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Negative inotropic effect of cyclic GMP in cardiac fiber fragments
Abstract:
The force of spontaneously beating cardiac cellular fragments obtained from mice heart by homogenization was recorded in presence of cyclic guanosine -3'.5'-monophosphate (cGMP) and cyclic 8-bromguanosine -3'.5'-monophosphate in concentrations of 3 X 10(-6) M - 33 X 10(-6) M. The nucleotide decreased the force and reduced the rate of spontaneity. Eventually the preparation became quiescent. It is thought that this nucleotide either reduces the capacity to sequester calcium or affects its release from the sarcotubular system.
Insights
Cyclic guanosine monophosphate (cGMP) and its analog reduced heart cell contraction force and rate. These nucleotides ultimately caused cardiac cellular fragments to stop beating, suggesting effects on cellular calcium handling.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Spontaneously beating cardiac cellular fragments are used to study heart muscle function.
- Cyclic nucleotides play roles in regulating cardiac contractility and rhythm.
Purpose of the Study:
- To investigate the effects of cyclic guanosine monophosphate (cGMP) and a related analog on the force and rate of spontaneously beating cardiac fragments.
- To explore the potential mechanisms by which these nucleotides influence cardiac cellular activity.
Main Methods:
- Cardiac cellular fragments were isolated from mouse hearts via homogenization.
- The contractile force and rate of these fragments were measured in the presence of varying concentrations of cGMP and cyclic 8-bromoguanosine monophosphate.
Main Results:
- Both cGMP and its analog significantly decreased the contractile force of the cardiac fragments.
- The rate of spontaneous contractions was reduced, and at higher concentrations, the fragments became quiescent (stopped beating).
Conclusions:
- cGMP and its analog exert inhibitory effects on cardiac cellular contractility and automaticity.
- The observed effects suggest that these cyclic nucleotides may interfere with intracellular calcium sequestration or release mechanisms within cardiac cells.