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Even though the mechanisms that mediate essential hypertension (HT) are not fully understood, an immunological-inflammatory mechanism could be the common pathway for diverse pathophysiological mechanisms. We analyze in a simplified way the participation of the immune system in HT. T lymphocytes (TL) and antigen presenting cells (APCs) are components of the immune system capable of generating proinflammatory cytokines. They cause endothelial damage, vasoconstriction, and decreased urinary sodium excretion. CD4+ and CD8+ TL are effector cells, causally implicated in the development of HT, whereas type γδ TL play their pathogenic role in HT enhancing endothelial dysfunction. Additionally, a immunomodulation decrease by regulatory TL, worsens endothelial dysfunction and reduces vasodilation in experimental HT. Results of recent studies indicate that lymphocyte activation would be mediated by antigens captured by antigen APCs for subsequent presentation to "naive" TL. On the other hand, proinflammatory states such as obesity, the change of the intestinal microbiota and the increase in salt intake favors TL and APC activation, contributing to HT development.

Background: Hemodialysis patients (HD) display high rates of cardiac disease and mortality. The cardiovascular morbidity and mortality of HD patients is attributable in a significant proportion to endothelial dysfunction, arterial stiffness, and vascular calcifications., Aim: To measure vascular reactivity in HD subjects and compare them with healthy volunteers., Material and Methods: Forty eight non diabetic patients aged 58 ± 4.6 years (29 males) on hemodialysis for a mean lapse of 4.8 years were studied. Arterial stiffness was measured in the radial artery. Pulse wave velocity was measured by noninvasive peripheral arterial tonometry in carotid and femoral arteries. Endothelial function was assessed, measuring reactive hyperemia response after a 5 min period of ischemia. As a control, all values were also measured in age and gender-matched healthy volunteers., Results: Arterial stiffness was significantly higher in HD patients than controls (23.9 ± 3.3 and 18.4 ± 3.4% respectively, p < 0.05). HD subjects had an increased pulse wave velocity (10.0 ± 0.8 and 7.6 ± 0.9 m/s respectively, p < 0.05). A reduction in the change in pulse amplitude pressure, as a measure of arterial dysfunction, was only observed in male patients (1.7 ± 0.4 and 2.7 ± 0.4 respectively p < 0.01)., Conclusions: Noninvasive assessment of peripheral vascular function may be useful for the identification of patients at risk for late cardiac events.

Background: Diabetes mellitus is an important risk factor for cardiovascular complications among patients on hemodialysis. However, the incidence of these complications among non diabetic patients on hemodialysis is not well known., Aim: To assess the incidence of cardiovascular complications in non diabetic patients on hemodialysis., Patients and Methods: Seventy five non diabetic patients aged 55.6 +/- 17 years (48 males), receiving hemodialysis three times a week were evaluated with laboratory tests, echocardiogram anda carotid ultrasound. In 26 patients, interleukin 6, tumor necrosis factor alpha, and intercellular adhesión molecule (ICAM-1) were also measured. Patients were followed during two years., Results: The mean lapse of dialysis therapy was 6.5 +/-5 years. The main cause of renal failure was hypertension. Sixty two percent had systolic hypertension, 86% had concentric left ventricular hypertrophy, 43% had atrial dilatation and 60% had calcifications in the thoracic aorta. Compared with normal controls, patients had higher levels of interleukin 6, tumor necrosis factor alpha and ICAM-1. Carotid media thickness was also higher and increased in the two years of follow up. No correlations were found between ventricular hypertrophy and dialysis lapse, packed red cell volume, calcium phosphorus product, parathormone levels or median arterial pressure. No cardiovascular events were recorded during the follow up period., Conclusions: Non diabetic patients on chronic hemodialysis have a high frequency of ventricular hypertrophy, carotid media thickening, aortic calcifications and an increase in proinflammatory cytokines.

Background: The presence of food in the intestinal lumen increases absorption from an isolated intestinal loop, the mechanisms involved are unknown. Casein, and its respective hydrolysate, increased D-xylose absorption in both normal volunteers and experimental animals; this effect was associated with prolonged small intestinal transit time and a decrease of motor activity., Aims: To separate from casein hydrolysate, groups of peptides and to investigate their effects on both D-xylose absorption and small intestinal motility., Material and Methods: Studies were performed on five dogs with a surgically implanted duodenal cannula. Three groups of peptides were separated by means of a Silica Gel 60 column and were continuously infused through the duodenal cannula. After 15 min, 5 g of D-xylose were injected in the duodenum, plasma levels were measured, and the area under the curve was estimated. Motility was recorded by means of infused catheters and external transducers., Results: Plasma levels of D-xylose were significantly increased during the infusion of one group of peptides compared to the others. In addition, the area under the curve: 3366 +/- 885 mg x min-1 observed with this group was significantly greater than the other two groups: 1432 +/- 183 mg x min-1 and 1137 +/- 280 mg x min-1 respectively. No statistically significant differences in motor activity were observed between the different groups of peptides., Conclusions: A group of peptides derived from casein was characterized by increasing D-xylose absorption. The presence of beta casomorphines might be the possible mechanism involved.

Background: Sodium and potassium ions are involved in the regulation of blood pressure and the genesis of hypertension., Aim: To assess internal potassium balance, as a measure of sodium pump activity, in subjects with essential hypertension and diabetic patients., Patients and Methods: Eleven hypertensive subjects, 5 non-insulin-dependent diabetics and 16 age matched controls were studied. An acute oral load of 0.8 mEq/Kg body weight of KCl was administered and blood samples were drawn every 30 min thereafter, until 120 min, to measure plasma K+ levels. Urinary K+ excretion during this period was also measured. In eight hypertensive patients, the test was repeated after two week of supplementation with 60 mEq/day of KCl. The maximal increase in plasma potassium levels and the time required to achieve the maximum concentration was recorded., Results: All patients had normal serum creatinine levels. Mean fasting blood glucose of diabetic patients was 133 +/- 15.1 mg/dl. No difference between patients and controls in maximal increase plasma potassium increase, was observed. In hypertensive patients the lapse to achieve the maximal potassium concentration was longer than in controls. After the period of potassium supplementation in hypertensive patients, there was a significant increase in basal plasma K+ levels and the temporal pattern of plasma potassium increase was similar to that of controls. Between 63 and 68% of retained K+ load was translocated to the intracellular space at 120 min in all study groups., Conclusions: Internal potassium balance is not significantly altered in subjects with essential hypertension or in non-insulin-dependent diabetics.