Plasma endothelin-1 (ET-1) levels were studied in 15 obese hypertensive (mean age 48.5 +/- 3.9 years) and 15 obese normotensive men (mean age 49.5 +/- 3.6 years) before and after weight loss due to an 800 kcal/day diet lasting 12 weeks. Circulating peptide concentrations were also assessed in nonobese hypertensive (n = 11) and normotensive men (n = 12). Baseline plasma ET-1 levels were similar in obese hypertensive (0.87 +/- 0.22 pg/ml) and obese normotensive men (0.91 +/- 0.30 pg/ml). In seven obese hypertensive men, caloric restriction normalized blood pressure levels (systolic: from 166.6 +/- 8.1 to 145.0 +/- 6.3 mmHg, P < 0.0001; diastolic: from 106.6 +/- 5.1 to 89.1 +/- 2.0 mmHg, P < 0.0001) and decreased body mass index (BMI) (from 33.4 +/- 1.6 to 29.6 +/- 2.1 kg/m2, P < 0.002) and plasma ET-1 levels (from 0.93 +/- 0.21 to 0.64 +/- 0.26 pg/ml, P < 0.05). In the remaining obese hypertensive men (n = 8), blood pressure levels were not normalized by caloric restriction despite a significant decrease of BMI and plasma ET-1 levels (from 0.83 +/- 0.23 to 0.60 +/- 0.16 pg/ml, P < 0.04). Weight loss also significantly decreased BMI and ET-1 (from 0.91 +/- 0.30 to 0.65 +/- 0.19 pg/ml, P < 0.01) in obese normotensive men. Baseline ET-1 and fasting insulin levels were significantly correlated in obese hypertensive (r = 0.518, P < 0.05) and obese normotensive men (r = 0.535, P < 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

The Montagna dei Fiori has received attention from geologists over the past decades because of both its Jurassic stratigraphy and its complex present-day structure. The latter is the result of multiple phases of deformation, from the Early Jurassic, during the opening of the Tethyan Ocean, to Neogene evolution of the Apennines fold-and-thrust belt. In this paper. we present a new stratigraphic interpretation of the Jurassic palaeogeography, based on a new geological mapping project in the area. Using this new stratigraphy. we constructed two forward models, using a combination of different fault/fold interactions, in order to unravel the kinematic evolution of the Montagna dei Fiori fault-related fold. The first model was constructed manually using the fault-bend and fault-propagation theories from an in configuration which included previous extensional features, whereas the second model was constructed using the software 2DMove (Midland Valley) using the fault-bend and In shear fault-propagation folding theories and starting from a layer-cake stratigraphy. Both forward models involved the same main steps and provided a reasonable geological simulation of the geometry of the Montagna dei Fiori structure. Copyright 2010 (C) John Wiley & Sons, Ltd

(50.5 (8.49) mm Hg, range 37-67 mm Hg), and systemic hypertension alone (160.7 (5-9)/100-6 (3.2) mm Hg) was present in 11 patients. Both conditions were present in 12 patients, while 11 patients had systemic sclerosis without pulmonary or systemic hypertension. There were no significant differences in plasma ET-1 levels between patients with pulmonary hypertension alone (1*62 (0.21) pg/ml) and those with systemic hypertension alone (1*65 (0.43) pg/ml). In particular, patients with normal pulmonary artery and systemic pressures (n = 11) had plasma ET-1 concentrations identical to those found in patients (n =12) with both pulmonary and systemic hypertension (1.70 (0.15) v 1-64 (0.35) pg/ml, respectively). No correlations were observed between plasma ET-1 and either pulmonary or systemic pressures. Conclusion-Systemic sclerosis is characterised by increased plasma ET-1 levels, but neither pulmonary nor systemic hypertension are accompanied by fiuther increase in plasma peptide levels. (Ann Rheum Dis 1995; 54: 730-734)

In order to verify the influence of salt sensitivity on the blood pressure response to orally administered kallikrein, we evaluated the efficacy of glandular kallikrein (derived from porcine pancreas) in 28 essential hypertensives (21 males and 9 females) aged between 40 and 62 years. After a placebo run-in period, the patients were assigned to receive oral kallikrein therapy (150 IU 3 times a day; n = 18 patients) or placebo (n = 10 patients) over a period of 8 days in a random double-blind fashion. In the salt-resistant patients (n = 8), kallikrein administration did not modify blood pressure levels. In the same group, natriuresis increased significantly after the treatment [from 94.51 ± 10.76 to Ill.65 ± 23.19 mEq/24 h (mmol/24 h), p < 0.039]. In the salt-sensitive patients (n = 10), blood pressure decreased with the kallikrein therapy (systolic: from 158.50 ± 9.20 to 144.50 ± 10.12 mm Hg, p < 0.005; diastolic: from 99.50 ± 2.16 to 90.0 ± 3.67 mm Hg, p < 0.024). In the same patients, urinary Na+ excretion increased considerably after the kallikrein treatment (from 101.07 ± 18.36 to 134.34 ± 18.27 mEq/ 24 h, p < 0.0001). Therefore, our data indicate that the oral kallikrein administration reduces blood pressure levels only in the salt-sensitive hypertensives. In both the salt-sensitive and the salt-resistant groups a marked increase in the 24-hour urinary excretion of sodium was observed after the kallikrein treatment. Therefore, the enhanced antihypertensive efficacy of the oral kallikrein administration observed in the sodium-sensitive patients is not only due to its natriuretic action but also to different kallikrein-related effects.