Angiotensin II Regulation of Renal Dopamine Uptake and Na+,K+-ATPase Activity

2009 ◽  
Vol 111 (4) ◽  
pp. p55-p60 ◽  
Author(s):  
Marcelo R. Choi ◽  
Cecilia Medici ◽  
Mariela M. Gironacci ◽  
Alicia H. Correa ◽  
Belisario E. Fernández
Keyword(s):  
Angiotensin Ii ◽  
Atpase Activity ◽  
Dopamine Uptake ◽  
Renal Dopamine

scholarly journals Regulation of Dopamine Uptake by Vasoactive Peptides in the Kidney

Scientifica ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-12
Author(s):  
N. L. Rukavina Mikusic ◽  
N. M. Kouyoumdzian ◽  
E. Rouvier ◽  
M. M. Gironacci ◽  
J. E. Toblli ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Inhibitory Effect ◽  
Renal Tissue ◽  
Dopamine Uptake ◽  
Tubular Cells ◽  
Vasoactive Peptides ◽  
Renal Dopamine ◽  
Atpase Inhibition ◽  
Sodium Handling

Considering the key role of renal dopamine in tubular sodium handling, we hypothesized that c-type natriuretic peptide (CNP) and Ang-(1-7) may regulate renal dopamine availability in tubular cells, contributing to Na+, K+-ATPase inhibition. Present results show that CNP did not affect either3H-dopamine uptake in renal tissue or Na+, K+-ATPase activity; meanwhile, Ang-(1-7) was able to increase3H-dopamine uptake and decreased Na+, K+-ATPase activity in renal cortex. Ang-(1-7) and dopamine together decreased further Na+, K+-ATPase activity showing an additive effect on the sodium pump. In addition, hydrocortisone reversed Ang-(1-7)-dopamine overinhibition on the enzyme, suggesting that this inhibition is closely related to Ang-(1-7) stimulation on renal dopamine uptake. Both anantin and cANP (4-23-amide) did not modify CNP effects on3H-dopamine uptake by tubular cells. The Mas receptor antagonist, A-779, blocked the increase elicited by Ang-(1-7) on3H-dopamine uptake. The stimulatory uptake induced by Ang-(1-7) was even more pronounced in the presence of losartan, suggesting an inhibitory effect of Ang-(1-7) on AT1 receptors on3H-dopamine uptake. By increasing dopamine bioavailability in tubular cells, Ang-(1-7) enhances Na+, K+-ATPase activity inhibition, contributing to its natriuretic and diuretic effects.

Abstract 341: Synergistic Effects of Renal Dopamine and Gastrin Receptors in Hypertension

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Yue Chen ◽  
Shuo Zhen ◽  
Laureano Asico ◽  
Pedro Jose ◽  
Chunyu Zeng
Keyword(s):  
Atpase Activity ◽  
Sodium Excretion ◽  
Synergistic Effects ◽  
Inhibitory Effect ◽  
Receptor Interaction ◽  
Gastrin Receptor ◽  
Wky Rats ◽  
Link Type ◽  
Renal Dopamine ◽  
Stimulation Of

Oral NaCl produces stronger natriuresis and diuresis as compared with venous infusion of same amount of NaCl, indicating the existence of renal-gastric axis. Although numerous hormones are secreted in gastrointestinal tract, gastrin is evident one due to its natriuretic effects and taken-up by the renal proximal tubule (RPT) cells. We hypothesize that there is an interaction between gastrin and dopamine receptor in kidney, which synergistically increases sodium excretion, the impaired interaction would be involved in the pathogenesis of hypertension. In WKY rats, infusion of gastrin, via renal artery, induced natriuresis and diuresis, which was blocked in the presence of CI988, a gastrin receptor blocker. Similarly, the natriuretic and diuretic effect of fenoldopam, a D1-like receptor agonist, was blocked by the D1-like receptor antagonist, SCH23390 , indicating that gastrin and fenoldopam, via individual receptor, play natriuretic and diuretic effects. Our further study found that lower dosages of gastrin or fenoldopam could not induce natriuresis and diuresis alone, while putting together induced natriuretic and diuretic effects. The above-mentioned effects were lost in SHRs. We also found, in the presence of SCH23390 , gastrin-mediated natriuresis and diuresis was partially blocked. Similarly, in the presence of CI988, the natriuretic and diuretic effects of fenoldopam were partially blocked, indicating the interaction between gastrin and D1-like receptor. The gastrin/D1-like receptor interaction was also confirmed in the RPT cells. Stimulation of one receptor increased the expression of the other. Stimulation of either D1-like receptor or gastrin receptor inhibited the Na + -K + -ATPase activity in RPT cells, while in the presence of SCH23390 , the inhibitory effect of gastrin on Na + -K + -ATPase activity was partially blocked. In the presence of CI988, D1-like receptor-mediated inhibitory effect of Na + -K + -ATPase activity in RPT cells was partially inhibited. It indicated the synergistic effect between gastrin and D1-like receptor would increase the sodium excretion in WKY rats; the impaired interaction might be involved in the pathogenesis of hypertension.

