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The diagnostic and prognostic implication of exaggerated blood pressure response to exercise has been controversial, with opinions ranging from a benign process to a harbinger of potential cardiovascular morbidity. Nonetheless, lowering of blood pressure and prevention of hypertension is in first instance preferable by lifestyle changes, and many studies have shown the inverse association between physical activity level and the incidence of cardiovascular diseases suggesting low aerobic fitness as a strong predictor for future cardiovascular disease and all-cause mortality in both healthy and cardiovascular disease patients, including those with hypertension. Endothelial function, large artery stiffness and neurohormonal response are surely implicated both in the development of exaggerated blood pressure response to exercise and in the positive effect of physical exercise in the prevention and management of hypertension and cardiovascular disease in general. In their interesting and well documented review published in this issue Kim and Ha broadly described the possible pathophysiologic mechanisms of exaggerated blood pressure response to exercise and its clinical implications: in this regard, a very interesting issue could be represented by the role of exercise training. In fact, there is an the ample evidence in the literature that physical activity could positively affect endothelial function, arterial stiffness, neurohormonal response and finally blood pressure levels both in healthy men and in hypertensive patients and so should be considered a very important element in the prevention and management of cardiovascular disease.

Background Central Nervous System (CNS) disorders often accompany the acquired immunodeficiency syndrome (AIDS) and are typified by neuropsychiatric symptoms, such as cognitive and motor impairments, sometimes paralleled by neuropathological hallmarks. Collectively, these events are referred to as HIV-1 associated dementia (HAD). Before the advent of the Highly Active Antiretroviral Therapy (HAART), about 20% of adult patients, but as many as 40% of children/adolescent infected subjects developed HAD. Nowadays, in the era of HAART, the prevalence of HAD has decreased, but a more subtle form of disorder, referred to as Minor Cognitive Motor Disorder (MCMD), has emerged in about 20% of symptomatic HIV-1 seropositive patients, including those receiving HAART. This work was aimed at investigating the impact of the HIV-1 viral protein Tat on central neurotransmission since this protein has been proposed as one of the viral component involved in the onset of central neuropsychiatric symptoms. Methods The approach used was the up-down superfusion of purified synaptosomes isolated from human neocortical specimens removed during neurosurgery from consenting patients suffering of brain tumours. Experiments were also carried out by using mouse purified synaptosomes or slices in an attempt to propose an animal model suitable to investigate Tat-induced modification to central nervous system. Functional studies were paralleled by biochemical investigation on the existence of receptor protein potential involved in the effects observed and changes to second messenger production. Results