The regulatory function of plasma-membrane Ca2+-ATPase (PMCA) in the heart

2007 ◽  
Vol 35 (5) ◽  
pp. 927-930 ◽  
Author(s):  
D. Oceandy ◽  
P.J. Stanley ◽  
E.J. Cartwright ◽  
L. Neyses
Keyword(s):  
Nitric Oxide ◽  
Plasma Membrane ◽  
Calcium Concentration ◽  
Regulatory Function ◽  
Minor Role ◽  
Sodium Calcium Exchanger ◽  
Excitable Cells ◽  
A Minor ◽  
Oxide Synthase ◽  
Calcium Extrusion

The PMCA (plasma-membrane Ca2+-ATPase) is a ubiquitously expressed calcium-extruding enzymatic pump important in the control of intracellular calcium concentration. Unlike in non-excitable cells, where PMCA is the only system for calcium extrusion, in excitable cells, such as cardiomyocytes, PMCA has been shown to play only a minor role in calcium homoeostasis compared with the NCX (sodium/calcium exchanger), another system of calcium extrusion. However, increasing evidence points to an important role for PMCA in signal transduction; of particular interest in cardiac physiology is the modulation of nNOS (neuronal nitric oxide synthase) by isoform 4b of PMCA. In the present paper, we will discuss recent advances that support a key role for PMCA4 in modulating the nitric oxide signalling pathway in the heart.

scholarly journals Inhibition of Nitric Oxide Synthase Prevents Muscarinic and Purinergic Functional Changes and Development of Cyclophosphamide-Induced Cystitis in the Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Patrik Aronsson ◽  
Renata Vesela ◽  
Martin Johnsson ◽  
Yasin Tayem ◽  
Vladimir Wsol ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Bladder Wall ◽  
Functional Results ◽  
Minor Role ◽  
Cell Distribution ◽  
Functional Changes ◽  
Nos Inhibitor ◽  
A Minor ◽  
Oxide Synthase

Nitric oxide (NO) has pivotal roles in cyclophosphamide- (CYP-) induced cystitis during which mucosal nitric oxide synthase (NOS) and muscarinic M5 receptor expressions are upregulated. In cystitis, urothelial muscarinic NO-linked effects hamper contractility. Therefore we wondered if a blockade of this axis also affects the induction of cystitis in the rat. Rats were pretreated with saline, the muscarinic receptor antagonist 4-DAMP (1 mg/kg ip), or the NOS inhibitor L-NAME (30 mg/kg ip) for five days. 60 h before the experiments the rats were treated with saline or CYP. Methacholine-, ATP-, and adenosine-evoked responses were smaller in preparations from CYP-treated rats than from saline-treated ones. Pretreatment with 4-DAMP did not change this relation, while pretreatment with L-NAME normalized the responses in the CYP-treated animals. The functional results were strengthened by the morphological observations; 4-DAMP pretreatment did not affect the parameters studied, namely, expression of muscarinic M5 receptors, P1A1 purinoceptors, mast cell distribution, or bladder wall enlargement. However, pretreatment with L-NAME attenuated the differences. Thus, the current study provides new insights into the complex mechanisms behind CYP-induced cystitis. The NO effects coupled to urothelial muscarinic receptors have a minor role in the development of cystitis. Inhibition of NOS may prevent the progression of cystitis.

Intracellular calcium in cultured rabbit oviduct epithelial cells

1996 ◽  
Vol 8 (2) ◽  
pp. 243 ◽  
Author(s):  
CJ Dickens ◽  
CI Cox ◽  
HJ Leese
Keyword(s):  
Plasma Membrane ◽  
Epithelial Cells ◽  
Intracellular Calcium ◽  
Fluid Secretion ◽  
Minor Role ◽  
Ion Substitution ◽  
Secretory Type ◽  
Oviduct Epithelial Cells ◽  
A Minor ◽  
Oviduct Fluid

Oviduct fluid is the medium in which fertilization and early embryonic development occur but little is known about the ionic basis of fluid secretion or its control. Since calcium ions (Ca2+) are involved in the mechanism of secretion in other epithelia, the intracellular calcium concentration ([Ca2+]i) was measured in single, rabbit oviduct epithelial cells in primary culture using the fluorescent dye Fura-2. The resting [Ca2+]i was constant (115 nM) in cells cultured for 2-7 days. Ion substitution experiments demonstrated the presence of a Na+/Ca(2+)-exchange system in the plasma membrane, whereas influx through channels was found to have only a minor role maintaining the resting [Ca2+]i. The addition of dibutyryl cAMP (db cAMP) induced two types of response: the first was an increase in [Ca2+]i, dependent on the presence of extracellular Ca2+, and the second was a zero response. Extracellular ATP induced a transient increase in [Ca2+]i owing to the release of Ca2+ from intracellular stores and Ca2+ entering the cell across the plasma membrane. It is proposed that these effects may be due to the presence of two types of cell in culture-the ciliated and non-ciliated (secretory type) oviduct epithelial cells.

