPase activity of the proximal tubule by 54 % ... Furthermore, it was observed that the inhibitory effect of Ang- ( 1-7 ) on the Na+-ATPase activity was completely reversed by 0.1 microM LY83583, an inhibitor of guanylate cyclase, and by 2 muM KT5823, a PKG ( protein kinase G ) inhibitor, and was mimicked by 10 nM d-cGMP ( dibutyryl cGMP ) ... Taken together, these data indicate that Ang- ( 1-7 ) inhibits the proximal tubule Na+-ATPase by interaction with the AT2 receptor that subsequently activates the G ( i/o ) protein/cGMP/PKG pathway
Carraro-Lacroix et al., Pflugers Arch 2006 : In the present study, we investigated the signaling pathways involved in the effects of ANG II on H ( + ) -ATPase activity and on the cytosolic free calcium concentration in immortalized rat proximal tubule cells, a permanent cell line derived from rat proximal tubules
Lara et al., Exp Physiol 2008 : The stimulatory effects of Ang ( 1-7 ) and PMA on Na+-ATPase activity are similar, non-additive and reversed by calphostin C, a specific inhibitor of PKC ... Our results show that the stimulatory effect of Ang ( 1-7 ) on Na+-ATPase activity through AT1R involves a Gq protein-phosphatidyl inositol-phospholipase Cbeta ( PI-PLCbeta ) pathway because : ( 1 ) the effect was reversed by GDPbetaS, a non-hydrolysable GDP analogue, and by a monoclonal Gq protein antibody ; ( 2 ) the effect was similar and not additive to that of GTPgammaS, a non-hydrolysable GTP analogue ; ( 3 ) Ang ( 1-7 ) induced a rapid decrease ( 30 s ) in phosphatidylinositol 4,5-bisphosphate levels, a PI-PLCbeta substrate ; and ( 4 ) U73122, a specific inhibitor of PI-PLCbeta, abolished Ang ( 1-7 ) -induced stimulation of Na+-ATPase activity
Carraro-Lacroix et al., Pflugers Arch 2009 : Long-term effects of angiotensin II (Ang II) on vacuolar H ( + ) -ATPase were studied in a SV40 transformed cell line derived from rat proximal tubules ( IRPTC )
De Souza et al., Biochim Biophys Acta 2010 : The results indicate that PKC could be the final target and an integrator molecule of different signaling pathways triggered by Ang II, which could explain the sustained activation of Na ( + ) -ATPase by Ang II
Choi et al., Nephron. Physiology 2010 : By this indirect way, ANG II stimulates renal Na ( + ), K ( + ) -ATPase activity through DA intracellular reduction
Javkhedkar et al., American journal of physiology. Renal physiology 2012 : In conclusion, at a high concentration ANG II ( µM ) activates renal NO signaling, which prevents stimulation of Na-K-ATPase in WKY rats
Neusser et al., J Hypertens 1994 (Hypertension) : The different effects of thapsigargin, a selective Ca-ATPase inhibitor , and of angiotensin II (Ang II) on the calcium storage pools were investigated
Marsigliante et al., J Mol Endocrinol 1997 : The data suggest that adaptation to sea water significantly increases Ang II-R concentration in the chloride cell and, together with the effects of Ang II on Na+/K+ATPase activity, suggest a role for this hormone in gill NaCl retention
Muscella et al., J Endocrinol 1997 : These results suggest that the AT1 receptor subtype mediates the Na+/K+ ATPase response to Ang II in these cells
López Ordieres et al., Regul Pept 1998 : In the presence of 10 ( -6 ) M Ang- ( 1-7 ), total ( Na, K+, Mg2+ ) -ATPase activity decreased 31 % in rat atrium and 13 % in sheep atrium but was unmodified in sheep liver, rat ventricle or crude brain membranes