Please use this identifier to cite or link to this item: http://nopr.niscair.res.in/handle/123456789/4457
Title: Bradycardia induced by <i style="">Mesobuthus tamulus</i> scorpion venom involves muscarinic receptor-G-protein-coupled cell signaling pathways
Authors: Deshpande, Shripad B.
Kanoo, Sadhana
Alex, Anitha B.
Keywords: Cardiac dysrhythmia
Guanylyl cyclase
Indian red scorpion
Methylene blue
Pertussis toxin
Issue Date: Apr-2008
Publisher: CSIR
Abstract: Indian red scorpion (<i style="">Mesobuthus tamulus</i>; MBT) envenomation produces various cardio-respiratory abnormalities including cardiac dysrhythmias. The underlying cell signaling pathways for the cardiac dysrhythmias produced by MBT venom are not known. The present study was therefore conducted to delineate the second messenger signaling pathways involved in MBT venom-induced atrial rhythm changes. The effects of venom and various antagonists were examined on spontaneously beating rat right atrial preparations <i style="">in vitro.</i> The<i style=""> </i>MBT-venom produced an increase (35%), a decrease (45%) and again an increase (50%) in rate at 0.03, 0.3 and 3.0 µg/ml of venom, respectively. On the other hand, force of contraction exhibited a concentration-dependent rise (up to 40%) at all concentrations of venom. Pretreatment with atropine (0.3 µM) blocked the decrease in atrial rate at 0.3 µg/ml concentration of venom while no such blockade was seen in force of contraction. Submaximal concentration of ACh (0.1 nM) decreased the atrial rate by 25%. In the presence of MBT venom (0.3 µg/ml), ACh-induced fall in atrial rate was enhanced. The venom-induced fall in atrial rate and augmentation of ACh response were blocked by pertussis toxin (PTx; a G<sub>i</sub>-inhibitor) or methylene blue (a G-cyclase inhibitor). The results indicate that the decrease in atrial rate produced by venom is mediated muscarinic by receptors <i>via</i> G<sub>i</sub>-guanylyl cyclase mediated cell signaling pathways.
Description: 229-233
URI: http://hdl.handle.net/123456789/4457
ISSN: 0019-5189
Appears in Collections:IJEB Vol.46(04) [April 2008]

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