Activation of microglia within paraventricular nucleus of hypothalamus is NOT involved in maintenance of established hypertension

Ko Takesue, Takuya Kishi, Yoshitaka Hirooka, Kenji Sunagawa

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background Inflammation within paraventricular nucleus of the hypothalamus (PVN), a key circulatory control center in the hypothalamus, is an important pathology of sympathetic hyperactivity. Brain inflammation is mainly mediated by microglia, innate immune cells in the brain. Activated microglia produce inflammatory cytokines with alteration of their morphology. Increase in inflammatory cytokines synthesis coincides with activation of microglia within PVN of angiotensin II-induced hypertensive model and myocardial infarction-induced heart failure model. Although the increase in inflammatory cytokines and the microglial activation within PVN were also seen in spontaneously hypertensive rats (SHR), the model of essential hypertension, their involvement in blood pressure regulation has still be fully clarified. In the present study, we examined whether activated microglia within PVN were involved in maintenance of established severe hypertension with sympathoexcitation. Methods Minocycline (25 mg/kg/day), an inhibitor of microglial activation, or vehicle were orally administered to stroke-prone SHR (SHRSP) and normotensive Wistar-Kyoto (WKY) rats for 2 weeks from 15-weeks-old, the age of established hypertension. Results Systolic blood pressure was comparable between minocycline treated-SHRSP and vehicle treated-SHRSP, whereas morphological analysis of microglia revealed smaller cell size in minocycline treated-SHRSP than vehicle treated-SHRSP, implying that minocycline deactivated microglia within PVN. Conclusions Activated microglia with morphological alteration within PVN are not involved in the maintenance of established severe hypertension, and inflammation within PVN could not be the therapeutic target of established hypertension.

Original languageEnglish
Pages (from-to)84-88
Number of pages5
JournalJournal of Cardiology
Volume69
Issue number1
DOIs
Publication statusPublished - Jan 1 2017

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Paraventricular Hypothalamic Nucleus
Microglia
Hypothalamus
Maintenance
Hypertension
Minocycline
Inbred SHR Rats
Cytokines
Blood Pressure
Inflammation
Inbred WKY Rats
Encephalitis
Cell Size
Angiotensin II
Heart Failure
Stroke
Myocardial Infarction
Pathology
Brain

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Activation of microglia within paraventricular nucleus of hypothalamus is NOT involved in maintenance of established hypertension. / Takesue, Ko; Kishi, Takuya; Hirooka, Yoshitaka; Sunagawa, Kenji.

In: Journal of Cardiology, Vol. 69, No. 1, 01.01.2017, p. 84-88.

Research output: Contribution to journalArticle

Takesue, Ko ; Kishi, Takuya ; Hirooka, Yoshitaka ; Sunagawa, Kenji. / Activation of microglia within paraventricular nucleus of hypothalamus is NOT involved in maintenance of established hypertension. In: Journal of Cardiology. 2017 ; Vol. 69, No. 1. pp. 84-88.
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N2 - Background Inflammation within paraventricular nucleus of the hypothalamus (PVN), a key circulatory control center in the hypothalamus, is an important pathology of sympathetic hyperactivity. Brain inflammation is mainly mediated by microglia, innate immune cells in the brain. Activated microglia produce inflammatory cytokines with alteration of their morphology. Increase in inflammatory cytokines synthesis coincides with activation of microglia within PVN of angiotensin II-induced hypertensive model and myocardial infarction-induced heart failure model. Although the increase in inflammatory cytokines and the microglial activation within PVN were also seen in spontaneously hypertensive rats (SHR), the model of essential hypertension, their involvement in blood pressure regulation has still be fully clarified. In the present study, we examined whether activated microglia within PVN were involved in maintenance of established severe hypertension with sympathoexcitation. Methods Minocycline (25 mg/kg/day), an inhibitor of microglial activation, or vehicle were orally administered to stroke-prone SHR (SHRSP) and normotensive Wistar-Kyoto (WKY) rats for 2 weeks from 15-weeks-old, the age of established hypertension. Results Systolic blood pressure was comparable between minocycline treated-SHRSP and vehicle treated-SHRSP, whereas morphological analysis of microglia revealed smaller cell size in minocycline treated-SHRSP than vehicle treated-SHRSP, implying that minocycline deactivated microglia within PVN. Conclusions Activated microglia with morphological alteration within PVN are not involved in the maintenance of established severe hypertension, and inflammation within PVN could not be the therapeutic target of established hypertension.

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