Ruthenium red and magnesium ion partially inhibit silver ion-induced release of calcium from sarcoplasmic reticulum of frog skeletal muscles.

Ôba, Toshiharu; Iwama, Hiroko; Aoki, Takako

doi:10.2170/jjphysiol.39.241

Cited by 12 publications

(5 citation statements)

References 26 publications

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“…By analogy with our work on SR vesicles, Ag+ and Hg2+ ions induced Ca2+ release from the SR network of skinned frog fibres and appeared to act by binding to a sulphydryl site on Ca2+-induced Ca2+ release channels (Aoki, Oba & Hotta, 1985; Oba, Iwama & Aoki, 1989). In intact frog fibres, the same heavy metals elicited contractions by an unknown action on T-tubule membrane proteins .…”

Section: Introductionsupporting

confidence: 60%

“…However, the omission of ATP-regenerating systems is of little consequence to force measurements when fibre diameters are in the range of 100 tm and the diffusion of ATP to the centre of the fibres is rapid compared to rates of ATP hydrolysis, as is the case for fibres bathed in millimolar ATP (Ferenczi, Goldman & Simmons, 1984) and high ionic-strength solutions to reduce ATPase activity (Yanagida, Kuranaga & Inoue, 1982). Previous studies on the interaction of Cd2+, Ag+ or Hg2+ with skinned fibres also omitted ATP-regenerating systems (Stephenson & Thieleczek, 1986, Oba et al 1989 an ATP-regenerating system (15 mM-CP plus 50 U ml-1 CK did not change either the time course or the amplitude of forces generated during Cal+-induced Ca 2 release (n = 6) or caffeine (n = 4) contractions, or contractures induced by a pCa of 2 (n = 6) (not shown). Possible fibre rundown.…”

Section: Analysis Of Tension Recordingsmentioning

confidence: 99%

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Sulphydryl reagents trigger Ca2+ release from the sarcoplasmic reticulum of skinned rabbit psoas fibres.

Salama

Abramson

Pike

1992

The Journal of Physiology

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SUMMARY1. By analogy with studies on sarcoplasmic reticulum (SR) vesicles, Ca2+ release induced by heavy metals and mercaptans (e.g. cysteine) was investigated in rabbit skinned psoas fibres through measurements of isometric tension.2. Heavy metals (at 2-5 /tM) elicited phasic contractions by triggering Ca2+ release from the SR and had the following order of potency: Hg2+ > Cu2+ > Cd2+ > Ag+ > Ni2+. Higher concentrations produced tonic contractions due to maintained high Ca2+ permeability of SR membranes.3. Contractions induced by heavy metals required a functional and Ca2+-loaded SR, were dependent on [Ca2+]free, blocked by Ruthenium Red (RR), inhibited by free Mg2+ and reduced glutathione (GSH) but not by oxidized glutathione (GSSG). Such contractions were not elicited through direct interactions) of heavy metals with the myofilaments.4. In the presence of catalytic concentrations of Hg2+ or Cu2+ (2-5 /UM), additions of cysteine (25-100 /LM) elicited rapid twitches, producing 70 % of maximal force with a time to half-peak of 2 s. Contractions induced by cysteine plus a catalyst required a functional SR network, were dependent on free [Mg2+] and were blocked by RR or GSH but not by GSSG.5. In the presence of Hg2+ (2-5 ,uM), low concentrations of cysteine (10 /uM) elicited tonic contractures, but subsequent or higher additions of cysteine (50-100 uM) caused further SR Ca2+ release and tension, followed by rapid and full relaxation.6. High cysteine (200-250 /tM, without Cu2+ or Hg2+) blocked contractions elicited by Cl-induced depolarization of sealed T-tubules. High cysteine probably acted as a sulphydryl reducing agent which promoted rapid relaxation of the fibres through the closure of Ca2+-release channels and ATP-dependent re-uptake of Ca2+ by the SR. 7. In some batches of skinned fibres (-10%), cysteine (5-50 /tM) alone (without Hg2+ or Cu2+ catalyst) produced rapid twitches. This implied that the catalysts) necessary to promote the sulphydryl oxidation reaction with exogenously added cysteine may be present in intact fibres but is usually lost by the skinning procedure.

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Section: Introductionsupporting

confidence: 60%

Section: Analysis Of Tension Recordingsmentioning

confidence: 99%

Sulphydryl reagents trigger Ca2+ release from the sarcoplasmic reticulum of skinned rabbit psoas fibres.

Salama

Abramson

Pike

1992

The Journal of Physiology

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“…Ruthenium red was used to isolate IP3-mediated calcium release from sarcoplasmic reticulum by blocking 45Ca uptake in the mitochondria (25). Ruthenium red also blocks membrane Ca-Mg ATPase activity (31 ), and calcium-mediated Ca release from sarcoplasmic reticulum (32). TG releases calcium from intracellular stores and prevents its reuptake, so it can be used as a means to estimate intracellular calcium pools (26).…”

Section: Methodsmentioning

confidence: 99%

Insulin attenuates agonist-mediated calcium mobilization in cultured rat vascular smooth muscle cells.

