Figure 1.

Pathophysiology of catecholamine-induced hypertensive crises and related cardiovascular complications. Norepinephrine and epinephrine display different binding affinities for adreno-receptors, leading to distinct clinical phenotypes according to the specific secreting pattern of the pheochromocytoma. Stimulation of α1 receptors, which show a higher affinity for norepinephrine, mediates an increase in peripheral vascular resistance, leading to sustained arterial hypertension and complications such as flash pulmonary edema, coronary artery vasospasm, myocardial infarction, aortic dissection, and hemorrhagic stroke. On the other hand, stimulation of cardiac β1 receptors, which have a greater affinity for epinephrine, leads to a positive chronotropic and inotropic effect, with the potential development of tachyarrhythmias, myocardial ischemia, and systolic hypertension. Finally, the stimulation of cardiac and vascular β2 receptors by epinephrine can lead to negative inotropism and vasodilation with subsequent hypotension and Tako-Tsubo like cardiomyopathy.