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Academic literature on the topic 'Intracellular pH; Hormone; ACE inhibitors'
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Journal articles on the topic "Intracellular pH; Hormone; ACE inhibitors"
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Hool, L. C., D. W. Whalley, M. M. Doohan, and H. H. Rasmussen. "Angiotensin-converting enzyme inhibition, intracellular Na+, and Na(+)-K+ pumping in cardiac myocytes." American Journal of Physiology-Cell Physiology 268, no. 2 (February 1, 1995): C366—C375. http://dx.doi.org/10.1152/ajpcell.1995.268.2.c366.
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Angiotensin-converting enzyme (ACE) inhibitors can reduce cardiac mass in both clinical and experimental cardiac hypertrophy. Because cytoplasmic Na+ and pH have been implicated as regulators of cell growth, we examined the effect of treatment with an ACE inhibitor on intracellular Na+ activity (alpha iNa) and pH (pHi) in the heart. After treatment of rabbits with captopril for 8 days alpha iNa was reduced relative to controls (3.6 +/- 0.4, n = 8, vs. 8.2 +/- 0.4 mM, n = 9, P < 0.001), whereas pHi was unchanged. To account for the difference in alpha iNa we measured electrogenic Na(+)-K+ pump activity in single isolated myocytes. Treatment with captopril increased pump currents at near-physiological levels of intracellular Na+ but had no effect at near-saturating levels of Na+. A similar increase in Na(+)-K+ pump activity occurred in rabbits treated with another ACE inhibitor, enalapril, but not with the vasodilator, hydralazine. We speculate that a decrease in alpha iNa after treatment with captopril may contribute to the well-documented ability of ACE inhibitors to reduce cardiac mass.
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STRATFORD, Suzanne, Daryll B. DEWALD, and Scott A. SUMMERS. "Ceramide dissociates 3′-phosphoinositide production from pleckstrin homology domain translocation." Biochemical Journal 354, no. 2 (February 22, 2001): 359–68. http://dx.doi.org/10.1042/bj3540359.
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Numerous hormones, cytokines and transforming oncogenes activate phosphoinositide 3-kinase (PI-3K), a lipid kinase that initiates signal transduction cascades regulating cellular proliferation, survival, protein synthesis and glucose metabolism. PI-3K catalyses the production of the 3′-phosphoinositides PtdIns(3,4)P2 and PtdIns(3,4,5)P3, which recruit downstream effector enzymes to the membrane via their pleckstrin homology (PH) domains. Recent studies have indicated that another signalling lipid, the sphingolipid ceramide, inhibits several PI-3K-dependent events, including insulin-stimulated glucose uptake and growth-factor-stimulated cell survival. Here we show that ceramide analogues specifically prevent the recruitment of the PtdIns(3,4,5)P3-binding proteins Akt/protein kinase B (PKB) or the general receptor for phosphoinositides-1 (GRP1). Specifically, the short-chain ceramide derivative C2-ceramide inhibited the platelet-derived growth factor (PDGF)-stimulated translocation of full-length Akt/PKB, as well as truncated proteins encoding only the PH domains of Akt/PKB or GRP1. C2-ceramide did not alter the membrane localization of the PH domain for phospholipase Cδ, which preferentially binds PtdIns(4,5)P2, nor did it affect the PDGF-stimulated production of PtdIns(3,4)P2 or PtdIns(3,4,5)P3. Interestingly, a glucosylceramide synthase inhibitor, 1-phenyl-2-decanoylamino-3-morpholinopropan-1-ol (PDMP), shown previously to increase intracellular ceramide concentrations without affecting PI-3K [Rani, Abe, Chang, Rosenzweig, Saltiel, Radin and Shayman (1995) J. Biol. Chem. 270, 2859–2867], recapitulated the inhibitory effects of C2-ceramide on PDGF-stimulated Akt/PKB phosphorylation. These studies indicate that ceramide prevents the translocation of certain PtdIns(3,4,5)P3-binding proteins, despite the presence of a full complement of PtdIns(3,4)P2 or PtdIns(3,4,5)P3. Furthermore, these findings suggest a mechanism by which stimuli that induce ceramide synthesis could negate the fundamental signalling pathways initiated by PI-3K.
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D’Arezzo, Silvia, Sandra Incerpi, Faith B. Davis, Filippo Acconcia, Maria Marino, Ricardo N. Farias, and Paul J. Davis. "Rapid Nongenomic Effects of 3,5,3′-Triiodo-l-Thyronine on the Intracellular pH of L-6 Myoblasts Are Mediated by Intracellular Calcium Mobilization and Kinase Pathways." Endocrinology 145, no. 12 (December 1, 2004): 5694–703. http://dx.doi.org/10.1210/en.2004-0890.
