Both arterial baroreceptor reflexes and cardiopulmonary reflexes are modified in human hypertension. The arterial baroreceptor reflex regulation of heart rate, when tested by both vasoactive drug injection and the neck chamber technique, has been shown to be reset and blunted. Arterial baroreceptor reflex control of blood pressure, studied by the neck chamber technique, has been found to be reset to more effectively buffer increases in blood pressure than blood pressure falls, but without any loss of overall reflex sensitivity. Cardiopulmonary reflexes, tested by passive leg raising and by application of lower body negative pressure, are also blunted, and their dysfunction involves not only control of peripheral vasoconstriction but also that of renin release. These readjustments of arterial and cardiopulmonary reflexes make buffering of blood pressure falls or of blood volume changes less effective in hypertension. These readjustments appear to be a consequence, rather than a cause, of hypertension. In particular, the blunting of cardiopulmonary reflexes is induced more by left ventricular hypertrophy than by hypertension. It is very marked in hypertensive patients with echocardiographic evidence of left ventricular hypertrophy and very significantly improves when left ventricular hypertrophy is made to regress by prolonged antihypertensive therapy; significant blunting of cardiopulmonary reflexes has also been found in young athletes with marked left ventricular hypertrophy but normal blood pressure. Whether structural changes in the carotid and aortic wall and possibly in the heart are equally important in the readjustment of arterial baroreceptor reflexes is incompletely clarified at the moment, although there are indications that functional and structural modifications may both be involved.