MECHANISMS OF BARORECEPTOR ACTIVATION

Citation
Mw. Chapleau et al., MECHANISMS OF BARORECEPTOR ACTIVATION, Clinical and experimental hypertension, 17(1-2), 1995, pp. 1-13
Citations number
34
Categorie Soggetti
Pharmacology & Pharmacy","Cardiac & Cardiovascular System
ISSN journal
10641963
Volume
17
Issue
1-2
Year of publication
1995
Pages
1 - 13
Database
ISI
SICI code
1064-1963(1995)17:1-2<1:MOBA>2.0.ZU;2-0
Abstract
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.