Approximately 50% of hypertensive patients are salt sensitive (they increase their Blood Pressure in response to sodium intake or volume expansion). Mechanisms underlying salt sensitivity are not completely elucidated although there is evidence that they may be genetically determined. The aim of this study is to establish the relation among some genetic polymorphisms of the renin-angiotensin system (RAAS) and the beta-3 subunit of the protein G and salt sensitivity. We studied 102 essential hypertensive patients, stage 1-2 and without target organ damage. Salt sensitivity was assessed by the rapid protocol of Weinberger. We determined by polymerase Chain reaction techniques the following polymorphisms: insertion/deletion (I/D) of the angiotensin-converting enzyme (ACE), A1166C of the angiotensin II type 1 receptor (AT1R), -344C/T and intron 2 conversion (IC) of the aldosterone synthase (CYP11B2), and C825T of the beta-3 subunit of the protein G (GNB3). 41 patients (40.19%) were salt sensitive. The distribution of the different polymorphisms was similar in both groups of patients, but subjects carriers of the W allele of the CYP11B2 IC polymorphism had a greater risk for salt sensitivity as compared with no carriers (37 of 41, 90.2% vs 4 of 41, 9.8%, OR 3.02, P<0.05). Although there is no association between salt sensitivity and the different studied genotypes of the RAAS and of the GNB3, our data show a greater risk for salt sensitivity among carriers of the W allele of the CYP11B2 1C polymorphism.

This study was undertaken to characterize blood pressure (by continuous blood pressure recording), renal hemodynamics, and excretory function in high-fructose-fed insulin-resistant dogs. We fed 10 mongrel dogs for 28 days with a normal sodium diet containing 60% of the calories either as fructose (n = 6) or dextrose (n = 4). Fructose-fed dogs developed insulin resistance by the 21st day of the experimental diet, as estimated by the mean glucose concentrations (in arbitrary units, AU) during the final hour of the insulin suppression test (640.3 +/- 57 AU fructose-fed dogs upsilon 397.5 +/- 24.7 AU dextrose fed dogs; P < .05). Neither of the groups showed any change in body weight, or in fasting plasma levels of glucose or insulin. There was no difference in mean arterial pressure between the groups before or during either diet, nor did we find any important alterations in renal function in these animals. We conclude that insulin resistance can be induced by a high-fructose diet in the dog. However, it is not accompanied by either hypertension or alteration in renal function. These findings emphasize the importance of continuously recording blood pressure under resting conditions and suggests that in the fructose-fed dog, insulin resistance does not appear to lead directly to hypertension.

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Increased levels of oxidative stress have been demonstrated in Preeclampsia in previous studies, but this finding has not been established in other hypertensive disorders in pregnancy (HDP). We measured different markers of lipid peroxidation and antioxidant defenses by spectrophotometry or enzymoimmunoanalysis in 339 pregnant women: 85 with gestational hypertension (GH), 88 chronic hypertension (CH), 104 Preeclampsia and 62 healthy pregnant control women (PCW). Lower activity of superoxide dismutase and higher levels of catalase were found in GH, CH and preeclampsia compared with PCW (964.4±116.5, 970.0±120.4, 971.2±137.5 and 1063.4±133.7 U g À1 Hb, Po0.001; and 313.0±71.7, 292.2±45.3, 297.1 ± 47.2, 215.5 ± 26.2 U mg À1 Hb, Po0.0001; respectively). Regarding the glutathione REDOX cycle, we found the following in GH, CH and preeclampsia compared with PCW: a decrease in its reduced form (2.6 ± 0.6, 2.7 ± 0.8, 2.7 ± 0.9, 3.3±1.3 lmol l À1 , Po0.003), a parallel increase in the oxidized form (185.6±68.9, 194.7±75.0, 184.3±78.3, 85.1±27.5 lmol l À1 , Po0.0001) and an increment in glutathione peroxidase (85.9±22.0, 86.4±20.9, 82.1±23.5 and 77.2 ± 19.7 U g À1 Hb, Po0.04) and glutathione reductase (6384.3 ± 1261.9, 6724.6 ± 1154.1, 6287.9 ± 1399.9 and 6044.4±1208.4 mU g À1 Hb, Po0.01, respectively). Nitrites/nitrates were higher in patients with preeclampsia than in PCW (31.50±15.08, 26.80±8.39 lmol l À1 , Po0.002). Although malondialdehyde and oxidized-LDL levels were similar among groups, free fatty acids were increased in every HDP (GH 514.6 ± 194.6, CH 501.3 ± 197.4, preeclampsia 555.2 ± 230.1 lmol l À1 ) compared with PCW (351.4 ± 146.1 lmol l À1 ), Po0.0001. Our results show an oxidation/reduction imbalance with an increase in oxidative stress coupled with a decreased capacity of antioxidant systems, not only in preeclampsia but also in every HDP.