Hypertension and the metabolic syndrome: Closely related central origin?

In primary hypertension a mild hyperresponsiveness of hypothalamic, sympath o-hormonal centres to psychosocial stimuli forms a major pathogenetic eleme nt, although high salt intake in some subjects may contribute via volume ex pansion. Hypertension is often associated with another "civilisation" disor der, the metabolic syndrome, defined as abdominal obesity, insulin resistan ce and dyslipidaemia. According to recent research, the metabolic syndrome has in all likelihood a central neuroendocrine origin in the form of enhanc ed engagement of the hypothalamic-pituitary-adrenal (HPA) axis. Here the pe ripheral endocrine perturbations act as triggers for both central obesity a nd the metabolic abnormalities. The reaction pattern characterising early primary hypertension is identical with, or closely related to, the "defence reaction", while that leading to the metabolic syndrome is similar to that of the "defeat reaction". Both b elong to the primitive survival reactions, common to all mammals, though ma n can control, or at least mask, his outward-behavioural part but not the n euro-hormonal expressions. Animal experiments show how frequent or chronic mental challenges are capab le of engaging these limbic-hypothalamic centres, affecting blood pressure regulation as well as endocrine-metabolic regulation. Furthermore, these ce ntres are tightly coupled functionally, and their signals to the periphery often combined. On a long-term basis their engagements appear to be decisiv e for the development of both primary hypertension and the metabolic syndro me, as suggested by intervention studies. In both these "disorders of civil isation", observations strongly indicate that psychosocial stress, socioeco nomic handicaps, lack of exercise, abuse and also psychiatric traits are in volved. Such factors, characteristic of current competitive society, probably cause mixed engagements of the two above-mentioned neuro-hormonal patterns, and thereby, with time, primary hypertension and the metabolic syndrome, with e nd-paints such as coronary artery disease, diabetes mellitus type2 and stro ke. Susceptibilty to such developments is probably enhanced by genetic fact ors This overview of recent developments therefore serves to emphasise how both primary hypertension and the metabolic syndrome seem to have a common cent ral origin. Central regulatory factors are often overlooked, partly because it is not realised that limbic-hypothalamic centres are the major regulato rs of both circulatory and metabolic events, and partly because of the long period of time required before these disease end-points are reached.