The determinants of the nerve activity generated at the baroreceptor e
ndings have been examined. 1) In the isolated carotid sinus, the place
ment of activated bovine aortic endothelial cells decreased barorecept
or activity (BRA) in a reversible manner. Both endothelin and nitric o
xide (NO) suppress BRA, whereas prostacyclin (PGl(2)) increases activi
ty. 2) The BRA in single units declines and often ceases during non-pu
lsatile increases in carotid sinus pressure sustained over several min
utes. This ''adaptation'' is attenuated by the transient potassium cha
nnel (l(A)) blocker 4-aminopyridine (4-AP) and not by inhibition of th
e Na+/K+ pump. 3) In preliminary studies, mechano-electrical transduct
ion was examined in isolated and cultured nodose ganglion neurons. Ope
ning of stretch-activated (SA) channels by suction on the cell-attache
d patch was seen infrequently; however, probing the neurons consistent
ly increased their intracellular calcium [Ca++](i) measured with fura-
2. This increase in [Ca++](i) is blocked by gadolinium (Gd3+), a triva
lent lanthanide reported to block SA channels. Gd3+ also blocks the BR
A in the carotid sinus. We conclude that paracrine factors significant
ly modulate BR sensitivity, that selective ionic mechanisms (the 4-AP
sensitive K+ channels) determine the degree of ''adaptation'' of BR to
elevated pressure, and that SA channels sensitive to Gd3+ may be the
mechano-electrical transducers in BR neurons.