The locations of recent supernovae near the Sun from modelling (60)Fe transport.

The signature of (60)Fe in deep-sea crusts indicates that one or more supernovae exploded in the solar neighbourhood about 2.2 million years ago. Recent isotopic analysis is consistent with a core-collapse or electron-capture supernova that occurred 60 to 130 parsecs from the Sun.

Expression of multiple CaV1.2 transcripts in rat tissues mediated by different promoters.

The expression of two different transcripts for Ca(V)1.2 in rat tissues mirrors that which has previously been described for human tissue, in that expression of transcripts expressing exon 1a is predominant only in heart, whereas expression of transcripts expressing exon 1b is greater in smooth muscle rich tissues such as aorta and intestine. Transcripts expressing exon 1b also predominate in brain and in diaphragm.

A new promoter for alpha1C subunit of human L-type cardiac calcium channel Ca(V)1.2.

The cardiac Ca channel known as alpha1C or Ca(V)1.2 is shown to express a new longer first exon equivalent to that formerly reported in rabbit heart or rat aorta. Ribonuclease protection assay indicates that this exon is found in the majority of Ca(V)1.

Expression and characterization of Edg-1 receptors in rat cardiomyocytes: calcium deregulation in response to sphingosine 1-phosphate.

Recent evidence indicates that sphingolipids are produced by the heart during hypoxic stress and by blood platelets during thrombus formation. It is therefore possible that sphingolipids may influence heart cell function by interacting with G-protein-coupled receptors of the Edg family. In the present study, it was found that sphingosine 1-phosphate (Sph1P), the prototypical ligand for Edg receptors, produced calcium overload in rat cardiomyocytes.

Dihydropyridine receptor isoform expression in adult rat skeletal muscle.

The expression of isoform-specific dihydropyridine receptor Ca2+ channel (DHPR) alpha1-subunit genes in rat diaphragm, soleus and extensor digitorum longus muscles was investigated using RNase protection assays. As expected, mRNA expression levels for the DHPR skeletal muscle isoform were highest in extensor digitorum longus. Unexpectedly, both diaphragm and soleus expressed mRNA for the cardiac isoform at a significant level.

Effects of three sarcoplasmic/endoplasmic reticulum Ca++ pump inhibitors on release channels of intracellular stores.

The three principal sarcoplasmic/endoplasmic reticulum Ca++ pump inhibitors have been compared for their effects on Ca++ fluxes across intracellular stores present in isolated skeletal muscle and brain membrane preparations. At moderate concentrations that only partially inhibited Ca++ pumping, all three inhibitors induced transient release of Ca++ from isolated sarcoplasmic reticulum membranes, and release was ruthenium red-sensitive, much faster and sustained at higher pump inhibitor concentrations. In contrast, in unidirectional 45Ca efflux assays, cyclopiazonic acid appeared to have little effect, thapsigargin decreased efflux and 2,5-di(tert-butyl)-1,4-benzohydroquinone increased efflux only slightly.

Dihydropyridine receptor gene expression in skeletal muscle from mdx and control mice.

The expression of isoform-specific dihydropyrine receptor-calcium channel (DHPR) alpha 1-subunit genes was investigated in mdx and control mouse diaphragm (DIA) and tibialis anterior (TA). RNase protection assays were carried out with a rat DHPR cDNA probe specific for skeletal muscle and a mouse DHPR cDNA probe specific for cardiac muscle. The level of expression of the gene encoding the cardiac DHPR was very weak in TA muscle from both control and mdx mice.

Dihydropyridine receptor and ryanodine receptor gene expression in long-term denervated rat muscles.

Following disruption of the nerve supply, extensor digitorum longus (EDL) and soleus (SOL) muscles in rats are known to exhibit alterations in excitation-contraction coupling. After total RNA isolation from the denervated and the contralateral control muscles performed at 25 and 50 days following denervation, RNase protection assays were carried out with four cDNA probes specific for the skeletal and cardiac isoforms of both the DHPR alpha 1-subunit and the RyR. Longterm denervation increased the expression of the mRNA for skeletal DHPR and skeletal RyR in SOL muscle, but it also significantly increased the expression of the mRNA for the cardiac isoform of the DHPR alpha 1 subunit in EDL muscle.

