OBJECTIVE: To evaluate the relationship between insulin, the renin-aldosterone system and blood pressure in obese subjects. DESIGN AND METHODS: A cross sectional study of a group of severely obese normotensive subjects who were surgical candidates (n 39; mean BMI: 47.8 AE 1.4) and a group of hypertensive patients (n 57; mean BMI: 28.0 AE 0.7) twenty-nine of whom had BMI b 27. All subjects were studied after 15 days on a balanced diet. Insulin, plasma renin activity and aldosterone were measured. RESULTS: Fasting insulin, plasma renin activity and aldosterone were higher in severely obese normotensive subjects than in hypertensive subjects (respectively 32.3 AE 3.0 vs 13.1 AE 1.0 mUal, P 0.0001; 1.34 AE 0.22 vs 0.88 AE 0.12 ngamlah, P 0.04; 137.2 AE 16.2 vs 87.9 AE 12.1 pgaml, P 0.015). Insulin was related to BMI and to aldosterone both in normotensive and in hypertensive patients. CONCLUSION: Hyperinsulinemia itself does not determine hypertension; in some people it could play a vasodilator role in opposition to the renin-aldosterone system.

The progressive decrease of glomerular function in subjects with hypertension is linked with insulin-resistance.

In hypertensive patients, smoking does not modify typical renal haemodynamic changes of arterial hypertension; however, it significantly increases the albumin excretion rate.

Vasoactive intestinal peptide (VIP) has been postulated as a nonadrenergic, non-cholinergic transmitter in the relaxation of vascular and non-vnscular systems. In order to synergize the vasoactivities of VIP with nitric oxide (NO), we synthesized a Snitrosylated derivative of VII', VIP-GIy-Cys-NO (VIPGC-NO). On aortic rings, VIPGC-NO exhibited a dose-dependent vnsorelaxation similar to S-nitrosoglutathiooe (GSNO), and both induced complete vasorelaxatiun at 1 pM, whereas, VIP at I i.tM only produced 19°/, relaxation. The degree of vnsorelaxation was proportional to the increases in cyclic GMP with no significant enhancvmant in cAMP level. On preoontracted tracheal rings, VIP, VIPGC-NO, VIPGC and GSNO produced relaxation with ECs0 0f74 + 5, 32 ± 6, 59 + 9, and 251+ 32 nM, respectively, which was consistent with increases in eGMP. A marked increase in cAMP was observed from the tracheal rings pretraated with VIP, VIPGC-NO and its parent V1P-Gly-Cys (VIPGC) as well as isoproterenol. Propranolol only blocked the airway relaxation induced by iseproterenol, but did not antagonize the ralaxation induced by VIP, VIPGC and VIPGC-NO. On rabbit sphincter of Odd±, VIP, VIPGC-NO and VIPGC inhibited both basic and ACh-induced contraction, whereas, GSNO was less potent than VIP and its derivatives over a range of 2 log units in this respect. On rat gastric fundus, these eompoands inhibited contraction amplitude and frequency induced with 5-HT in the order of inhibitory potency VIP> V1PGC-NO> VIPGC> isoproterenol > GSNO. Our data suggest that NO is selective in relaxing vascular smooth muscle via the cGMP pathway, whereas VIP is selective in relaxing nonvascular smooth muscles via the activation of both cGMP and cAMP pathways. Key Words: Vasonctive intestinal polypeptide; eGMP, cAMP S-nitrosylated-VIP; Nitric oxide; S-nitrosothione; D023 ENDOTHELIAL DYSFUNCTION IN A GROUP OF ESSENTIAL HYPERTENSIVE PATIENTS RELATED TO SALT-SENSITIVITYE. Bragulat, A. de la Sierra*, MT. Antonio, E. G6mez-Angelats, V. Giner, C. Sierra, MT. Aguilera*, W. Jimdnez, A. Coea*. Hypertension Unit. Hospital Clinic, Barcelona. SPAIN. The aim of the study was to evaluate the degree of endothelial dysfunction in a group of essential hypertensive (EH) patients related to their saltsensitivity. Fourteen never ~eated EH patients without evidence of target organ damage were studied. Salt-sensitive hypertension was defined as a signitieant rise (p

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