4.5 Article

Hypothalamic paraventricular nucleus augments baroreflex sensitivity, role of angiotensin II

Journal

BRAIN RESEARCH
Volume 1802, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.brainres.2022.148218

Keywords

Paraventricular nucleus; Angiotensin; Arterial pressure; Heart rate; Baroreflex gain

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This study in anesthetized rats found that AngII does not provide tonic activity in the parvocellular part of the paraventricular nucleus (PVNp) under normal conditions. However, drugs microinjected into the PVNp attenuated the frequency component of baroreflex, and AngII attenuated the heart rate response of baroreflex through AT1 and AT2 receptors.
The hypothalamic paraventricular nucleus (PVN) is an important brain region involved in control of the car-diovascular system. Direct injection of angiotensin II (AngII) into the PVN produces a short or long pressor response. This study was performed in anesthetized rats to find whether the parvocellular part of the para-ventricular nucleus (PVNp) affects the baroreflex. And if so, what is the effect of AngII injected into the PVNp on the baroreflex? Drugs were microinjected into the PVNp while blood pressure and heart rate were recorded continuously. We found that microinjection of AT1 and AT2 receptor antagonists into the PVNp region did not affect the baseline mean arterial pressure (MAP) and heart rate (HR) indicating that under normal conditions AngII may not provide tonic activity, at least in anaesthetized animals. Bilateral microinjections of a synaptic blocker (CoCl2) into the PVNp attenuated the baroreflex gains in responses to loading and unloading of baro-receptors, indicating that PVNp is involved in the baroreflex rate component. Microinjection of AngII into the PVNp increased MAP and HR. However, AngII slightly attenuated the baroreflex rate component using its two receptors AT1 and AT2. Collectively, these findings suggest that the PVNp as a whole is involved in the baror-eflex. But AngII attenuates the heart rate response of the baroreflex through AT1 and AT2 receptors.

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