OBJECTIVE: To ascertain in obesity the role of body fat distribution (the strongest predictor of morbility and mortality in obese subjects) in determining the degree of endothelial dysfunction, an early marker of atherosclerotic disease. SUBJECTS: 18 premenopausal women with uncomplicated obesity excluding other cardiovascular risk factors and 12 age-matched slim healthy women. MEASUREMENTS: Endothelium-dependent vasodilation, studied as diameter variation in response to an increase in shear-stress, was evaluated in the right common femoral artery of obese and slim subjects by a non invasive approach and compared to glyceril-trinitrate vasodilation. To characterize better the vascular functional andaor structural properties, we studied the arterial wall distensibility by an echo-tracking system. Adipose tissue regional distribution was determined by computerised axial tomography. RESULTS: The endothelium-dependent vasodilation was signi®cantly impaired in obese subjects (P`0.005 versus non-obese subjects) while glyceril-trinitrate vasodilation and arterial distensibility were similar in the two groups. In our obese subjects endothelial-dependent vasodilation was inversely correlated to body fat distribution (visceralasubcutaneous adipose tissue ratio: r À0.624, P 0.0058). In contrast, metabolic parameters (except C-peptide response during oral glucose tolerance test (OGTT): r À0.587, P 0.01), blood pressure values and body weight did not correlate with the endothelial function. CONCLUSION: Uncomplicated obesity per se is characterised by an alteration of the endothelial function; the degree of this vascular damage is predicted by body fat distribution independently of body weight and metabolic and other haemodynamic parameters, and correlates with an index of insulin secretion.

The results confirm the hypothesis that dysfunction of autonomic control of the cardiovascular response may be a contributing pathogenetic factor in NTG, inducing a chronic ischemia of the optic nerve.

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SUMMARY Intracellular free calcium, [Ca 2 + ],, was studied in platelets of essential hypertensive subjects and normotensive controls under basal conditions and after stimulation with epinephrine, norepinephrine, angiotensin II, ouabain, and thrombin, using the fluorescent calcium indicator quin 2. Basal [Ca 2+ ], was significantly higher in hypertensive subjects (n = 32) than in normotensive controls (n = 30; 167.4 ± 5.0 vs 143.2 ± 3.1 nmol/L; p<0.001). Epinephrine, norepinephrine, angiotensin II, and ouabain had no effect on platelet calcium, whereas thrombin induced a dose-dependent increase in [Ca 2+ ]| in both the presence and absence of extracellular calcium. This [Ca 2+ ]| increase in the presence of extracellular calcium, which depends mainly on calcium influx, was significantly higher (p<0.05) in platelets of hypertensive subjects at all thrombin concentrations (ranging from 0.025-0.1 U/ml), while the [Ca 2+ ]| increase in the absence of extracellular calcium, which depends only on release from intracellular stores, was similar in hypertensive subjects and controls. These results suggest that, in essential hypertension, there is not only increased platelet resting [Ca 2+ ]| but also an increase in agonist-mediated calcium influx, which appears to indicate a cell membrane abnormality in the platelets of subjects with essential hypertension.

Urinary excretion of kallikrein has been studied in a patient with hypokalemic alkalosis, hyperplasia of the renal juxtaglomerular apparatus and hyperreninemia, secondary aldosteronism and resistance to the pressor effect of angiotensin II (Bartter's syndrome). Urinary kallikrein was found exceedingly high in several determination, whereas it was low in patients with essential hypertension and high in patients with primary aldosteronism. Urinary kallikrein decreased after spironolactone therapy. The rise of kallikrein excretion (which is not related to plasma renin) in this case is probably caused by a direct action of the chronic excess of plasma aldosterone; it could not be accounted for as secondary to natriuresis.