Heart failure is associated with increased activity of sympathetic nervous system. As to the latter's effector organs, attention has been mainly drawn by heart and systemic circulation. In this study we investigated whether and how the neurogenic vasomotility of the lesser circulation is modified. Therefore, we compared 12 patients with heart failure in III NYHA functional class, with 10 subjects, undergoing hemodynamic study for diagnostic reasons and found to be normal. The neurogenic reactivity of pulmonary vessels was assayed by means of 2 sympathetic stimuli: arithmetic test (AT) and cold pressor test (CPT), performed both with and without obstruction to right heart venous return. This was obtained by expanding a balloon in inferior vena cava, in order to rid the neurogenic component of pulmonary vasomotility of the interference of the normally prevailing mechanical component (consisting in adaptations to flow variations). AT caused pulmonary vasodilation in normal subjects, as a passive consequence of the increase of cardiac output and, therefore, of pulmonary flow. Caval obstruction, by simply restraining this increase, induced a clearly neurogenic vasoconstrictor response. On the contrary, in failing patients, a slight vasodilation, independently from the condition of venous return, was observed. This took place in spite of the constant absence of any variations of cardiac output, which both indicates the reduction of myocardial function and helps to show the diminished nervous influence on pulmonary circulation. On the other hand, CPT had a vasoconstrictor effect in both groups, though potentiated by the reduction of transpulmonary flow in normal subjects only.(ABSTRACT TRUNCATED AT 250 WORDS)