In man, cardiac receptors exert a continuous restraint on sympathetic activity. Reflexes originating from the heart also restrain renin and vasopressin secretion, thereby being involved both in blood pressure and in blood volume homeostasis. We have shown that these reflexes are markedly depressed in subjects with left ventricular hypertrophy (LVH) due to hypertension and that this is also the case when, in normotensive subjects, LVH is caused by prolonged physical training. In both instances, the cardiogenic reflex impairment is associated with derangement of blood pressure homeostasis. Either spontaneous regression of LVH by physical training cessation or antihypertensive treatment is followed by a marked improvement of the cardiogenic reflex. Thus, LVH also affects the 'afferent' function of the heart. 'Physiological', as well as pathological, hypertrophy has a similar adverse effect. This effect is reversible, however, and the reflex function can be restored by regression of hypertrophy.