oa Editorial

Despite the large amount of information collected over the past years, several aspects related to the link between blood pressure and metabolic abnormalities remain unclear. This is particularly the case for the pathophysiology of the blood pressure/metabolic relationships and, more specifically, for the hypothesis that abnormalities in sympathetic cardiovascular function may represent the driving force responsible on one side for the blood pressure elevation and on the other for the hypertension-related metabolic disarray. First, direct and indirect evidence suggest that high blood pressure states are characterized by an adrenergic overactivity. Overdrive is present in the hypertensive state of the young, middle-age and elderly patients, in which it parallels the clinical severity of the hypertensive state. On the other hand, the obese state displays signs of adrenergic activation, such as increased resting heart rate values and elevated plasma norepinephrine values. An augmented sympathetic neural discharge to skeletal muscle as well as an increased spillover rate of norepinephrine from sympathetic nerve endings has been shown. As Dr Guido Grassi et al., mentioned in this issue, the mechanisms responsible for the hyperadrenergic drive described in hypertension, obesity, diabetes and in the other metabolic disease which may include both metabolic, humoral and reflex factors, such as the insulin resistance condition, the hyperleptinemic state, the activation of the renin-angiotensin system and the chemoreflex stimulation are parasympathetic impairment and sympathetic drive over expression. In the PAMELA study by Bombelli et al., blood glucose and serum cholesterol levels progressively increase while HDL-C progressively decreases with increasing clinic blood pressure category or home and 24-hour blood pressure quartile. The percentage of subjects with impaired fasting glucose or diabetes mellitus also progressively increases from the lowest to the highest category of clinic blood pressure and quartile of home or 24-hour blood pressure. By a multivariate analysis systolic and diastolic clinic, home and 24-hour blood pressure all appeared among factors independently associated to blood glucose and serum cholesterol level in the PAMELA population. Dr Patricio Lopez Jaramillo et al., in its paper reflects also that cardiac autonomic function is altered in subjects with one or more metabolic abnormalities, but without insulin resistance. Thus, they proposed that an over autonomic function may precede insulin resistance in the initiation of the Metabolic Sindrome. Furthermore, Nitric oxide seems to be also involved in the relationship between authonomic nervous system and endothelial dysfunction. Neuronal Nitric Oxide contributes to the regulation of renal function and NO performs an important role in kidney protection in opposing the effects of chronic renal renin-angiotensin system over activation, which contributes to renal hypertension and injury. Furthermore, the vascular and cardio protective functions of NO extend beyond the endothelium to involve neuronal NO and its role as a neuromodulator of the autonomic nervous system, maintaining vagal tone and suppressing sympathetic nervous system over activity through both central and peripheral nervous system signaling.....