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Abstract l-T3 and l-T4 activated the Na+/H+ exchanger of L-6 myoblasts, with a fast nongenomic mechanism, both in the steady state and when cells undergo acid loading with ammonium chloride. Monitored with the intracellular pH-sensitive fluorescent probe 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein, activation of the exchanger appeared to be initiated at the plasma membrane, because T3-agarose reproduced the effect of l-T3, and triiodothyroacetic acid, a hormone analog previously shown to inhibit membrane actions of thyroid hormone, blocked the action of l-T3 on the exchanger. We show here for the first time that transduction of the hormone signal in this nongenomic response requires tyrosine kinase-dependent phospholipase C activation and two different signaling pathways: 1) mobilization of intracellular calcium, assessed by the fluorescent probe fura-2, through activation of inositol trisphosphate receptors and without contributions from extracellular calcium or ryanodine receptors; and 2) protein phosphorylation involving protein kinase C and MAPK (ERK1/2), as shown by the use of kinase inhibitors and by immunoblotting for activated kinases.
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Wu, Bingjie, Jingjing Jiang, Minghui Gui, Lin Liu, Qiqige Aleteng, Shanshan Wang, Xiaojing Liu, Yan Ling, and Xin Gao. "Serum-Free Thyroxine Levels Were Associated with Pulmonary Hypertension and Pulmonary Artery Systolic Pressure in Euthyroid Patients with Coronary Artery Disease." International Journal of Endocrinology 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/4832608.
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The aim of this study was to evaluate the association between thyroid hormone levels, pulmonary hypertension (PH), and pulmonary artery systolic pressure (PASP) in euthyroid patients with coronary artery disease (CAD). A cross-sectional study was conducted in individuals who underwent coronary angiography and were diagnosed as CAD from March 2013 to November 2013. 811 subjects (185 women and 626 men) were included in this study. PASP was measured by transthoracic Doppler echocardiography. 86 patients were diagnosed as PH and had significantly higher free thyroxine (FT4) levels than those without PH. Multiple logistic regression analysis demonstrated an independent association of FT4 levels with PH after adjustment of gender, age, body mass index, systolic blood pressure, left ventricular ejection fraction, hypertension, and medication use of calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and nitrates. Serum-free triiodothyronine (FT3) and thyroid-stimulating hormone (TSH) were not associated with PH. Furthermore, multivariate linear regression analysis showed that FT4 levels emerged as an independent predictor for PASP, while FT3 and TSH levels were not associated with PASP. Our study demonstrated that, in euthyroid patients with CAD, FT4 was an independent risk factor for PH, and FT4 levels were independently associated with PASP.
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Michea, Luis, Ana M. Delpiano, Catalina Hitschfeld, Lorena Lobos, Sergio Lavandero, and Elisa T. Marusic. "Eplerenone Blocks Nongenomic Effects of Aldosterone on the Na+/H+ Exchanger, Intracellular Ca2+ Levels, and Vasoconstriction in Mesenteric Resistance Vessels." Endocrinology 146, no. 3 (March 1, 2005): 973–80. http://dx.doi.org/10.1210/en.2004-1130.
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There is increasing evidence for rapid nongenomic effects of aldosterone. Aldosterone has been demonstrated to alter intracellular pH and calcium in isolated cells. However, few studies have correlated these effects with aldosterone-mediated physiological responses. Therefore, we studied rapid effects of aldosterone on vascular reactivity, intracellular Ca2+, and pH in resistance vessels. Furthermore, we explored whether the new antimineralocorticoid drug eplerenone could effectively block nongenomic aldosterone-mediated effects. The vasoconstrictor action of aldosterone was examined directly by determining the diameter of small resistance mesenteric vessels (160–200 μm resting diameter), simultaneously with intracellular pH or Ca2+. Aldosterone (10 nm) caused a rapid constriction of resistance vessels (8.1% ± 1.0% reduction in the diameter below control conditions, P < 0.05). Aldosterone potentiated phenylephrine-mediated constriction in small and large mesenteric vessels. Aldosterone induced a rapid increase of intracellular Ca2+ and cellular alkalinization. Vasoconstrictor action of aldosterone and nongenomic effects on the sodium-proton exchanger (NHE1) activity or intracellular Ca2+ responses was abolished by eplerenone. The vasoconstrictor response of aldosterone was related to phosphatidylinositol 3-kinase (PI3-K): the hormone decreased protein kinase B phosphorylation; pharmacological inhibition of PI3-K (10 μm LY294002 or 1 μm wortmannin) increased arterial contractility. Inhibitors of ERK 1/2 phosphorylation (15 μm PD98059) had no effect on aldosterone-mediated vasoconstriction. Inhibition of protein kinase C with 1 μm bi-sindolylmaleimide I and/or inhibition of NHE1 with 100 μm amiloride abolished aldosterone vasoconstrictor action of resistance mesenteric arteries. We conclude that aldosterone-mediated increase in vascular tone is related to a nongenomic mechanism that involves protein kinase C, PI3-K, and NHE1 activity. Eplerenone is an effective blocker of nongenomic effects of aldosterone in vascular tissue.
