Abstract
BackgroundCirculating monocytes and tissue macrophages play complex roles in the pathogenesis of hypertension and the resulting target organ damage. In this study, we observed alterations in the monocyte phenotype and inflammatory state of hypertensive patients with left ventricular hypertrophy (LVH) and studied the effects of irbesartan in these patients. This study might reveal a novel mechanism by which irbesartan alleviates LVH, and it could provide new targets for the prevention and treatment of hypertensive target organ damage.MethodsCD163 and CD206 expression on monocytes and IL-10 and TNF-α levels in the serum of hypertensive patients with or without LVH and of healthy volunteers were detected. Furthermore, we treated monocytes from the LVH group with different concentrations of irbesartan, and then, CD163, CD206, IL-10 and TNF-α expression was detected.ResultsWe found, for the first time, that the expression of CD163, CD206 and IL-10 in the LVH group was lower than that in the non-LVH group and healthy control group, but the TNF-α level in the LVH group was significantly higher. Irbesartan upregulated the expression of CD163 and CD206 in hypertensive patients with LVH in a concentration-dependent manner. Irbesartan also increased the expression of IL-10 and inhibited the expression of TNF-α in monocyte culture supernatants in a concentration-dependent manner.ConclusionsOur data suggest that inflammation was activated in hypertensive patients with LVH and that the monocyte phenotype was mainly proinflammatory. The expression of proinflammatory factors increased while the expression of anti-inflammatory factors decreased. Irbesartan could alter the monocyte phenotype and inflammatory status in hypertensive patients with LVH. This previously unknown mechanism may explain how irbesartan alleviates LVH.Trail registration The study protocols were approved by the Ethical Committee of the Second Affiliated Hospital of Dalian Medical University. Each patient signed the informed consent form.
Highlights
Circulating monocytes and tissue macrophages play complex roles in the pathogenesis of hypertension and the resulting target organ damage
The systolic blood pressure (SBP) and diastolic blood pressure (DBP) of the left ventricular hypertrophy (LVH) and non-LVH groups were higher than those of the control group (P < 0.05), but there was no significant difference between the LVH and non-LVH groups (P > 0.05)
We found that irbesartan could upregulate the expression of CD163 and CD206 in monocytes of hypertensive patients with LVH in a concentration-dependent manner, of which the 10–6 mol/L group was the most significant (P < 0.01) (Fig. 4)
Summary
Circulating monocytes and tissue macrophages play complex roles in the pathogenesis of hypertension and the resulting target organ damage. We observed alterations in the monocyte phenotype and inflammatory state of hypertensive patients with left ventricular hypertrophy (LVH) and studied the effects of irbesartan in these patients. This study might reveal a novel mechanism by which irbesartan alleviates LVH, and it could provide new targets for the prevention and treatment of hypertensive target organ damage. 270 million patients with hypertension in China, accounting for approximately 1/5 of the global number of patients with hypertension, and 30% of the patients with hypertension were complicated by left ventricular hypertrophy (LVH) [1]. LVH is considered to be an important marker of target organ damage in hypertension and is an important predictor of coronary heart disease, heart failure and stroke. Patients with LVH have a significantly increased risk of cognitive impairment, atherosclerosis, atrial fibrillation and other diseases. The prevention and alleviation of LVH has become a long-term goal of hypertension treatment
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