301 Adiponectin and Aldosterone Levels is Associated with Arterial Stiffness in Resistant Hypertension (original) (raw)

Journal of Hypertension, 2012

Abstract

ABSTRACT Objective: Obesity, arterial stiffness, cardiac hypertrophy, high aldosterone and endothelial dysfunction may interact to cause resistant hypertension (RHTN). Lower adiponectin (APN) and aldosterone excess may be significantly associated with hypertension. However, the importance of hypoadiponectinemia as a complicating factor for the lack of blood pressure (BP) control in RHTN has not been demonstrated. Methods: Ninety-six RHTN patients were divided into uncontrolled (UCRHTN, n=44) and controlled (CRHTN, n=52) subgroups. APN and aldosterone, office BP and ambulatory BP measurement (ABPM), endothelium-dependent brachial artery responses [flow-mediated dilation (FMD)], left ventricular mass index (LVMI) and pulse wave velocity (PWV) were evaluated. Results: UCRHTN had increased aldosterone (12.6 +/- 1.4 vs. 8.9 +/- 0.8 ng/dL, p=0.02) as well as LVMI (142.2 +/- 6.0 vs. 122.9 +/- 4.3 g/m2, p=0.02) and PWV (12.0 +/- 0.3 vs. 9.2 +/- 0.2 m/s, p<0.0001). However, lower APN (6.9 +/- 0.7 vs. 9.5 +/- 0.8 [mu]g/mL, p=0.01) and impaired FMD response (6.6 +/- 0.3 vs. 7.5 +/- 0.3%, p=0.001) were found in this same subgroup. Brachial and ABPM pulse pressures were inversely associated with APN (r = - 0.45, p=0.002; r= - 0.33, p=0.03, respectively) as well as aldosterone and PWV (r = - 0.38, p=0.01; r = - 0.36, p=0.02, respectively) in UCRHTN. PWV was only significantly influenced by APN levels in UCRHTN ([beta]= - 0.16, SE= 0.05, p=0.01). APN did not correlate with the same parameters in CRHTN. Conclusion: Hypoadiponectinemia and high aldosterone may be implicated in antihypertensive therapy resistance in respect to arterial rigidity.

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