Ca2+ feedback on "quantal" Ca2+ release involving ryanodine receptors.

The influence of luminal and cytoplasmic Ca2+ on the ability of ryanodine-sensitive stores to undergo multiple partial ("quantal") releases has been assessed. Increased luminal Ca2+ levels do indeed modulate sarcoplasmic reticulum Ca2+ release by lowering the threshold agonist concentration required to elicit release, but the decrease in luminal Ca2+ that accompanies a partial release is not sufficient by itself to terminate release. Similarly, an increase in cytoplasmic Ca2+ lowers the threshold agonist concentration required to elicit release; thus, the bulk cytoplasmic Ca2+ levels attained during a release would only stimulate further release, not terminate it before it reached completion.

Sphingosylphosphocholine modulates the ryanodine receptor/calcium-release channel of cardiac sarcoplasmic reticulum membranes.

Sphingosylphosphocholine (SPC) modulates Ca2+ release from isolated cardiac sarcoplasmic reticulum membranes; 50 microM SPC induces the release of 70 80% of the accumulated calcium. SPC release calcium from cardiac sarcoplasmic reticulum through the ryanodine receptor, since the release is inhibited by the ryanodine receptor channel antagonists ryanodine. Ruthenium Red and sphingosine.

Involvement of ryanodine receptors in sphingosylphosphorylcholine-induced calcium release from brain microsomes.

Sphingosylphosphorylcholine (SPC) releases Ca2+ from brain microsomes. SPC-induced CA2+ release differs from IP3-induced Ca2+ release in that it is more extensive in the cerebrum than in the cerebellum. SPC has little effect on [3H] IP3 binding but enhances [3H] ryanodine binding, as expected for an activator of ryanodine receptors.

Sphingosine effects on the contractile behavior of skinned cardiac myocytes.

Sphingosine modulates myocyte beating behavior by acting on the sarcoplasmic reticulum calcium release channel, the ryanodine receptor. Chemically skinned myocytes isolated from adult rabbit ventricles exhibited spontaneous asynchonous contractions in response to micromolar levels of calcium. These cells do not have a functional sarcolemma but exhibit spontaneous contraction-relaxation cycles which are controlled by the sarcoplasmic reticulum.

Many agonists induce "quantal" Ca2+ release or adaptive behavior in muscle ryanodine receptors.

Ryanodine receptors have recently been shown to undergo an unusual kind of inactivation process termed adaptation, which bears similarities to the transient calcium releases induced in other systems by successive incremental additions of inositol-1,4,5-trisphosphate. Such releases are sometimes termed "quantal". In this study we report that many agonists induce similar behavior in muscle sarcoplasmic reticulum and that the responses depend not on the calcium pumps therein but rather on the ryanodine receptors.

Modulation of cardiac sarcoplasmic reticulum ryanodine receptor by sphingosine.

Excitation contraction (EC) coupling in muscle cells involves the movement of calcium through the calcium release channel of the sarcoplasmic reticulum (SR) membrane known as the ryanodine receptor. We have recently shown that the novel second messenger, sphingosine, can block calcium release from skinned skeletal muscle fibers and from isolated skeletal muscle SR membranes (Sabbadini et al., J Biol Chem 267: 15475-15484, 1992).

Potentiation of sarcoplasmic reticulum Ca2+ release by 2,3-butanedione monoxime in crustacean muscle.

The effect of the chemical phosphatase 2,3-butanedione monoxime (BDM) on various aspects of excitation/contraction coupling in crustacean muscle was investigated. Despite having a depressant effect on vertebrate skeletal and cardiac muscle, BDM was a potentiator of contraction in crustacean muscle. At concentrations of 1-3 mM BDM caused an increase of potassium contractures in bundles of fibers isolated from crayfish muscle.

Arachidonic acid-induced Ca2+ release from isolated sarcoplasmic reticulum.

