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Measurement of Cyclic Guanosine Monophosphate (cGMP) in Solid Tissues using Competitive Enzyme-Linked Immunosorbent Assay (ELISA)
Published on: July 3, 2025
Platelet cyclic GMP levels in unstable angina and myocardial infarction
Massimo Pistono1, Serena Bergerone, Luisella Carrieri
1Department of Cardiology, University of Torino, Torino, Italy.
Insights
Platelet cyclic GMP (cGMP) levels are elevated in unstable angina and acute myocardial infarction patients, indicating altered nitric oxide-cyclic GMP pathways. Unstable angina patients show higher cGMP response to sodium nitroprusside, suggesting distinct mechanisms in these coronary syndromes.
Area of Science:
- Cardiology
- Biochemistry
- Platelet Physiology
Background:
- Platelet hyperactivation is observed in coronary syndrome.
- The nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway regulates platelet aggregation.
- Investigating alterations in this pathway is crucial for understanding unstable angina (UA) and acute myocardial infarction (AMI).
Purpose of the Study:
- To investigate the platelet nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway in patients with unstable angina (UA) and acute myocardial infarction (AMI).
- To determine if alterations in platelet aggregation regulation are present in these patient groups.
Main Methods:
- Platelet cyclic guanosine monophosphate (cGMP) levels were measured using a radioimmunoassay kit.
- Measurements were taken under basal conditions and after stimulation with sodium nitroprusside (SNP).
- SNP stimulation served as an indirect assessment of soluble guanylate cyclase (sGC) activity.
Main Results:
- Basal platelet cGMP levels were significantly higher in patients with UA and AMI compared to controls.
- Final cGMP levels after SNP stimulation were significantly elevated in UA patients compared to both AMI patients and controls.
- No significant difference in SNP-stimulated cGMP levels was observed between AMI patients and controls.
Conclusions:
- Elevated basal platelet cGMP in UA and AMI suggests enhanced platelet-derived NO synthesis.
- This may be due to increased intraplatelet calcium and platelet endothelial nitric oxide synthase (cNOS) activation.
- UA and AMI exhibit distinct behaviors regarding SNP-dependent cGMP production, with UA showing higher activity and AMI demonstrating a loss of functional soluble guanylate cyclase (sGC).
Background:
Several studies showed that there is a state of platelet hyperactivaction in patients with coronary syndrome: the aim of this study is to investigate if the platelet nitric oxide-cyclicGMP (NO-cGMP) pathway, that regulates platelet aggregation is altered in patients with unstable angina (UA) and acute myocardial infarction (AMI).
Methods And Results:
Population included 11 patients with UA, 12 patients with AMI and 23 controls. Platelet cGMP was measured by a radioimmunoassay kit, under basal conditions and after stimulation with sodium nitroprusside (SNP), which maximally stimulates soluble guanylate cyclase (sGC), used as an indirect measurement of active sGC. Basal platelet cGMP values were significantly (P<0.001) higher in patients with UA and AMI than in controls (UA, 1089 +/- 412 pmol/10(10) platelets; AMI, 1071 +/- 507 pmol/10(10) platelets; controls, 492 +/- 201 pmol/10(10) platelets). The final cGMP level reached after SNP stimulation was significantly more elevated in UA, compared with both AMI (P<0.05) and controls (P<0.02) (UA, 4428 +/- 2723 pmol/10(10) platelets; AMI, 2728 +/- 655 pmol/10(10) platelets; controls, 2772 +/- 1031 pmol/10(10) platelets); on the contrary no significant difference between AMI and controls was observed.
Conclusions:
Basal platelet cGMP is significantly higher in both UA and AMI groups. This observation suggests that: (1) platelet-derived NO synthesis may be enhanced inUA and AMI, due to increase of intraplatelet calcium level and of platelet cNOS activation; (2) platelets from UA and AMI patients are continuously stimulated by the high-level NO production due to increased iNOS expression. As far as SNP-dependent cGMP production is concerned, UA and AMI behave as two separate conditions. SNP-stimulated activity in UA is higher than in controls, while a loss of functional sGC is observed in AMI.
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