Lercanidipine effect on polymorphonuclear leukocyte-related inflammation and insulin resistance in essential hypertension patients.

Abstract

IntroductionInflammation, insulin resistance, and oxidative stress (OS) are among the mechanisms that have been implicated in the pathogenesis of essential hypertension (EH). Peripheral polymorphonuclear leukocytes (PMNLs) are primed in EH patients, releasing uncontrolled superoxide anions contributing to OS in these patients. PMNL priming correlates with insulin resistance and PMNL intracellular calcium ([Ca2+]i). Recent studies have attributed additional anti-ischemic and antioxidative characteristics to the antihypertensive drug, lercanidipine, a third-generation calcium-channel blocker. The purpose of this study was to evaluate the possible nontraditional effect of 2 months of lercanidipine treatment on insulin resistance and on PMNL-related inflammation in EH patients.MethodsNon-smoking EH patients with untreated mild-to-moderate high blood pressure (BP) were included. Low-grade inflammation was reflected by PMNL apoptosis and by white blood cell (WBC) and PMNL counts. Systemic inflammation was measured by plasma fibrinogen, C-reactive protein (CRP), and transferrin and albumin levels. Fasting serum insulin levels served as a marker of insulin resistance.ResultsTwo months of lercanidipine treatment showed a significant decrease in BP, WBC, and PMNL counts, PMNL apoptosis, CRP, and serum insulin levels, and a significant increase in serum albumin levels. Rates of superoxide release from PMNLs, WBC and PMNL counts, and insulin levels positively correlated with mean arterial BP values.ConclusionThe use of lercanidipine can be favorable in EH patients due to its combined anti-PMNL priming and anti-inflammatory effects, in addition to its antihypertensive characteristics.