Potential for pharmacology of ryanodine receptor/calcium release channels.

Calcium release channels, known also as ryanodine receptors (RyRs), play an important role in Ca2+ signaling in muscle and nonmuscle cells by releasing Ca2+ from intracellular stores. Mammalian tissues express three different RyR isoforms comprising four 560-kDa (RyR polypeptide) and four 12-kDa (FK506 binding protein) subunits. The large protein complexes conduct monovalent and divalent cations and are capable of multiple interactions with other molecules.

Ruthenium red modifies the cardiac and skeletal muscle Ca(2+) release channels (ryanodine receptors) by multiple mechanisms.

The effects of ruthenium red (RR) on the skeletal and cardiac muscle ryanodine receptors (RyRs) were studied in vesicle-Ca(2+) flux, [(3)H]ryanodine binding, and single channel measurements. In vesicle-Ca(2+) flux measurements, RR was more effective in inhibiting RyRs at 0.2 microM than 20 microM free Ca(2+).

Effects of 2,3-butanedione 2-monoxime on Ca2+ release channels (ryanodine receptors) of cardiac and skeletal muscle.

Single channel and [3H]ryanodine binding measurements were performed to test for a direct functional interaction between 2,3-butanedione 2-monoxime (BDM) and the skeletal and cardiac muscle sarcoplasmic reticulum Ca2+ release channels (ryanodine receptors). Single channel measurements were carried out in symmetric 0.25 m KCl media using the planar lipid bilayer method.

Selectivity and permeation in calcium release channel of cardiac muscle: alkali metal ions.

Current was measured from single open channels of the calcium release channel (CRC) of cardiac sarcoplasmic reticulum (over the range +/-180 mV) in pure and mixed solutions (e.g., biionic conditions) of the alkali metal ions Li+, K+, Na+, Rb+, Cs+, ranging in concentration from 25 mM to 2 M.

Imperatoxin A induces subconductance states in Ca2+ release channels (ryanodine receptors) of cardiac and skeletal muscle.

Single-channel and [3H]ryanodine binding experiments were carried out to examine the effects of imperatoxin activator (IpTxa), a 33 amino acid peptide isolated from the venom of the African scorpion Pandinus imperator, on rabbit skeletal and canine cardiac muscle Ca2+ release channels (CRCs). Single channel currents from purified CRCs incorporated into planar lipid bilayers were recorded in 250 mM KCl media. Addition of IpTxa in nanomolar concentration to the cytosolic (cis) side, but not to the lumenal (trans) side, induced substates in both ryanodine receptor isoforms.

Permeation through the calcium release channel of cardiac muscle.

Current voltage (I-V) relations were measured from the calcium release channel (CRC) of the sarcoplasmic reticulum of cardiac muscle in 12 KCl solutions, symmetrical and asymmetrical, from 25 mM to 2 M. I-V curves are nearly linear, in the voltage range +/- 150 mV approximately 12kT/e, even in asymmetrical solutions, e.g.

Evidence for a role of C-terminal amino acid residues in skeletal muscle Ca2+ release channel (ryanodine receptor) function.

The effects of deleting 1, 3 and 15 amino acid residues from the highly conserved C-terminus of the tetrameric skeletal muscle ryanodine receptor (RyR) complex were determined. Immunoblot analysis indicated similar expression levels in HEK293 cells for full-length and mutant proteins. Full-length and RyR lacking the last amino acid showed [3H]ryanodine binding and single channel activities typical of native receptors.

Effects of ayurvedic treatment on amoebic colitis.

This is a report of the clinical trial done on some patients of amoebic colitis with the Ayurvedic medicines like AMRATAKA (Spondias pinnata Linn f Kurz) and PARNAVEEJA (Bryophyllum pinnatum Lam. Kurz) and Dasamoola Ksheera Paka vasti in the department of Kayachikitsa, Institute of medical sciences, Banaras Hindu University.

Regulation of skeletal muscle Ca2+ release channel (ryanodine receptor) by Ca2+ and monovalent cations and anions.

The effects of ionic composition and strength on rabbit skeletal muscle Ca2+ release channel (ryanodine receptor) activity were investigated in vesicle-45Ca2+ flux, single channel and [3H]ryanodine binding measurements. In <0.01 microM Ca2+ media, the highest 45Ca2+ efflux rate was measured in 0.

Sarcoplasmic reticulum lumenal Ca2+ has access to cytosolic activation and inactivation sites of skeletal muscle Ca2+ release channel.

The effects of sarcoplasmic reticulum lumenal (trans) Ca2+ on cytosolic (cis) ATP-activated rabbit skeletal muscle Ca2+ release channels (ryanodine receptors) were examined using the planar lipid bilayer method. Single channels were recorded in symmetric 0.25 M KCl media with K+ as the major current carrier.

Calmodulin activation and inhibition of skeletal muscle Ca2+ release channel (ryanodine receptor).

The calmodulin-binding properties of the rabbit skeletal muscle Ca2+ release channel (ryanodine receptor) and the channel's regulation by calmodulin were determined at < or = 0.1 microM and micromolar to millimolar Ca2+ concentrations. [125I]Calmodulin and [3H]ryanodine binding to sarcoplasmic reticulum (SR) vesicles and purified Ca2+ release channel preparations indicated that the large (2200 kDa) Ca2+ release channel complex binds with high affinity (KD = 5-25 nM) 16 calmodulins at < or = 0.

A self-associating hepatitis B surface antigen-derived peptide that is immunogenic in alum.

We previously described an oligomeric synthetic peptide derived from the hepatitis B surface antigen that displayed a limited tendency to form self-associating macromolecular structures in solution. Here it is demonstrated that amino-terminal myristylation of this peptide results in near quantitative aggregation of the oligomeric peptide. The myristylated peptide is highly immunogenic when used in conjunction with alum as adjuvant in both the rabbit and rhesus monkey models.

A case of fluoxetine-induced serum sickness.

After 3-4 weeks of taking fluoxetine for depression, a 27-year-old man developed fever, skin eruptions, arthralgia, and lymphadenopathy. His clinical symptoms and results of laboratory assessment were consistent with a diagnosis of serum sickness reaction to the fluoxetine.