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Harvey, B., I. Lacoste, and J. Ehrenfeld. "Common channels for water and protons at apical and basolateral cell membranes of frog skin and urinary bladder epithelia. Effects of oxytocin, heavy metals, and inhibitors of H(+)-adenosine triphosphatase." Journal of General Physiology 97, no. 4 (April 1, 1991): 749–76. http://dx.doi.org/10.1085/jgp.97.4.749.
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We have compared the response of proton and water transport to oxytocin treatment in isolated frog skin and urinary bladder epithelia to provide further insights into the nature of water flow and H+ flux across individual apical and basolateral cell membranes. In isolated spontaneous sodium-transporting frog skin epithelia, lowering the pH of the apical solution from 7.4 to 6.4, 5.5, or 4.5 produced a fall in pHi in principal cells which was completely blocked by amiloride (50 microM), indicating that apical Na+ channels are permeable to protons. When sodium transport was blocked by amiloride, the H+ permeability of the apical membranes of principal cells was negligible but increased dramatically after treatment with antidiuretic hormone (ADH). In the latter condition, lowering the pH of the apical solution caused a voltage-dependent intracellular acidification, accompanied by membrane depolarization, and an increase in membrane conductance and transepithelial current. These effects were inhibited by adding Hg2+ (100 microM) or dicyclohexylcarbodiimide (DCCD, 10(-5) M) to the apical bath. Net titratable H+ flux across frog skin was increased from 30 +/- 8 to 115 +/- 18 neq.h-1.cm-2 (n = 8) after oxytocin treatment (at apical pH 5.5 and serosal pH 7.4) and was completely inhibited by DCCD (10(-5) M). The basolateral membranes of the principal cells in frog skin epithelium were found to be spontaneously permeable to H+ and passive electrogenic H+ transport across this membrane was not affected by oxytocin. Lowering the pH of the basolateral bathing solution (pHb) produced an intracellular acidification and membrane depolarization (and an increase in conductance when the normal dominant K+ conductance of this membrane was abolished by Ba2+ 1 mM). These effects of low pHb were blocked by micromolar concentrations of heavy metals (Zn2+, Ni2+, Co2+, Cd2+, and Hg2+). Lowering pHb in the presence of oxytocin (50 mU/ml) produced a transepithelial current (3 microA.cm-2 at pHb 5.5) which was blocked by 100 microM of Hg2+, Zn2+, or Ni2+ at the basolateral side, and by DCCD (10(-5) M) or Hg2+ (100 microM) from the apical side. The net hydroosmotic water flux (JH2O) induced by oxytocin in frog bladder sacs was blocked by inhibitors of H(+)-adenosine triphosphatase (ATPase). Diethylstilbestrol (DES 10(-5) M), oligomycin (10(-8) M), and DCCD (10(-5) M) prevented JH2O when present in the lumen. These effects cannot be attributed to inhibition of metabolism since cyanide (10(-4) M), or 2-deoxyglucose (10(-3) M) had no effect on JH2O.(ABSTRACT TRUNCATED AT 400 WORDS)
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Klip, A., T. Ramlal, and E. J. Cragoe. "Insulin-induced cytoplasmic alkalinization and glucose transport in muscle cells." American Journal of Physiology-Cell Physiology 250, no. 5 (May 1, 1986): C720—C728. http://dx.doi.org/10.1152/ajpcell.1986.250.5.c720.
