Journal article
New insights into the influence of pulsatile pressure on the arterial baroreceptor reflex
Clinical and experimental hypertension. Part A, Theory and practice, Vol.10 Suppl 1(S1), pp.179-191
1988
DOI: 10.3109/10641968809075971
PMID: 3072123
Abstract
Pulsatile arterial pressure as compared to static pressure has important influences on baroreceptor activation and on the central mediation of the baroreflex. First, the static pressure-baroreceptor activity curve is sigmoid and the slope or gain peaks abruptly at pressures near 100 mmHg. In contrast, the pulsatile pressure-activity curve is linear over a wide range of pressure and the maximum gain is reduced. Second, exposure of baroreceptors to elevated levels of static pressure causes a rapid resetting or desensitization of the receptors within minutes. Baroreceptor resetting is absent or blunted when the elevated pressure is pulsatile. Third, inhibition of sympathetic activity is greater during pulsatile vs. static pressure even when baroreceptor activity per unit time is less. This central facilitation of the baroreflex is related to the lack of adaptation of central neurons to the pulse phasic afferent activity. The results indicate: 1) the extended linear range of the pressure-activity relation during pulsatile pressure may enable the baroreceptors to accurately detect changes in arterial pressure over a wider pressure range than that predicted from experiments using static pressure; and 2) pulsatile pressure can reduce resetting and promote reflex inhibition of sympathetic activity both by sensitizing the baroreceptors and by centrally facilitating the reflex.
Details
- Title: Subtitle
- New insights into the influence of pulsatile pressure on the arterial baroreceptor reflex
- Creators
- M W Chapleau - Cardiovascular Center, University of Iowa College of Medicine, Iowa City 52242G HajduczokF M Abboud
- Resource Type
- Journal article
- Publication Details
- Clinical and experimental hypertension. Part A, Theory and practice, Vol.10 Suppl 1(S1), pp.179-191
- Publisher
- United States
- DOI
- 10.3109/10641968809075971
- PMID
- 3072123
- ISSN
- 0730-0077
- eISSN
- 1525-6006
- Grant note
- HL40428 / NHLBI NIH HHS HL14388 / NHLBI NIH HHS
- Language
- English
- Date published
- 1988
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
- Record Identifier
- 9984025690102771
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