Mechanisms of Baroreceptor Activation

M. W Chapleau; G Hajduczok; R. V Sharma; R. E Wachtel; J. T Cunningham; M. J Sullivan; P. M Abboud

doi:10.3109/10641969509087050

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Mechanisms of Baroreceptor Activation

M. W Chapleau, G Hajduczok, R. V Sharma, R. E Wachtel, J. T Cunningham, M. J Sullivan and P. M Abboud

Clinical and experimental hypertension (1993), Vol.17(1-2), pp.1-13

1995

DOI: 10.3109/10641969509087050

PMID: 7735260

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Abstract

The determinants of the nerve activity generated at the baroreceptor endings have been examined. 1) In the isolated carotid sinus, the placement of activated bovine aortic endothelial cells decreased baroreceptor activity (BRA) in a reversible manner. Both endothelin and nitric oxide (NO) suppress BRA, whereas prostacyclin (PGI2) increases activity. 2) The BRA in single units declines and often ceases during non-pulsatile increases in carotid sinus pressure sustained over several minutes. This "adaptation" is attenuated by the transient potassium channel (IA) blocker 4-aminopyridine (4-AP) and not by inhibition of the Na+/K+ pump. 3) In preliminary studies, mechano-electrical transduction was examined in isolated and cultured nodose ganglion neurons. Opening of stretch-activated (SA) channels by suction on the cell-attached patch was seen infrequently; however, probing the neurons consistently increased their intracellular calcium [Ca++]i measured with fura-2. This increase in [Ca++]i is blocked by gadolinium (Gd3+), a trivalent lanthanide reported to block SA channels. Gd3+ also blocks the BRA in the carotid sinus. We conclude that paracrine factors significantly 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.

Details

Title: Subtitle: Mechanisms of Baroreceptor Activation
Creators: M. W Chapleau - 1Department of Internal Medicine and Physiology, Biophysics Cardiovascular Research Center University of Iowa, Department of Veterans Affairs Medical Center, Iowa City, Iowa, USA
G Hajduczok - 1Department of Internal Medicine and Physiology, Biophysics Cardiovascular Research Center University of Iowa, Department of Veterans Affairs Medical Center, Iowa City, Iowa, USA
R. V Sharma - University of Iowa
R. E Wachtel - 1Department of Internal Medicine and Physiology, Biophysics Cardiovascular Research Center University of Iowa, Department of Veterans Affairs Medical Center, Iowa City, Iowa, USA
J. T Cunningham - 1Department of Internal Medicine and Physiology, Biophysics Cardiovascular Research Center University of Iowa, Department of Veterans Affairs Medical Center, Iowa City, Iowa, USA
M. J Sullivan - 1Department of Internal Medicine and Physiology, Biophysics Cardiovascular Research Center University of Iowa, Department of Veterans Affairs Medical Center, Iowa City, Iowa, USA
P. M Abboud - 1Department of Internal Medicine and Physiology, Biophysics Cardiovascular Research Center University of Iowa, Department of Veterans Affairs Medical Center, Iowa City, Iowa, USA
Resource Type: Journal article
Publication Details: Clinical and experimental hypertension (1993), Vol.17(1-2), pp.1-13
DOI: 10.3109/10641969509087050
PMID: 7735260
NLM abbreviation: Clin Exp Hypertens
ISSN: 1064-1963
eISSN: 1525-6006
Publisher: Informa UK Ltd
Language: English
Date published: 1995
Academic Unit: Molecular Physiology and Biophysics; Cardiovascular Medicine; Anesthesia; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
Record Identifier: 9984025433902771

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