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Insulin stimulates glucose uptake into muscle within minutes, preceding stimulation of glycolysis. Signals involved in stimulation of glycolysis include cytoplasmic alkalinization and specific intracellular proteolytic products. In contrast, the signals that mediate stimulation of glucose transport remain unknown. Here we explore whether the insulin-induced cytoplasmic alkalinization is an early event that precedes activation of sugar uptake, whether such alkalinization is causally related to stimulation of sugar uptake, and whether proteolytic activity mediates stimulation of hexose transport. Cytoplasmic pH (pHi) was measured in suspended skeletal muscle cells of the L6H9 line with the intracellularly trapped fluorescent pH indicator bis(carboxyethyl)carboxy fluorescein. At 37 degrees C, insulin (1 X 10(-7) M) produced an increase in pHi of 0.11 units in 10 min. This increase became apparent 2 min after addition of the hormone, and maximal elevation of pHi was observed after 10 min, remaining elevated for up to 60 min. Removal of the hormone with anti-insulin antiserum did not reverse pHi back to the resting level. The alkalinization was prevented by amiloride, by 5-(N,N'-disubstituted)amiloride analogues, and by isosmotic replacement of Na+ with N-methylglucamine+ or choline+. This suggests that insulin activates Na+-H+ exchange. In contrast, stimulation of 2-deoxy-D-glucose transport by insulin was not affected by replacement of external Na+ or by addition of amiloride. Monensin, an exogenous Na+-H+ exchanger, did not stimulate sugar transport even though it increased pHi. Proteinase inhibitors that block hormonal stimulation of glycolysis were ineffective in preventing stimulation of 2-deoxy-D-glucose transport by insulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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Schmidt, W. K., and H. P. Moore. "Ionic milieu controls the compartment-specific activation of pro-opiomelanocortin processing in AtT-20 cells." Molecular Biology of the Cell 6, no. 10 (October 1995): 1271–85. http://dx.doi.org/10.1091/mbc.6.10.1271.
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Newly synthesized prohormones and their processing enzymes transit through the same compartments before being packaged into regulated secretory granules. Despite this coordinated intracellular transport, prohormone processing does not occur until late in the secretory pathway. In the mouse pituitary AtT-20 cell line, conversion of pro-opiomelanocortin (POMC) to mature adrenocorticotropic hormone involves the prohormone convertase PC1. The mechanism by which this proteolytic processing is restricted to late secretory compartments is unknown; PC1 activity could be regulated by compartment-specific activators/inhibitors, or through changes in the ionic milieu that influence its activity. By arresting transport in a semi-intact cell system, we have addressed whether metabolically labeled POMC trapped in early secretory compartments can be induced to undergo conversion if the ionic milieu in these compartments is experimentally manipulated. Prolonged incubation of labeled POMC trapped in the endoplasmic reticulum or Golgi/trans-Golgi network did not result in processing, thereby supporting the theory that processing is normally a post-Golgi/trans-Golgi network event. However, acidification of these compartments allowed effective processing of POMC to the intermediate and mature forms. The observed processing increased sharply at a pH below 6.0 and required millimolar calcium, regardless of the compartment in which labeled POMC resided. These conditions also resulted in the coordinate conversion of PC1 from the 84/87 kDa into the 74-kDa and 66-kDa forms. We propose that POMC processing is predominantly restricted to acidifying secretory granules, and that a change in pH within these granules is both necessary and sufficient to activate POMC processing.
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Carraro-Lacroix, Luciene R., Gerhard Malnic, and Adriana C. C. Girardi. "Regulation of Na+/H+ exchanger NHE3 by glucagon-like peptide 1 receptor agonist exendin-4 in renal proximal tubule cells." American Journal of Physiology-Renal Physiology 297, no. 6 (December 2009): F1647—F1655. http://dx.doi.org/10.1152/ajprenal.00082.2009.
