Inactivation of the paraventricular nucleus attenuates the cardiogenic sympathetic afferent reflex in the spontaneously hypertensive rat.
J Hypertens
; 42(1): 70-78, 2024 01 01.
Article
em En
| MEDLINE
| ID: mdl-37889604
ABSTRACT
BACKGROUND:
Myocardial ischemia causes the release of bradykinin, which stimulates cardiac afferents, causing sympathetic excitation and chest pain. Glutamatergic activation of the paraventricular hypothalamic nucleus (PVN) in the spontaneously hypertensive rat (SHR) drives elevated basal sympathetic activity. Thus, we tested the hypothesis that inactivation of the PVN attenuates the elevated reflex response to epicardial bradykinin in the SHR and that ionotropic PVN glutamate receptors mediate the elevated reflex.METHODS:
We recorded the arterial pressure and renal sympathetic nerve activity (RSNA) response to epicardial bradykinin application in anesthetized SHR and Wistar Kyoto (WKY) rats before and after PVN microinjection of GABA A agonist muscimol or ionotropic glutamate receptor antagonist kynurenic acid.RESULTS:
Muscimol significantly decreased the arterial pressure response to bradykinin from 180.4â±â5.8 to 119.5â±â6.9âmmHg in the SHR and from 111.8â±â7.0 to 84.2â±â8.3âmmHg in the WKY and the RSNA response from 186.2â±â7.1 to 142.7â±â7.3% of baseline in the SHR and from 201.0â±â11.5 to 160.2â±â9.3% of baseline in the WKY. Kynurenic acid significantly decreased the arterial pressure response in the SHR from 164.5â±â5.0 to 126.2â±â7.7âmmHg and the RSNA response from 189.9â±â13.7to 168.5â±â12.7% of baseline but had no effect in the WKY.CONCLUSION:
These results suggest that tonic PVN activity is critical for the full manifestation of the CSAR in both the WKY and SHR. Glutamatergic PVN activity contributes to the augmented CSAR observed in the SHR.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Núcleo Hipotalâmico Paraventricular
/
Bradicinina
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article