Net Release Of Ca2 Research Articles

Element Budgets in a Forested Watershed in Southern China: Estimation of a Proton Budget

We evaluated the element budgets in a forested watershed in Jiulianshan, southern China. The element input in bulk precipitation was characterized by high depositions of H+, NH4+, Ca2+, and SO42−, i.e., 400, 351, 299, and 876 eq/ha/yr, respectively. The outputs of H+, NH4+, and SO42− from the watershed were very low, while those of Ca2+ and Mg2+ were high, 712 and 960 eq/ha/yr, respectively. The element budgets suggested that i) the net retentions of H+, NH4+, and SO42− in this watershed were high, and ii) the net release of Mg2+ from this watershed was high mainly due to weathering. The net release of Ca2+ was not so high because of the high atmospheric deposition, while atmospheric deposition of Mg2+ was not so high (130 eq/ha/yr). Decrease of acid neutralizing capacity in the soil, i.e., net soil acidification, was caused mainly by the net release of Mg2+. Moreover, the net retention of SO42− also contributed to soil acidification.

Access to intracellular calcium during development in the feline gastric antrum.

Circular smooth muscle cells from the feline newborn antrum, unlike the adult, are unable to respond to myogenic agonists in the absence of extracellular calcium or to exogenous inositol 1,4,5-trisphosphate (IP3). This study examined the reasons behind the relative inaccessibility of intracellular calcium stores in the newborn period. IP3 binding was determined in antral smooth muscle homogenates from adult cats and newborns by evaluating the competitive binding of D-myo-[3H]IP3 and unlabeled IP3. Receptor density (Bmax) (fmol/mg of protein) and binding affinity (Kd) were determined. The Kd was similar in adults (31 +/- 4 nM) and newborns (28 +/- 7 nM); however, the Bmax was markedly decreased in the newborn (647 +/- 181.0 fmol/mg) compared with the adult (1755 +/- 275 fmol/mg). In adult and newborn antral cells, thapsigargin, which causes a net release of Ca2+ from intracellular stores by inhibiting Ca(2+)-ATPase-dependent reuptake activity, caused an early contraction at 30 s that was maintained for at least 20 min. We conclude that, in the newborn, dynamic intracellular calcium stores are present in the smooth muscle of the feline antrum and that differences in accessibility of intracellular calcium stores may be related to changes in the release of calcium from IP3-sensitive stores.

The H2O2-generating enzyme, xanthine oxidase, decreases luminal Ca2+ content of the IP3-sensitive Ca2+ store in vascular endothelial cells.

Xanthine oxidase inhibits agonist-stimulated Ca2+ signaling in calf pulmonary artery endothelial cells by an H2O2-dependent mechanism. We investigated the effect of xanthine oxidase on luminal Ca2+ content of the inositol-1,4,5-trisphosphate (IP3)-sensitive Ca2+ store. Luminal Ca2+ content was estimated from the net release of Ca2+ activated by 2,5-di-t-butylhydroquinone (BHQ), an inhibitor of microsomal Ca2+ pumps. Initially, xanthine oxidase depleted the IP3-sensitive Ca2+ store of releasable Ca2+, but with more prolonged incubation, the enzyme also depleted non-IP3-sensitive stores. In addition, xanthine oxidase inhibited capacitative Ca2+ influx. Similar results were observed when thapsigargin was substituted for BHQ. Depletion of luminal Ca2+ content within the IP3-sensitive Ca2+ store contributes to xanthine oxidase inhibition of Ca2+ signaling in vascular endothelial cells.

Effects of 2,3-butanedione monoxime on sarcoplasmic reticulum of saponin-treated rat cardiac muscle

We have studied the effects of 2,3-butanedione monoxime (BDM) on the sarcoplasmic reticulum (SR) of saponin-treated rat cardiac trabeculae. Rapid application of 20 mM caffeine released Ca2+ from the SR, which was detected using the fluorescent Ca2+ indicator indo 1. The amplitude of the caffeine-induced Ca2+ transient was used as an index of the Ca2+ content of the SR before, during, and after exposure to various concentrations of BDM. BDM (1-5 mM) had little effect on caffeine-induced Ca2+ release. At these levels of BDM, force was inhibited predominantly by a direct action of BDM on the myofilaments. However, with higher concentrations (5-30 mM), BDM caused a concentration-dependent decrease in the amount of Ca2+ released from the SR in response to caffeine. This action of BDM may contribute to the negative inotropic effect of the drug in intact cardiac preparations by reducing the amount of Ca2+ available for release during systole. Rapid application of BDM induced a net release of Ca2+ from the SR. Both BDM and caffeine-induced Ca2+ releases were abolished following treatment of the muscle with 10 microM ryanodine. BDM failed to release Ca2+ in the absence of ATP or after substitution of ATP with nonhydrolyzable adenine nucleotides. In contrast, caffeine released Ca2+ in the absence of ATP. The possible involvement of the Ca(2+)-uptake pump in the action of BDM on the SR is discussed.

