Platelet-induced suppression of baroreceptor activity is mediated by a stable diffusible factor.

We have demonstrated recently that platelets aggregating in the carotid sinus decrease baroreceptor sensitivity. The goals of the present study were to determine whether platelet-induced suppression of baroreceptor activity is mediated by a diffusible, transferable factor and, if true, whether the factor is short-lived or stable. Baroreceptor activity was recorded from the isolated carotid sinus during slow ramp increases in nonpulsatile pressure in rabbits anesthetized with sodium pentobarbital. Intraluminal exposure of the carotid sinus to washed rabbit platelets resuspended in Krebs buffer (3-5 x 10(8) cells/ml) and activated by thrombin decreased baroreceptor activity significantly (n = 7, P < 0.05). Maximum baroreceptor activity recorded at a pressure of 140 mmHg was reduced to 81 +/- 7% of the control maximum. Injection of cell-free supernatant obtained from filtered thrombin-activated platelets also suppressed baroreceptor activity to a similar extent after 10 min (n = 7) and after 2 h (n = 5) of incubation when maximum baroreceptor activity was reduced to 84 +/- 5 and 82 +/- 5% of the control maximum, respectively. The inhibitory influence of activated platelets and platelet supernatant on baroreceptor activity was still apparent after 10-60 min of heating (95 degrees C) (n = 5) and was reversible upon removal of platelets and supernatant from the sinus. The results indicate that activated platelets release a stable diffusible factor that suppresses baroreceptor activity. We speculate that this 'inhibitory factor' may contribute to impairment of the baroreceptor reflex and neurally-mediated increases in arterial pressure in atherosclerotic and thrombotic states.