A methylpyrrole-carboxylate from RYANIA that disrupts the RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL to modify CALCIUM release from SARCOPLASMIC RETICULUM resulting in alteration of MUSCLE CONTRACTION. It was previously used in INSECTICIDES. It is used experimentally in conjunction with THAPSIGARGIN and other inhibitors of CALCIUM ATPASE uptake of calcium into SARCOPLASMIC RETICULUM.
Also Known As:
Ryanodol, 3-(1H-pyrrole-2-carboxylate)
Networked: 294 relevant articles (10 outcomes, 21 trials/studies)

Relationship Network

Bio-Agent Context: Research Results


1. Hidalgo, Cecilia: 3 articles (01/2015 - 01/2008)
2. Donoso, Paulina: 3 articles (09/2008 - 12/2003)
3. Sánchez, Gina: 3 articles (09/2008 - 12/2003)
4. Ogawa, Yasuo: 3 articles (03/2007 - 12/2005)
5. Pollock, Neil: 2 articles (01/2015 - 06/2010)
6. Caputo, Carlo: 2 articles (12/2013 - 08/2008)
7. Knollmann, Björn C: 2 articles (04/2013 - 01/2009)
8. Katina, I E: 2 articles (11/2008 - 07/2002)
9. Nasledov, G A: 2 articles (11/2008 - 07/2002)
10. Macho, Pilar: 2 articles (01/2008 - 12/2003)

Related Diseases

1. Contracture
2. Ischemia
3. Anoxia (Hypoxia)
4. Cardiac Arrhythmias (Arrythmia)
5. Shock
02/14/1991 - "These data demonstrate that the Ca2(+)-induced Ca2+ release via the ryanodine-sensitive Ca2+ channel in canine cardiac SR was reduced during endotoxin shock. "
04/01/1998 - "Heat shock or PMA treatment of vector- or HSF1 cDNA-transfected cells to induce HSP-70 also attenuated the NaCN-induced increase in [Ca2+]i, perhaps because of a decrease in Vmax for the uptake of external Ca2+. Removal of external Ca2+ or treatment with inhibitors of Na+/Ca2+ exchangers eliminated the NaCN-induced increase in [Ca2+]i in HSP-70 cDNA-transfected cells, but ryanodine treatment did not. "
08/01/2008 - "We present evidence for the first time that the increase in [Ca(2+)](i) in rat cerebellar Type-1 astrocytes, resulting from moderate hypotonic shock, is mediated by Ca(2+) release from ryanodine-operated Ca(2+)(i) stores, and that the magnitude of the intracellular Ca(2+) signal induced by hypotonicity in the short term (up to 240 s) is small and controlled by the activity of the Na(+)/Ca(2+) exchanger operating in its extrusion mode. "
12/01/2013 - "Experiments using 2-aminoethoxydiphenyl borate, nifedipine, or Mn(2+) quenching, strongly suggest that the increased [Ca(2+)](myo) by ryanodine or hypertonic shock is mediated by potentiated SOCE activation. "
07/01/1992 - "Caffeine, ATP, and AMP-PCP activated while calmodulin, SKF-525A, ruthenium red, and Mg2+ inhibited [3H]ryanodine binding in both groups but the A0.5 (concentration requires for half-maximum activation) and the I50 (concentration requires for half-maximum inhibition) for the above-mentioned activators and inhibitors, respectively, were unaffected during endotoxin shock. "

Related Drugs and Biologics

1. Caffeine (No Doz)
2. Calcium
3. Thapsigargin
4. Calcium Channels (Calcium Channel)
5. Nifedipine (Adalat)
6. Adenosine Triphosphatases (ATPase)
7. Diltiazem (Cardizem)
8. diacetylmonoxime (KBDO)
9. Complementary DNA (cDNA)
10. Flecainide (Tambocor)

Related Therapies and Procedures

1. Induced Heart Arrest (Cardioplegia)
2. Microelectrodes
3. Aftercare (After-Treatment)
4. Heart Transplantation (Grafting, Heart)
5. Therapeutics