Arachidonic acid has been shown to release Ca2+ from isolated skeletal and cardiac sarcoplasmic reticulum (SR) vesicles. The release took place nearly equally well from all fractions of the SR and was only partially inhibited by ruthenium red, suggesting that some other pathway is involved in addition to the SR Ca2+ release channel. Arachidonic acid increased SR Ca2+ efflux even in the presence of several different SR Ca2+ pump inhibitors.

Involvement of sarcoplasmic reticulum 'Ca2+ release channels' in excitation-contraction coupling in vertebrate skeletal muscle.

1. Pharmacological blockers of calcium-induced calcium release from isolated skeletal sarcoplasmic reticulum (SR) vesicles have been introduced into frog skeletal muscle fibres to determine their effects on excitation-contraction coupling. 2.

Effects of alkaline pH on sarcoplasmic reticulum Ca2+ release and Ca2+ uptake.

Alkalinization-induced Ca2+ release from isolated frog or rabbit sarcoplasmic reticulum vesicles appears to consist of two distinct components: 1) a direct activation of ruthenium red-sensitive Ca2+ release channels in terminal cisternae and 2) an increased ruthenium red-insensitive Ca2+ efflux through some other efflux pathway distributed throughout the sarcoplasmic reticulum. The first of these releases exhibits an alkalinization-induced inactivation process and does not depend on the ruthenium red-insensitive form of Ca2+ release as a triggering agent for secondary Ca(2+)-induced Ca2+ release. Both releases are inhibited when the extravesicular (i.

Pulmonary complications in the patient with acute head injury: neurogenic pulmonary edema.

Neurogenic pulmonary edema (NPE) is a serious complication associated with various central nervous system insults. Experimental and clinical data support the occurrence of pulmonary edema as a result of neurogenic factors. Patients with NPE have increased intracranial pressure and respiratory distress, and their care presents a challenge to critical care nurses.

Pharmacologic differentiation between inositol-1,4,5-trisphosphate-induced Ca2+ release and Ca2+- or caffeine-induced Ca2+ release from intracellular membrane systems.

Various known Ca2+ channel blockers and intracellular Ca2+ antagonists have been tested for effects of inositol-1,4,5-trisphosphate (IP3)-induced Ca2+ release from isolated canine brain microsomes. In agreement with previous reports, heparin, p-chloromercuribenzoic acid, W-7, cinnarizine, flunarizine, certain local anesthetics, La3+, and Ca2+ inhibit the release of Ca2+ induced by addition of IP3. In addition, we report here pronounced inhibition of IP3-induced Ca2+ release by low levels of Cd2+, by relatively high concentrations of TMB-8, and by phytic acid.

Direct inhibition of inositol-1,4,5-trisphosphate-induced Ca2+ release from brain microsomes by K+ channel blockers.

Tetraethylammonium and 9-tetraethylammonium have previously been reported to inhibit inositol-1,4,5-trisphosphate (IP3)-induced Ca2+ release from brain microsomes, purportedly by blocking potassium channels [Biochem. J. 258:617-620 (1988)].

Pharmacology of calcium release from sarcoplasmic reticulum.

Calcium release from sarcoplasmic reticulum (SR) has been elicited in response to additions of many different agents. Activators of Ca2+ release are here tentatively classified as activators of a Ca2+-induced Ca2+ release channel preferentially localized in SR terminal or as likely activators of other Ca2+ efflux pathways. Some of these pathways may be associated with several different mechanisms for SR Ca2+ release that have been postulated previously.

Heavy metal-induced Ca2+ release from sarcoplasmic reticulum.

Two distinct forms of Ca2+ release from isolated sarcoplasmic reticulum vesicles in response to additions of heavy metals (silver and mercurials) are described. One form of heavy metal-induced Ca2+ release involves the ruthenium red-sensitive Ca2+ release channel localized in terminal cisternae. The other form of heavy metal-induced Ca2+ release appears to involve all portions of the sarcoplasmic reticulum and is insensitive to ruthenium red.