Serum Heat Shock Protein 90 Alpha: A New Marker of Hypertension-Induced Endothelial Injury?

Abstract

Hypertension-induced endothelial dysfunction is associated with an impaired bioavailability of nitric oxide regulated through interactions between nitric oxide synthase and heat shock protein-90 (Hsp-90). The role of Hsp-90 in the development of arterial hypertension remains unclear. The objective of the study was to evaluate serum concentrations of Hsp-90a in patients with arterial hypertension in comparison to their normotensive counterparts. The study was performed on 49 adults (mean age 55.6 years) with an elevated waist circumference. The individuals presented no subjective feeling of any disease, admitted no drug treatment for any condition, and had not previously been diagnosed with the metabolic syndrome. Patients were screened for arterial hypertension and other component disorders of the metabolic syndrome. Hsp-90a concentrations were evaluated by enzyme-linked immunosorbent assay (ELISA). Twenty-eight subjects were diagnosed with arterial hypertension, while 21 individuals had normal blood pressure. Twenty-five patients satisfied the metabolic syndrome diagnostic criteria. Hsp-90a concentrations were significantly higher (p = 0.002) in the individuals with arterial hypertension than in their normotensive counterparts (median ± interquartile range): 19.42 ng/mL ± 5.17 vs. 16.86 ng/mL ± 3.18. The concentrations of Hsp-90a correlated positively with systolic blood pressure (R = 0.39; p = 0.005) and diastolic blood pressure (R = 0.29; p = 0.046). An increase in Hsp-90a concentrations in patients with arterial hypertension may be a compensatory mechanism for the impaired bioavailability of nitric oxide. The role of Hsp-90a as an early marker of hypertension-associated endothelial injury should be confirmed in further studies on a larger group of patients.