scholarly journals Enhanced Natriuresis and Diuresis in Wistar Rats Caused by the Costimulation of Renal Dopamine D3and Angiotensin II Type 2 Receptors

2015 ◽  
Vol 28 (10) ◽  
pp. 1267-1276 ◽  
Author(s):  
Sufei Yang ◽  
Yu Han ◽  
Shuo Zheng ◽  
Xun Kou ◽  
Laureano D. Asico ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Wistar Rats ◽  
Renal Dopamine

Effects of ouabain, low K+, and aldosterone on hypoxic pressor reactivity of rat lungs

1985 ◽  
Vol 248 (1) ◽  
pp. H55-H60 ◽  
Author(s):  
J. Herget ◽  
I. F. McMurtry
Keyword(s):  
Angiotensin Ii ◽  
Energy Metabolism ◽  
Atpase Activity ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Response Curves ◽  
Hypoxic Response ◽  
Rat Lungs ◽  
Hypoxic Vasoconstriction ◽  
Low K

It can be postulated that inhibition of lung tissue Na+-K+-ATPase might potentiate hypoxic pulmonary vasoconstriction by depolarizing some excitable cell or, in contrast, that it might blunt the hypoxic response by reducing cellular metabolic rate and sensitivity to hypoxia. Thus the purpose of this study was to test in isolated rat lungs whether hypoxic pressor reactivity was related inversely or positively to Na+-K+-ATPase activity. Dose-pressor response curves to hypoxia, angiotensin II, or KCl were measured under control conditions and after exposure either to one of two inhibitors of Na+-K+-ATPase, ouabain, and low-K+ solution or to a stimulator of Na+-K+ pumping, aldosterone. Ouabain and low K+ depressed the response to hypoxia but had little effect on that to angiotensin II. The response to KCl was increased by ouabain. Aldosterone potentiated the hypoxic response. These results do not support the idea that membrane depolarization due to inhibition Na+-K+ pumping is a component of hypoxic vasoconstriction. They do suggest a positive relationship between Na+-K+-ATPase activity and hypoxic pressor reactivity and are consistent with the idea that Na+-K+-ATPase activity might influence hypoxic reactivity indirectly by altering cellular energy metabolism. It is also possible that the results were somehow due to changes in intracellular [Na+] or transmembrane Na+ gradient, rather than to changes in energy metabolism.

Adenosine reverses the stimulatory effect of angiotensin II on the renal Na+-ATPase activity through the A2 receptor

2005 ◽  
Vol 129 (1-3) ◽  
pp. 9-15 ◽  
Author(s):  
C.P. Gomes ◽  
L.R. Leão-Ferreira ◽  
C. Caruso-Neves ◽  
A.G. Lopes
Keyword(s):  
Angiotensin Ii ◽  
Atpase Activity

Effects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: reversal of increased β-myosin heavy chain gene expression

2006 ◽  
Vol 84 (8-9) ◽  
pp. 935-941 ◽  
Author(s):  
Baohua Wang ◽  
Jingping Ouyang ◽  
Zhengyuan Xia
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Thyroid Hormone ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Mrna Expression ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Ang Ii ◽  
Hypertrophic Growth

Thyroid hormone-induced cardiac hypertrophy is similar to that observed in physiological hypertrophy, which is associated with high cardiac contractility and increased α-myosin heavy chain (α-MHC, the high ATPase activity isoform) expression. In contrast, angiotensin II (Ang II) induces an increase in myocardial mass with a compromised contractility accompanied by a shift from α-MHC to the fetal isoform β-MHC (the low ATPase activity isoform), which is considered as a pathological hypertrophy and inevitably leads to the development of heart failure. The present study is designed to assess the effect of thyroid hormone on angiotensin II-induced hypertrophic growth of cardiomyocytes in vitro. Cardiomyocytes were prepared from hearts of neonatal Wistar rats. The effects of Ang II and 3,3′,5-triiodo-thyronine (T3) on incorporations of [3H]-thymine and [3H]-leucine, MHC isoform mRNA expression, PKC activity, and PKC isoform protein expression were studied. Ang II enhanced [3H]-leucine incorporation, β-MHC mRNA expression, PKC activity, and PKCε expression and inhibited α-MHC mRNA expression in cardiomyocytes. T3 treatment prevented Ang II-induced increases in PKC activity, PKCε, and β-MHC mRNA overexpression and favored α-MHC mRNA expression. Thyroid hormone appears to be able to reprogram gene expression in Ang II-induced cardiac hypertrophy, and a PKC signal pathway may be involved in such remodeling process.

