Evidences That Sympathetic Overactivity and Neurogenic Hypertension Correlate with Changes in the Respiratory Pattern in Rodent Models of Experimental Hypoxia

© 2023. The Author(s), under exclusive license to Springer Nature Switzerland AG..

The main question of this chapter is as follows: What is the contribution of changes in the sympathetic-respiratory coupling to the hypertension observed in some experimental models of hypoxia? Although there is evidence supporting the concept that sympathetic-respiratory coupling is increased in different models of experimental hypoxia [chronic intermittent hypoxia (CIH) and sustained hypoxia (SH)], it was also observed that in some strains of rats and in mice, these experimental models of hypoxia do not affect the sympathetic-respiratory coupling and the baseline arterial pressure. The data from studies performed in rats (different strains, male and female, and in the natural sleep cycle) and mice submitted to chronic CIH or SH are critically discussed. The main message from these studies performed in freely moving rodents and in the in situ working heart-brainstem preparation is that experimental hypoxia changes the respiratory pattern, which correlates with increased sympathetic activity and may explain the hypertension observed in male and female rats previously submitted to CIH or SH.

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:1427

Enthalten in:

Advances in experimental medicine and biology - 1427(2023) vom: 15., Seite 23-33

Sprache:

Englisch

Beteiligte Personen:

Machado, Benedito H [VerfasserIn]

Links:

Volltext

Themen:

Chronic intermittent hypoxia
Journal Article
Neurogenic hypertension
Peripheral chemoreflex
Rodents models of hypoxia
Sustained hypoxia
Sympathetic-respiratory coupling

Anmerkungen:

Date Completed 19.06.2023

Date Revised 19.06.2023

published: Print

Citation Status MEDLINE

doi:

10.1007/978-3-031-32371-3_3

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM358239206