Neuropeptide Y (NPY), a putative sympathetic neurotransmitter and neuromodulator, is released during sympathetic nerve stimulation and causes vasoconstriction and cardiodepression. Whether the release of NPY contributes to stress-induced cardiovascular responses was assessed by studying i) plasma levels of circulating NPY-immunoreactivity (NPY-ir) during various stress paradigms and ii) mechanisms of action of NPY in the cardiovascular system of the rat. Plasma NPY-ir was increased by all stress situations, such as transfer to a new environment (by 52%), exposure to cold water (4 degrees C) (by 117%) and hemorrhage (4 ml/300 g body weight) (by 231%). The cold water, stress-induced, maximal increase in circulating plasma NPY-ir was delayed in relation to the peak pressor response by 10-20 min. Administration of NPY caused dose-dependent pressor responses that were greater in pithed rats--which have all centrally mediated circulatory reflexes removed--than in conscious rats. Infusion of a low pressor (8.5 +/- 1.5 mm Hg) dose of norepinephrine into conscious rats potentiated NPY-mediated pressor responses 2-fold and also tended to increase bradycardic effect of a higher dose of NPY (by 19%). Thus hypertensive and bradycardiac actions of NPY appear to depend on the level of adrenergic activity and on the interactions at the level of vascular smooth muscle, heart, and baroreceptor reflexes. During a hyperadrenergic state such as stress, cardiovascular effects of NPY may be greatly accentuated. NPY may enhance and prolong the stress-induced hypertensive responses while antagonizing adrenergic cardiostimulation.