Related Experiment Video

Updated: Jun 27, 2026

Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection
08:52

Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection

Published on: February 17, 2015

Cardiac dysrhythmia produced by Mesobuthus tamulus venom involves NO-dependent G-Cyclase signaling pathway

Sadhana Kanoo1, Maloy B Mandal, Anitha B Alex

  • 1Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, 221 005, India.

Naunyn-Schmiedeberg'S Archives of Pharmacology
|November 28, 2008
PubMed

Insights

Indian red scorpion venom affects heart rate and force via G-protein coupled pathways. These cardiotoxic effects involve nitric oxide (NO) and muscarinic receptors, influencing atrial function.

Area of Science:

  • Cardiovascular Pharmacology
  • Toxicology
  • Neuropharmacology

Background:

  • Indian red scorpion (Mesobuthus tamulus) venom contains toxins that can affect cardiovascular function.
  • G-protein coupled pathways play a crucial role in regulating cardiac activity and response to toxins.

Purpose of the Study:

  • To investigate the role of G-protein coupled pathways in mediating the cardiotoxic effects of Indian red scorpion venom.
  • To elucidate the specific signaling mechanisms involved in venom-induced atrial dysrhythmia.

Main Methods:

  • Isometric contractions of rat right atrial preparations (spontaneously beating and paced) were recorded in vitro.
  • Cumulative concentration-response curves for venom were generated.
  • The effects of pharmacological inhibitors (atropine, NO synthase inhibitor, guanylyl cyclase inhibitor, Ca(2+) channel antagonist) were assessed.

Main Results:

  • Venom decreased atrial rate and increased force in spontaneously beating atria, effects sensitive to atropine, NO synthase inhibition, and guanylyl cyclase inhibition.
  • Nifedipine blocked force changes but not rate changes in spontaneously beating atria.
  • In paced atria, venom caused a concentration-dependent decrease in force, attenuated by nifedipine.

Conclusions:

  • Venom-induced atrial dysrhythmia is mediated by muscarinic receptor-dependent NO-guanylyl cyclase signaling pathways.
  • Distinct mechanisms underlie venom-induced rate and force modifications in atrial preparations.

More Related Videos

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice09:20

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

Published on: July 5, 2021

Ambulatory ECG Recording in Mice08:00

Ambulatory ECG Recording in Mice

Published on: May 27, 2010

Related Concept Videos

Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
Electrophysiology of Normal Cardiac Rhythm01:19

Electrophysiology of Normal Cardiac Rhythm

The normal cardiac rhythm is a synchronized electrical activity that facilitates the regular and coordinated contraction of the heart muscle. This process is essential for efficient blood circulation throughout the body. The fundamental elements involved in establishing and maintaining this rhythm include the unique electrical properties of cardiac muscle cells, the sinoatrial (SA) node's pacemaker function, the specialized conducting system, and the ionic mechanisms underlying each phase of...
G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Conduction System of the Heart01:19

Conduction System of the Heart

Autorhythmicity is a term that refers to the heart's inherent ability to generate electrical signals and instigate muscle contractions. This self-regulating conduction system within the heart consists of two key components: the pacemaker cells and specialized conducting cells.
The pacemaker cells are located in two primary nodes: the sinoatrial (SA) node and the atrioventricular (AV) node. The SA node pacemaker cells can autonomously depolarize, triggering an action potential that leads to the...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...