Saito¹,

Hori²,

Fittingoff³

et al. 1993

J. Clin. Invest.

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Insulin has been shown to attenuate pressor-induced vascular contraction, but the mechanism for this vasodilatory action is unknown. This study examines the effect of insulin on angiotensin II (ANG II)-induced increments in cytosolic calcium in cultured rat vascular smooth muscle cells (VSMC). 20-min incubations with insulin (10 ,U/ml to 100 mU/ml) did not alter basal intracellular calcium concentration (ICa2I,), but inhibited the response to 100 nM ANGII in a dose-dependent manner (ANG II alone, 721±54 vs. ANG II + 100 mU/ml insulin, 315±35 nM, P < 0.01). A similar effect of insulin on ANGII action was observed in calcium poor buffer. Moreover, insulin did not effect calcium influx. ANG II receptor density and affinity were not affected by 24-h incubation with insulin. To further clarify the mechanisms of these observations, we measured ANG II-induced production of inositol 1,4,5-triphosphate (IP3), and IP3-releasable 45Ca. Insulin treatment did not alter ANG Il-stimulated IP3 production. However, IP3-stimulated release of45Ca in digitonin permeabilized cells was significantly reduced after 5-min incubations with 100 mU/ml insulin. Thapsigargin induced release of calcium stores was also blocked by insulin. Thus, insulin attenuates ANG 11-stimulated ICa2"I, primarily by altering IP3-releasable calcium stores. Insulin effects on ANG II-induced ICa2`Ii were mimicked by preincubation of VSMC with either sodium nitroprusside or 8-bromo-cGMP. As elevations in cGMP in vascular tissue lower ICa2I1j, it is possible that insulin affects IP3 release of calcium by a cGMP-dependent mechanism that would contribute to its vasodilatory effects. (J. Clin. Invest. 1993. 92:1161-1167

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“…Bar graph shows effect of parathyroid hormone-( to block calcium-magnesium ATPase activity and calciuminduced calcium mobilization. 24 ' 25 Cells were washed twice with Hanks' buffered salt solution (Sigma) and incubated with either 100 nmol/L PTH(l-34), PTHrp(l-34), 10 mmol/L forskolin, or vehicle for 5 minutes at ambient temperature. After rapid removal of the treatment buffer, cells were immediately treated with 35 mmol/L digitonin (Sigma) in a HEPESbuffered salt solution with or without 10 mmol/L IP 3 (Calbiochem) for 5 minutes, and then 1-mL aliquots were collected for counting.…”

Section: Measurement Of Inositol 145 -Trisphosphate-releasable Calciummentioning

confidence: 99%

Parathyroid hormone analogues inhibit calcium mobilization in cultured vascular cells.

Hino¹,

Nyby²,

Fittingoff³

et al. 1994

Hypertension

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Parathyroid hormone and parathyroid hormonerelated protein lower blood pressure and relax contracted arteries. Parathyroid hormone also attenuates angiotensin H-induced vasoconstriction. To determine the cellular mechanism or mechanisms by which parathyroid hormone analogues antagonize pressor effects, we examined the effect of these peptides on angiotensin II-induced calcium mobilization in fura 2-AMloaded cultured rat vascular smooth muscle cells. Either 100 nmol/L parathyroid hormone or parathyroid hormone-related protein significantly reduced the amount of calcium mobilized by 100 nmol/L angiotensin II. The attenuating effect of these peptides was mimicked by 10 mmol/L forskolin and 10 mmol/L isobutylmethylxanthine and was not dependent on the presence of extracellular calcium. This effect of the parathyroid hormone analogues was reduced when cells were pretreated with 100 mmol/L 2',5'-dideoxyadenosine, an adenylate cyclase inhibitor. Combined inhibition of cyclic nucleotide-dependent protein N umerous studies have consistently demonstrated that parathyroid hormone (PTH), as either intact hormone or the N-terminal 1-34 fragment of PTH [PTH(l-34)], relaxes contracted vessels and lowers blood pressure in a variety of animal species.15 PTH can also attenuate vasopressor responses to angiotensin II (Ang II) and norepinephrine when coinfused with these pressors in rats. 6 Although initially identified as a factor in the generation of hypercalcemia in a variety of malignancies, PTH-related protein (PTHrp) has subsequently been found to be present in a variety of normal tissue, including vascular smooth muscle. 7 The N-terminal fragment of this hormone, PTHrp(l-34), appears to affect target cells much like PTH(l-34) does and appears to bind to the same receptor or receptors as PTH(l-34) in bone, kidney, and renal vascular cells. 89Acute exposure to PTHrp(l-34) has been shown to cause vasodilation in vivo, 10 and it has been suggested that PTHrp may have an autocrine or paracrine function in modulating blood flow in certain tissues such as myometrium. 11Although it has been established that PTH and PTHrp acutely decrease blood pressure and relax vasReceived June 14,1993; accepted in revised form December 13, 1993.From the Department of Endocrinology, Veterans Affairs Medical Center, Sepulveda, and the UCLA School of Medicine, Los Angeles, Calif.Correspondence to Arnold S. Brickman, MD, Endocrinology Department (HIE), Sepulveda VAMC, 16111 Plummer St, Sepulveda, CA 91343. kinases eliminated the inhibitory effect of parathyroid hormone, whereas protein kinase C inhibition had no effect. Parathyroid hormone analogues decreased the amount of calcium released by inositol 1,4,5 -trisphosphate in digitoninpermeabilized vascular smooth muscle cells. This effect was inhibited by treatment with 2',5'-dideoxyadenosine. These results suggest that these peptides attenuate inositol 1,4,5-trisphosphate-sensitive calcium mobilized by angiotensin II via an adenylate cyclase-dependent mechanism. This may be a mechanism ...

show abstract

Ruthenium red and magnesium ion partially inhibit silver ion-induced release of calcium from sarcoplasmic reticulum of frog skeletal muscles.

Cited by 12 publications

References 26 publications

Sulphydryl reagents trigger Ca2+ release from the sarcoplasmic reticulum of skinned rabbit psoas fibres.

Sulphydryl reagents trigger Ca2+ release from the sarcoplasmic reticulum of skinned rabbit psoas fibres.

Insulin attenuates agonist-mediated calcium mobilization in cultured rat vascular smooth muscle cells.

Parathyroid hormone analogues inhibit calcium mobilization in cultured vascular cells.

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