1. Recordings of vasoconstrictor sympathetic activity in peroneal muscle fascicles, blood pressure, and heart rate were made in twelve subjects while stimulating carotid sinus receptors by continuous or sinusoidal (cycle durations 7.5, 15 and 30 sec) neck suction. Neural activity, quantified by counting the number of pulse synchronous sympathetic bursts (burst incidence), was correlated to the pressure sensed by carotid sinus receptors (= calculated diastolic transmural carotid pressure) and to pressure sensed by arterial baroreceptors not located in the neck (= diastolic blood pressure). 2. Sinusoidal neck suction induced rhythmical modulation of sympathetic activity which became less noticeable with increasing modulation of sympathetic activity which became less noticeable with increasing cycle duration. Static suction led to a non-significant reduction of sympathetic burst incidence. 3. With sinusoidal stimuli the amplitude of the transmural carotid pressure variations were maximal at a cycle duration of 7.5 sec and decreased successively at cycles of 15 and 30 sec. Amplitudes of induces variations in R-R intervals in the e.c.g. changed in a similar way but in contrast induced variations in diastolic blood pressure were minimal at a cycle duration of 7.5 sec and maximal at 15 sec. It is suggested that the main rate limiting factors for the blood pressure responses is the sluggishness of the peripheral vascular beds. 4. Sinusoidal neck suction always prolonged mean R-R interval. This stimulus increased mean burst incidence in subjects with few bursts at rest and decreased burst incidence in subjects with many bursts at rest. These changes of burst incidence were linearly related to the increases of R-R intervals. The findings demonstrate interindividual differences in balance between cardiac and peripheral vasoconstrictor responses to changes of baroreceptor activity. 5. It is concluded that fast changes in carotid sinus pressure effectively modulate sympathetic outflow to the muscles and thereby contribute to transient compensatory blood pressure responses. Static blood pressure control, on the other hand, probably depends more on baroreceptor control over the effector organs.