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The gut incretin hormone glucagon-like peptide 1 (GLP-1) is released in response to ingested nutrients and enhances insulin secretion. In addition to its insulinotropic properties, GLP-1 has been shown to have natriuretic actions paralleled by a diminished proton secretion. We therefore studied the role of the GLP-1 receptor agonist exendin-4 in modulating the activity of Na+/H+ exchanger NHE3 in LLC-PK1 cells. We found that NHE3-mediated Na+-dependent intracellular pH (pHi) recovery decreased ∼50% after 30-min treatment with 1 nM exendin-4. Pharmacological inhibitors and cAMP analogs that selectively activate protein kinase A (PKA) or the exchange protein directly activated by cAMP (EPAC) demonstrated that regulation of NHE3 activity by exendin-4 requires activation of both cAMP downstream effectors. This conclusion was based on the following observations: 1) the PKA antagonist H-89 completely prevented the effect of the PKA activator but only partially blocked the exendin-4-induced NHE3 inhibition; 2) the MEK1/2 inhibitor U-0126 abolished the effect of the EPAC activator but only diminished the exendin-4-induced NHE3 inhibition; 3) combination of H-89 and U-0126 fully prevented the effect of exendin-4 on NHE3; 4) no additive effect in the inhibition of NHE3 activity was observed when exendin-4, PKA, and EPAC activators were used together. Mechanistically, the inhibitory effect of exendin-4 on pHi recovery was associated with an increase of NHE3 phosphorylation. Conversely, this inhibition took place without changes in the surface expression of the transporter. We conclude that GLP-1 receptor agonists modulate sodium homeostasis in the kidney, most likely by affecting NHE3 activity.
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Sileno, Giuseppe, Silvia Brazzo, Paola Baiardi, Massimo Torreggiani, Vittoria Esposito, Marco Colucci, Ettore Pasquinucci, Giuseppe Locatelli, Chiara Morelli, and Ciro Esposito. "P1106DETERMINANTS OF SERUM POTASSIUM IN HEMODIALYSIS PATIENTS. DOES JUST ONE COUNT?" Nephrology Dialysis Transplantation 35, Supplement_3 (June 1, 2020). http://dx.doi.org/10.1093/ndt/gfaa142.p1106.
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Abstract Background and Aims Potassium (K) is mostly an intracellular ion, with a complex homeostasis that is deeply modified in ESRD patients undergoing hemodialysis (HD). Several factors (diet, insulin, acid-base balance, aldosterone, etc) may contribute to determine the level of serum extracellular K, but it is not clear which factor contributes the most. We aimed to evaluate the importance of several factors in inducing hyperkalemia in HD patients. Methods Chronic tri-weekly HD patients were evaluated. Patients on diuretics or on potassium binders were excluded. For every patient we recorded age, sex, Kt/V and we measured the post-HD kalemia on the day before the long interHD interval. On the day after the long interHD interval we evaluated: pre-HD K, glucose, creatinine, aldosterone, LDH, CPK, arterial blood gases, ECG, overhydration by bioelectrical impedance analysis, body weight increase after the long interHD interval and daily urinary output. K amount introduced by diet was calculated by a dietitian from each patient’s daily food diary. Treatment with ARB, ACE-inhibitors, beta-blockers, insulin or heparin was recorded. Data are presented as mean±SD for each variable analyzed. Correlations between the serum K values and change in serum K (delta K) and the other patient medical data were determined through the two-tailed Pearson’s test or Spearman test according to data distribution. Results We enrolled 56 patients (male 53.6%), aged 72±13, with a mean Kt/V 1.44±0.25. Mean post-HD kalemia was 3.65±0.4 mmol/L, mean pre-HD kalemia was 5.23±0.72 mmol/L, with a mean delta 1.58±0.64 mmol/L. Medium pH was 7.37±0.01, with serum bicarbonate 20.15±4.0 mmol/L. Overhydration estimated by bioelectrical impedance analysis was 2.3±0.6 L, while mean daily intake of K was 1697.13±711.13 mg. We found a strong positive correlation between delta K and pre-HD kalemia (r=0.79, p<0.0001). Surprisingly, a positive correlation was found between delta K and serum bicarbonate (r=0.27, p=0.04), while no correlations were present between delta K, mean pre-HD kalemia and dietary intake of K (p=ns). No difference in delta K was found between anuric and not anuric patients. No other statistically significant differences were found. Conclusion Potassium homeostasis is markedly altered in ESRD and several factors contribute to determine the serum K values. In this study we found that delta potassium correlates to pre-HD kalemia. We did not study the temporal kinetic of K increase, but it is reasonable to infer that a significant post-HD rebound may contribute to increase kalemia, as dietary intake of K was not found to correlate to delta K or to serum K after the long interdialytic interval. The positive correlation between delta K and serum bicarbonate is unexpected and difficult to explain. However, since we did not measure serum bicarbonate post-HD, we may speculate that patients with high delta K and serum bicarbonate might have even higher levels of bicarbonate after HD. In conclusion, our study shows that none of the examined factors prevales in determining high serum potassium in HD patients.
Dissertations / Theses on the topic "Intracellular pH; Hormone; ACE inhibitors"
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Mielke, Marilyn. "Mechanisms underlying the inotropic response to angiotensin II in the heart." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325976.
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