Toxicology and applied pharmacologyJun 14, 2016

Telmisartan’s effects on high blood pressure may involve immune signaling and metabolism control in the brain’s blood pressure center

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 6, 2026

Abstract

Hypertensive rats showed significantly higher levels of angiotensin II type 1 receptors and lower levels of PPAR-γ in the hypothalamic paraventricular nucleus.

Treatment with the AT1-R antagonist telmisartan reduced mean arterial pressure in hypertensive rats.
Telmisartan treatment improved cardiac hypertrophy and decreased levels of pro-inflammatory cytokines in hypertensive rats.
The reduction in inflammation was associated with decreased levels of TLR4, MyD88, and NF-κB in the hypothalamic paraventricular nucleus.
Increased levels of PPAR-γ were observed in the hypothalamic paraventricular nucleus following telmisartan treatment in hypertensive rats.
Similar effects were not observed in normotensive rats, indicating a specific response in hypertensive conditions.

Simplified

Previous findings from our laboratory and others indicate that the main therapeutic effect of angiotensin II type 1 receptor (AT1-R) antagonists is to decrease blood pressure and exert anti-inflammatory effects in the cardiovascular system. In this study, we determined whether AT1-R antagonist telmisartan within the hypothalamic paraventricular nucleus (PVN) attenuates hypertension and hypothalamic inflammation via both the TLR4/MyD88/NF-κB signaling pathway and peroxisome proliferator-activated receptor-γ (PPAR-γ) in the PVN in hypertensive rats. Spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats were treated for 4weeks through bilateral PVN infusion with the AT1-R antagonist telmisartan (TEL, 10μg/h), or losartan (LOS, 20μg/h), or the PPAR-γ antagonist GW9662 (GW, 100μg/h), or vehicle via osmotic minipump. Mean arterial pressure (MAP) was recorded by a tail-cuff occlusion method. PVN tissue and blood were collected for the measurement of AT1-R, PPAR-γ, pro-inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6), inducible nitric oxide synthase (iNOS), TLR4, MyD88, nuclear factor-kappa B (NF-κB) activity and plasma norepinephrine (NE), respectively. Hypertensive rats exhibited significantly higher level of AT1-R and lower level of PPAR-γ in the PVN. PVN treatment with TEL attenuated MAP, improved cardiac hypertrophy, reduced TNF-α, IL-1β, IL-6, iNOS levels, and plasma NE in SHR but not in WKY rats. These results were associated with reduced TLR4, MyD88 and NF-κB levels and increased PPAR-γ level in the PVN of hypertensive rats. Our findings suggest that TLR4/MyD88/NF-κB signaling and PPAR-γ within the PVN are involved in the beneficial effects of telmisartan in hypertension.

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Telmisartan’s effects on high blood pressure may involve immune signaling and metabolism control in the brain’s blood pressure center

Abstract

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