The aim of the present study was to compare cytokine secretion in healthy young and old subjects. Peripheral blood mononuclear cells were isolated from 55 healthy volunteers (aged 23-77 years) and cultured for 24 h in the presence or the absence of lipopolysaccharide (LPS) and 1,25-dihydroxyvita-min D₃. Interleukin-lΒ (IL-1), tumor necrosis factor a (TNF) and prostaglandin E₂ were measured in the culture superna-tants with specific immunoassays. The unstimulated and LPS-stimulated production of IL-1 was significantly higher in the group of subjects older than 55 years than in the group aged less than 55 years. Likewise, there were positive correlations between age and the unstimulated and LPS-stimulated IL-1 secretion (r= 0.50 and 0.63, respectively, p < 0.01 in both cases). However, there were no age-related differences in the secretion of IL-1 in the presence of 1,25-dihydroxyvitamin D or in the secretion of TNF or prostaglandin E₂ in any culture condition. These results suggest the existence of subtle abnormalities in cytokine secretion in healthy aged subjects, in comparison with younger individuals. In theory, the increased secretion of IL 1 might play a role in the pathophysiology of some diseases which are frequent in old people, such as osteoporosis.

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Dopamine modulates cardiovascular function by actions in the central and peripheral nervous system, by altering the secretion/release of prolactin, pro-opiomelanocortin, vasopressin, aldosterone, and renin, and by directly affecting renal function. Dopamine produced by the renal proximal tubule exerts an autocrine/paracrine action via two classes of dopamine receptors, D1-like (D1 and D5) and D2-like (D2, D3, and D4), that are differentially expressed along the nephron. The autocrine/paracrine function of dopamine, manifested by tubular rather than by haemodynamic mechanisms, becomes most evident during extracellular fluid volume expansion. This renal autocrine/paracrine function is lost in essential hypertension and in some animal models of genetic hypertension. The molecular basis for the dopaminergic dysfunction in hypertension may involve an abnormal post-translational modification of dopamine receptors.

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