Reduced renal dopamine D1 receptor function in streptozotocin-induced diabetic rats

2004 ◽  
Vol 286 (3) ◽  
pp. F451-F457 ◽  
Author(s):  
Aditi Marwaha ◽  
Anees Ahmad Banday ◽  
Mustafa F. Lokhandwala
Keyword(s):  
Atpase Activity ◽  
Sodium Excretion ◽  
Type I Diabetes ◽  
Receptor Activation ◽  
Diabetic Rats ◽  
D1 Receptor ◽  
Skf 38393 ◽  
Receptor Expression ◽  
Type I ◽  
Renal Dopamine

Dopamine, via activation of renal D1 receptors, inhibits the activities of Na-K-ATPase and Na/H exchanger and subsequently increases sodium excretion. Decreased renal dopamine production and sodium excretion are associated with type I diabetes. However, it is not known whether the response to D1 receptor activation is altered in type I diabetes. The present study was designed to examine the effect of streptozotocin-induced type I diabetes on renal D1 receptor expression and function. Streptozotocin treatment of Sprague-Dawley rats caused a fourfold increase in plasma levels of glucose along with a significant decrease in insulin levels compared with control rats. Intravenous administration of SKF-38393, a D1 receptor agonist, caused a threefold increase in sodium excretion in control rats. However, SKF-38393 failed to produce natriuresis in diabetic rats. SKF-38393 caused a concentration-dependent inhibition of Na-K-ATPase activity in renal proximal tubules of control rats. However, the ability of SKF-38393 to inhibit Na-K-ATPase activity was markedly diminished in diabetic rats. D1 receptor numbers and protein abundance as determined by [3H]SCH-23390 ligand binding and Western blot analysis were markedly reduced in diabetic rats compared with control rats. Moreover, SKF-38393 failed to stimulate GTPγS binding in proximal tubular membranes from diabetic rats compared with control rats. We conclude that the natriuretic response to D1 receptor activation is reduced in type I diabetes as a result of a decrease in D1 receptor expression and defective receptor G protein coupling. These abnormalities may contribute to the sodium retention associated with type I diabetes.

scholarly journals Angiotensin II Stimulates Vacuolar H+-ATPase Activity in Renal Acid-Secretory Intercalated Cells from the Outer Medullary Collecting Duct

2007 ◽  
Vol 18 (7) ◽  
pp. 2085-2093 ◽  
Author(s):  
Florina Rothenberger ◽  
Ana Velic ◽  
Paul A. Stehberger ◽  
Jana Kovacikova ◽  
Carsten A. Wagner
Keyword(s):  
Angiotensin Ii ◽  
Atpase Activity ◽  
Collecting Duct ◽  
Intercalated Cells ◽  
Medullary Collecting Duct

Angiotensin II decreases system A amino acid transporter activity in human placental villous fragments through AT1 receptor activation

2006 ◽  
Vol 291 (5) ◽  
pp. E1009-E1016 ◽  
Author(s):  
Eiji Shibata ◽  
Robert W. Powers ◽  
Augustine Rajakumar ◽  
Frauke von Versen-Höynck ◽  
Marcia J. Gallaher ◽  
...  
Keyword(s):  
Amino Acid ◽  
Angiotensin Ii ◽  
Atpase Activity ◽  
Renin Angiotensin System ◽  
Coupled System ◽  
Receptor Activation ◽  
Isobutyric Acid ◽  
Transport Systems ◽  
System A ◽  
Placental Villi

Reduced transport of amino acids from mother to fetus can lead to fetal intrauterine growth restriction (IUGR). The activities of several amino acid transport systems, including system A, are decreased in placental syncytiotrophoblast of IUGR pregnancies. Na+-K+-ATPase activity provides an essential driving force for Na+-coupled system A transport, is decreased in the placenta of IUGR pregnancies, and is decreased by angiotensin II in several tissues. Several reports have shown activation of the fetoplacental renin-angiotensin system (RAS) in IUGR. We investigated the effect of angiotensin II on placental system A transport and Na+-K+-ATPase activity in placental villi. Placental system A activity in single primary villous fragments was measured as the Na+-dependent uptake of α-(methylamino)isobutyric acid, and Na+/K+ ATPase activity was measured as ouabain-sensitive uptake of 86rubidium. Angiotensin II decreased system A activity in a concentration-dependent fashion (10–500 nmol/l). Angiotensin II type 1 receptor (AT1-R) antagonists losartan and AT1-R anti-peptide blocked the angiotensin II effect, but the angiotensin II type 2 receptor antagonist PD-123319 was without effect. System A activity was not altered by preincubation with AT1-R-independent vasoconstrictors, and antioxidants did not prevent the decrease in activity mediated by angiotensin II. Angiotensin II decreased Na+-K+-ATPase activity by an AT1-R dependent mechanism, and inhibition of Na+-K+-ATPase activity decreased system A activity in a dose-response fashion. These data suggest that angiotensin II, via AT1-R signaling, decreases system A activity by suppressing Na+-K+-ATPase in human placental villi, consistent with possible adverse effects of enhanced placental RAS on fetal growth.

Urodilatin increases renal dopamine uptake: intracellular network involved

2011 ◽  
Vol 67 (2) ◽  
pp. 243-247 ◽  
Author(s):  
Marcelo R. Choi ◽  
Marisa R. Citarella ◽  
Brenda M. Lee ◽  
Florencia Lucano ◽  
Belisario E. Fernández
Keyword(s):  
Dopamine Uptake ◽  
Renal Dopamine
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