Plasma aldosterone and its relationships with left ventricular mass in essential hypertensive patients with the metabolic syndrome.

BACKGROUND: The association of aldosterone with the metabolic syndrome (MetS) has not been fully elucidated. The aim of our study was to evaluate the relationships of plasma aldosterone concentration (PAC) with MetS and left ventricular mass (LVM) in nondiabetic Caucasian patients with essential hypertension. METHODS: Measurements were taken with the patients off antihypertensive medications. The measurements included 24-h blood pressure (BP) readings, plasma renin activity (PRA) and aldosterone, and an echocardiogram. RESULTS: Subjects with MetS (n = 201) had higher age-adjusted PAC (10.2 +/- 5.8 vs. 11.6 +/- 5.9 ng/dl; P = 0.01) and greater age-adjusted LVM indexed for height2.7 (LVMH2.7) (56 +/- 19 vs. 62 +/- 20 g/m2; P = 0.001) than those without MetS (n = 249). The difference in respect of PAC between the two groups was independent of PRA and was attributable mainly to obesity. After adjusting for potential confounders, LVMH2.7 was associated with MetS as a whole (beta = 0.11; P = 0.02) and with body mass index (BMI) (beta = 0.19; P < 0.0001) in the overall population. The latter relationship was attenuated (beta = 0.15; P = 0.001) after further adjustment for PAC. In the MetS group the association of LVMH2.7 with PAC held (beta = 0.19; P = 0.007) in multivariate analyses. In subjects without MetS, this relationship had only borderline statistical significance. CONCLUSIONS: Our results suggest that the elevated PAC related to obesity may help to explain the increased LVM observed in association with MetS, and may contribute to enhancing the cardiovascular risk associated with MetS.

Influence of the metabolic syndrome on aortic stiffness in never treated hypertensive patients.

BACKGROUND AND AIM: Metabolic syndrome (MS) carries an increased risk for cardiovascular events and there is a growing awareness that large artery stiffening is a powerful predictor of cardiovascular morbidity and mortality. Little is known about the relationship of MS with aortic stiffness. The aim of our study was to analyze, in patients with essential hypertension, the influence of MS, defined according to the criteria proposed by the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (NCEP-ATP III), on carotid-femoral pulse wave velocity (PWV), a measure of aortic stiffness. METHODS: Ninety-three untreated essential hypertensives, aged between 23 and 61 years, without diabetes mellitus, were studied. All subjects underwent routine blood chemistry, oral glucose tolerance test with glucose and insulin determinations, albumin excretion rate (AER) measurement, 24-h ambulatory blood pressure monitoring, and measurement of carotid-femoral PWV, by means of a computerized method. RESULTS: Patients with MS (n = 28) showed higher age-adjusted carotid-femoral PWV (10.1 +/- 1.4 vs 9.3 +/- 1.4 m/s; p = 0.01) when compared to subjects without MS. This difference held after controlling for gender and for 24-h mean blood pressure (MBP) (p = 0.02) and lost its statistical significance after further adjustment for AER. In a multiple regression model, excluding the individual components of MS, in which metabolic syndrome was added along with age, gender, smoking habit, LDL cholesterol, HOMA index, 24-h MBP and 24-h heart rate, MS remained independently associated with carotid-femoral PWV (beta = 0.29; p = 0.002). The statistical significance of this association disappeared after the inclusion into this model of AER. CONCLUSIONS: Metabolic syndrome is associated with an increased aortic stiffness. Main explanatory factors of this association are age, systolic blood pressure and albumin excretion rate.

Renal plasma flow, filtration fraction and microalbuminuria in hypertensive patients: effects of chronic smoking.

INTRODUCTION: Albumin excretion rate is usually increased in people who smoke, but the physiological basis of this phenomenon is not fully understood. METHODS: The effect of chronic smoking on renal haemodynamics was studied in a cohort of 66 men. Twenty-seven were smokers and 36 were hypertensive. In all subjects, the albumin excretion rate was evaluated; in hypertensive patients, a renoscintigraphic evaluation of renal plasma flow and glomerular filtration were carried out and the filtration fraction was calculated. RESULTS: The hypertensive smoking population presented an increased urinary albumin excretion rate in comparison with hypertensive non-smoking patients. No significant differences were found for the mean values of renal plasma flow, the glomerular filtration rate and the filtration fraction between hypertensive smokers and hypertensive non-smoking patients. CONCLUSIONS: In hypertensive patients, smoking does not modify typical renal haemodynamic changes of arterial hypertension; however, it significantly increases the albumin excretion rate.

Insulin resistance and glomerular hemodynamics in essential hypertension.

BACKGROUND: Arterial hypertension is an important cause of end-stage renal failure. Insulin has been shown to modify glomerular hemodynamics in hypertensive subjects. The aim of this work, therefore, was to observe the relationships between renal hemodynamics and insulin resistance in arterial hypertension. METHODS: Sixty-two non-diabetic hypertensive patients and 25 healthy normal subjects were studied. Renal plasma flow and the glomerular filtration fraction were determined by renoscintigraphy and the insulin sensitivity by an oral glucose test. RESULTS: Renal plasma flow in hypertensive subjects was lower than expected and was related to pressure values, whereas the mean glomerular filtration rates were not different in the two groups. In most patients the filtration fraction was higher than expected. A lower glomerular filtration rate and lower filtration fraction were found in patients with higher insulin resistance. CONCLUSIONS: The progressive decrease of glomerular function in subjects with hypertension is linked with insulin-resistance.