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. 2023 Nov 14;12(22):7081.
doi: 10.3390/jcm12227081.

Platelet Cyclic GMP Levels Are Reduced in Patients with Primary Aldosteronism

Carla Sala  1   2 , Marta Rescaldani  3 , Elisa Gherbesi  1 , Gianni Bolla  1   2 , Cesare Cuspidi  4 , Massimiliano Ruscica  1   5 , Stefano Carugo  1   2
Affiliations

Platelet Cyclic GMP Levels Are Reduced in Patients with Primary Aldosteronism

Carla Sala et al. J Clin Med. .

Abstract

Background and aim: Nitric oxide inhibits platelet aggregation by increasing the second messenger cyclic guanosine-3',5'-monophosphate (cGMP) through the activation of soluble guanylyl cyclase in target cells. Within this context, the oxidative stress associated with the aldosterone excess impairs the nitric oxide availability. Thus, the aim of the present study was to assess the impact of chronic aldosterone excess on the platelet nitric oxide/cGMP pathway in humans.

Methods: The levels of cGMP were evaluated in platelets of male patients, 12 with primary aldosteronism (PA) and 32 with uncomplicated essential hypertension (EH), matched for age and blood pressure (BP) values.

Results: PA and EH patients were 52.8 ± 3 years old and 51.6 ± 1.6 years old, respectively. Systolic and diastolic BP were 158 ± 5.0 mmHg and 105.9 ± 2.3 mmHg in PA and did not differ compared to EH patients (156.6 ± 2.4 mmHg and 104.7 ± 1.2 mmHg). Mean aldosterone levels were significantly higher in PA (25.5 ± 8.8 ng/dL) compared toEH (8.11 ± 0.73 ng/dL), whereas potassium was significantly lower in PA (3.52 ± 0.18 mEq/L) compared to EH (4.08 ± 0.04 mEq/L). Aldosterone and potassium were inversely related (r = -0.49, p = 0.0006) in the whole study population (n = 44). Platelet cGMP was significantly lower in PA (5.1 ± 0.36 pM/109 cells) than in EH (7.1 ± 0.53 pM/109 cells), and in the entire study cohort, it was directly related to plasma potassium (r = 0.43, p = 0.0321).

Conclusions: These results show an impairment of nitric oxide/cGMP signaling in platelets of PA patients. This effect is likely related to the potassium-depleting effect of chronic aldosterone excess. Future studies are needed to understand whether the platelet nitric oxide/cGMP system is involved in the atherothrombotic events in these patients.

Keywords: cyclic guanosine-3′,5′-monophosphate; essential hypertension; nitric oxide; primary aldosteronism.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Scatter-plot of cGMP in platelets. Primary aldosteronism (PA, n = 12; blue dots) and Essential hypertension (EH, n = 32; red dots); p, values. cGMP, cyclic guanosine-3′,5′-monophosphate.
Figure 2
Figure 2
Correlation analyses between (A) plasma levels of potassium and aldosterone and (B) between plasma levels of cGMP and ANP in patients with primary aldosteronism (n = 12; blue dots) and essential hypertension (n = 32; red dots). cGMP, cyclic guanosine-3′,5′-monophosphate; ANP, atrial natriuretic peptide.
Figure 3
Figure 3
Correlation analysis between platelet and plasma cGMP in patients with primary aldosteronism (n = 12; blue dots) and essential hypertension (n = 32; red dots). cGMP, cyclic guanosine-3′,5′-monophosphate.
Figure 4
Figure 4
Correlation analyses between platelet cGMP and (A) aldosterone and (B) potassium in patients with primary aldosteronism (n = 12; blue dots) and essential hypertension (n = 32; red dots). cGMP, cyclic guanosine-3′,5′-monophosphate.
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