From:  Cardiovascular effects of endocrine hypertension: insights from primary aldosteronism, pheochromocytoma, and Cushing syndrome

 Pathophysiologic mechanisms linking hormonal excess to cardiac injury.

Mechanistic pathwayPAPPGLCSCommon outcomeRef. No.
Mineralocorticoid receptor activation+++++Fibrosis, hypertrophy[3, 4, 11, 12, 41]
β-Adrenergic overstimulation++++/–Myocyte necrosis, arrhythmia[2328, 47]
Oxidative stress+++++++Mitochondrial damage[11, 12, 24, 30, 44]
Endothelial dysfunction+++++++Arterial stiffness[17, 23, 48, 50]
Inflammation and cytokine activation+++++++Fibrosis, remodeling[11, 12, 24, 43, 46]

In CS, β-adrenergic overstimulation is primarily indirect, resulting from cortisol-induced upregulation of adrenergic receptors and enhanced sympathetic sensitivity. –: denotes absence or negligible contribution; +/–: denotes weak or indirect involvement; +: denotes mild involvement; ++: denotes moderate involvement; +++: denotes strong and well-established involvement. PA: primary aldosteronism; PPGL: pheochromocytoma and paraganglioma; CS: Cushing syndrome.