scholarly journals Resting Tension Affects eNOS Activity in a Calcium-Dependent Way in Airways

2007 ◽  
Vol 2007 ◽  
pp. 1-6 ◽  
Author(s):  
Eudoxia Kitsiopoulou ◽  
Apostolia A. Hatziefthimiou ◽  
Konstantinos I. Gourgoulianis ◽  
Paschalis-Adam Molyvdas
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Calcium Concentration ◽  
Kinase Inhibitors ◽  
Calcium Dependent ◽  
Enos Activity ◽  
Resting Tension ◽  
Smooth Muscle Contractions ◽  
Oxide Synthase ◽  
Inducible Nos

The alteration of resting tension (RT) from 0.5 g to 2.5 g increased significantly airway smooth muscle contractions induced by acetylcholine (ACh) in rabbit trachea. The decrease in extracellular calcium concentration[Ca2+]ofrom 2 mM to 0.2 mM reduced ACh-induced contractions only at 2.5 g RT with no effect at 0.5 g RT. The nonselective inhibitor of nitric oxide synthase (NOS),NG-nitro-L-arginine methyl ester (L-NAME) increased ACh-induced contractions at 2.5 g RT. The inhibitor of inducible NOS, S-methylsothiourea or neuronal NOS, 7-nitroindazole had no effect. At 2.5 g RT, the reduction of[Ca2+]ofrom 2 mM to 0.2 mM abolished the effect of L-NAME on ACh-induced contractions. The NO precursor L-arginine or the tyrosine kinase inhibitors erbstatin A and genistein had no effect on ACh-induced contractions obtained at 2.5 g RT. Our results suggest that in airways, RT affects ACh-induced contractions by modulating the activity of epithelial NOS in a calcium-dependent, tyrosine-phosphorylation-independent way.

scholarly journals Nitric oxide production in murine spleen cells: role of interferons and prostaglandin E2in the generation of cytotoxic activity

1996 ◽  
Vol 5 (1) ◽  
pp. 62-68 ◽  
Author(s):  
Dominique Vaillier ◽  
Richard Daculsi ◽  
Norbert Gualdel
Keyword(s):  
Nitric Oxide ◽  
Cytotoxic Activity ◽  
Minor Role ◽  
No Production ◽  
Spleen Cells ◽  
Kinase C ◽  
Murine Spleen ◽  
Ifn Γ ◽  
A Minor

The production of nitric oxide (NO) was measured in cultures of spleen cells stimulated by lipopolysaccharide (LPS), IL-2 or LPS + IL-2. We observed that NO synthesis is increased by IFN-γ but inhibited by IFN-α/β. This is not the case when IL-2 is present in the cultures, since interferons play a minor role in the regulation of the NO production. When IL-2 and LPS were associated in the cultures, the IFN-α/β role seems more important than that of IFN-γ. PGE2inhibits NO production in LPS supplemented cultures but has a slight effect in the presence of IL-2 and no effect with IL-2 + LPS. 3-isoButyl-1-methylxanthine (IBMX), an inhibitor of phosphodiesterases, induces a decrease of IFN production. In the presence of H-7, an inhibitor of protein kinase C (PKC), NO production is reduced when the cultures are supplemented by LPS or IL-2 but not when IL-2 and LPS are both added. H-7 also reduced IFN production. In the presence of NG-monomethyl-L-arginine (N-MMA), an inhibitor of NO synthesis, IFN production was increased, with no change in the cytotoxic activity. Hence, interferons regulate NO production by mouse spleen cells and, in return, NO modulates the generation of IFN.

scholarly journals The N-terminal portion of autoinhibitory element modulates human endothelial nitric-oxide synthase activity through coordinated controls of phosphorylation at Thr495 and Ser1177

2014 ◽  
Vol 34 (4) ◽  
Author(s):  
Pei-Rung Wu ◽  
Bo-Rui Chen ◽  
Chi-Chun Hsieh ◽  
Wei-Chung Lin ◽  
Kenneth K. Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Regulatory Function ◽  
Terminal Portion ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
First Time ◽  
Nitric Oxide Synthase Activity

Our findings demonstrate for the first time that AIE insert exerts its regulatory function by coordinate phosphorylation on eNOS Ser1177 and Thr495, highlighting the importance of AIE in regulating agonist-induced eNOS activation.

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