Transport and release of calcium by sarcoplasmic reticulum in chemically skinned ventricular muscle of the rat.

Strips of rat ventricle were treated with EGTA (5 mM) for 24 h at 4 degrees C and used to perform isotopical measurements of transport and release of Ca2+ in the SR in situ. 45Ca accumulated by these preparations showed dependence on time of incubation until it reached saturation after 30 min. Rate and capacity of Ca2+ accumulation were calculated in 0.075 nmol mg ww-1 min-1 and 0.402 nmol mg ww-1, respectively. These values were increased by a factor of 2.6 and 8.6 when K oxalate was present in the incubation media as could be expected for Ca2+ transported by SR. Ca2+ release was assayed on 45Ca desaturation curves at three free Ca2+ concentrations: 0.3, 1 and 10 microM. Significant increases in the velocity of Ca2+ efflux and net release of Ca2+ were induced only by 1 microM free Ca2+, and the Ca2+ release could be inhibited by 75% when 50 microM of ruthenium red was included in the washout solution. These results are in agreement with those obtained in assessing the SR function by mechanical measurements in skinned cardiac cells or by biochemical determinations in isolated cardiac SR vesicles. In spite of the fact that the resolution time is not as high as that required for the physiological handling of Ca2+ by SR, this methodology looks promising for approaching the SR function in cardiac pathologies as well as the effects of drugs on transport and release of Ca2+ by cardiac SR.

Inorganic phosphate decreases the Ca2+ content of the sarcoplasmic reticulum in saponin-treated rat cardiac trabeculae.

1. Measurements of [Ca2+] were made in saponin-permeabilized rat ventricular trabeculae using the fluorescent indicator Indo-1. Application of caffeine (20 mM) caused a transient rise in [Ca2+] within the preparation as a result of Ca2+ release from the sarcoplasmic reticulum (SR). The size of the caffeine-induced Ca2+ transient was related to the amount of Ca2+ accumulated by the SR prior to addition of caffeine. Caffeine-induced Ca2+ release was abolished by ryanodine (10 microM), an inhibitor of SR Ca2+ release. 2. At a bathing [Ca2+] of 0.2 microM, the amount of Ca2+ released from the SR on addition of caffeine was sufficient to generate a tension transient. Ca2+ and tension responses were stabilized by application of caffeine at regular intervals (2 min). Addition of 10 mM inorganic phosphate (Pi) induced a transient increase in [Ca2+] within the preparation due to a net release of Ca2+ from the SR. The amplitude of subsequent caffeine-induced Ca2+ transients were reduced to 65 +/- 7.5% (mean +/- S.D., n = 13) of control. In addition, the accompanying tension transient fell to 45 +/- 6.9% of control. Removal of Pi caused a transient decrease in the [Ca2+] within the preparation consistent with a net increase in Ca2+ uptake by the SR. Subsequent caffeine-induced Ca2+ and tension transients returned to control levels. 3. Inclusion of Pi (2-30 mM) in the perfusing solution decreased the size of caffeine-induced Ca2+ and tension transients in a dose-dependent manner. 4. Addition of 10 mM ADP caused a transient increase in [Ca2+] and depressed subsequent caffeine-induced Ca2+ transients to a greater extent than 10 mM Pi. Despite the reduction in Ca2+ release from the SR, tension responses were larger in the presence of 10 mM ADP than under control conditions. This is a consequence of an increase in Ca(2+)-activated force by ADP. 5. A decrease in the amplitude of caffeine-induced Ca2+ transients also occurred on changing from a solution containing 1 mM ADP and 10 mM Pi to a solution with 10 mM ADP and 1 mM Pi. This confirms the previous observation that ADP is more effective than Pi at reducing caffeine-induced Ca2+ released from the SR. 6. Spontaneous oscillations of [Ca2+] and tension occurred in the presence of 0.5 microM Ca2+.(ABSTRACT TRUNCATED AT 400 WORDS)