Vanadate inhibition of sarcoplasmic reticulum Ca2+-ATPase and other ATPases

O'Neal, Steven G.; Rhoads, David B.; Racker, Efraim

doi:10.1016/0006-291x(79)91855-2

Cited by 219 publications

(79 citation statements)

References 24 publications

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“…It is to be noted that our results leads to ADP/O ratios for pyruvate and malate of 2.4 ± 0.7, both in the absence or presence of V 10 or V 1 , a value which is close to the theoretical value of 3 [36]. vanadium) [39,40]. NADH levels in mitochondria were also not affected by the vanadate solutions.…”

Section: Effect Of Decavanadate On Mitochondrial Oxygen Consumptionsupporting

confidence: 85%

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

Soares¹,

Gutiérrez‐Merino²,

Aureliano³

2007

Journal of Inorganic Biochemistry

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Decavanadate induced rat liver mitochondrial depolarization at very low concentrations, half-depolarization with 39 nM decavanadate, while it was needed a 130-fold higher concentration of monomeric vanadate (5 lM) to induce the same effect. Decavanadate also inhibits mitochondrial repolarization induced by reduced glutathione in vitro, with an inhibition constant of 1 lM, whereas no effect was observed up to 100 lM of monomeric vanadate. The oxygen consumption by mitochondria is also inhibited by lower decavanadate than monomeric vanadate concentrations, i.e. 50% inhibition is attained with 99 nM decavanadate and 10 lM monomeric vanadate. Thus, decavanadate is stronger as mitochondrial depolarization agent than as inhibitor of mitochondrial oxygen consumption. Up to 5 lM, decavanadate does not alter mitochondrial NADH levels nor inhibit neither F O F 1 -ATPase nor cytochrome c oxidase activity, but it induces changes in the redox steady-state of mitochondrial b-type cytochromes (complex III). NMR spectra showed that decameric vanadate is the predominant vanadate species in decavanadate solutions. It is concluded that decavanadate is much more potent mitochondrial depolarization agent and a more potent inhibitor of mitochondrial oxygen consumption than monomeric vanadate, pointing out the importance to take into account the contribution of higher oligomeric species of vanadium for the biological effects of vanadate solutions.

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Section: Effect Of Decavanadate On Mitochondrial Oxygen Consumptionsupporting

confidence: 85%

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

Soares¹,

Gutiérrez‐Merino²,

Aureliano³

2007

Journal of Inorganic Biochemistry

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“…A 50% inhibition of the steady state rate of the Ca2*-ATPase was obtained at -10 PM vanadate or above which is much higher than the affinity for the E state measured here [7,8]. This weak inhibitory effect on the ATPase activity, confirmed by us (not shown), indicates that most of the steady state intermediates formed are less susceptible to vanadate than the calcium free E conformation, being either the E-Mg-P or the Et' .…”

Section: Discussionsupporting

confidence: 52%

“…Binding to the phosphorylation site is facilitated by K+ and Mg2+ and locks the enzyme in the Ez state . Vanadate inhibition of Ca2+-ATPase activity of sarcoplasmic reticulum has been reported in [7,8], the apparent affinity for the inhibitor being however much lower than for the __ (Na',K+)ATPase.…”

Section: Introductionmentioning

confidence: 99%

Vanadate inhibition of the Ca²⁺‐dependent conformational change of the sarcoplasmic reticulum Ca²⁺‐ATPase

Dupont

Bennett

1982

FEBS Letters

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“…Ouabain has been found to inhibit renin release [14,29,49,58,59] and additional evidence was obtained to show that this inhibition is a calcium dependent process [14,25,58]. Inhibition of the calcium ATPase by vanadate also inhibits part of the extrusion of calcium and therefore leads to a rise in the intracellular calcium concentration [56]. Vanadate has also been found to inhibit renin release [18,47].…”

Section: Role Of Calcium In the Intracellular Control Of Renin Releasementioning

confidence: 99%

Intracellular control of renin release — An overview

Kurtz

1986

Klin Wochenschr

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The renin angiotensin aldosterone system is an important regulator of the extracellular volume and of the control of blood pressure. It is mainly controlled in its activity by the rate of renin release from the kidney. Within the kidney renin is produced, stored and released from the so-called granular juxtaglomerular cells. These cells are modified smooth muscle cells and are found in the tunica media of the afferent arteriole, just adjacent to the glomerulus. They resemble morphologically vascular smooth muscle cells but have also characteristic features of secretory cells with respect to a welldeveloped endoplasmic reticulum, a prominent Golgi-apparatus and membrane bound granules containing renin [6,73].Since the rate of renin release from juxtaglomerular cells has a direct effect on blood pressure and because an enhanced rate of renin release is known to be a major reason of hypertension, the mechanisms controlling renal renin release have attracted considerable interest among physiologists, pharmacologists and clinicians.So far four basic mechanisms controlling renin release from the kidney have been described [26]. These comprise 1. The intra-renal blood pressure, which influences renin release by an as yet undefined baroreceptor.2. The amount of NaCl-load sensed by the macula densa segment of the distal tubule (macula densa sensor).3. The sympathetic nervous system 4. A large number of humoral factors like catecholamines, angiotensin II, vasopressin, atrial natriuretic peptide as well as metabolites as for example adenosine.In spite of the large body of findings about the modulation and alteration of renal renin release, the intracellular mechanisms by which renin release is controlled within the juxtaglomerular cells are not clearly understood.During the last years the mechanisms of physiological and pharmacological alterations of renin release have been reviewed [26, 36, 39]. The present contribution wants to concentrate on the intracellular processes that influence renin release from juxtaglomerular cells. The available information will be discussed in front of the background of the present knowledge about the general mechanisms of secretion.For a variety of secretory cells including adrenal medulla and cortex, pituitary, exocrine and endocrine pancreas, neutrophils and platelets it has been found that the secretory process is triggered by the intracellular levels of calcium and cyclic nucleotides and further by the activity of protein kinase C [12,33,64,68,[70][71][72]. I shall therefore discuss in special the role of intracellular calcium, intracellular cyclic AMP and cyclic GMP and protein kinase C activity in the control of renin release from juxtaglomerular cells. In this context I will also present our own results obtained from studies on the intracellular control of renin release from isolated juxtaglomerular cells. Role of Calcium in the Intracellular Control of Renin ReleaseThe typical secretory process in a large number of secreting cells has been found to be biphasic. The secretory process ...

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Vanadate inhibition of sarcoplasmic reticulum Ca2+-ATPase and other ATPases

Cited by 219 publications

References 24 publications

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

Vanadate inhibition of the Ca²⁺‐dependent conformational change of the sarcoplasmic reticulum Ca²⁺‐ATPase

Intracellular control of renin release — An overview

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Vanadate inhibition of sarcoplasmic reticulum Ca2+-ATPase and other ATPases

Cited by 219 publications

References 24 publications

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

Vanadate inhibition of the Ca2+‐dependent conformational change of the sarcoplasmic reticulum Ca2+‐ATPase

Intracellular control of renin release — An overview

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Vanadate inhibition of the Ca²⁺‐dependent conformational change of the sarcoplasmic reticulum Ca²⁺‐ATPase