Paeonol improves renal and vascular angiotensin II type 1 receptor function via inhibiting oxidative stress in spontaneously hypertensive rats

ABSTRACT

Background

Oxidative stress has been shown to play a critical role in the pathogenesis of hypertension. Paeonol, a major phenolic component extracted from Moutan Cortex, exerts a beneficial effect in preventing cardiovascular disease via reducing oxidative stress. The present study investigated the protective mechanism of paeonol against high blood pressure in spontaneous hypertension rats (SHRs).

Methods

Wistar-Kyoto (WKY) rats and SHRs received vehicle or peaonol in the drinking water for 5 weeks. Blood pressure was measured by tail-cuff plethysmography and oxidative stress in kidney and vascular tissue was examined by enzyme-linked immunosorbed assay. The functions of angiotensin II type 1 receptors (AT₁R) in the kidney and mesenteric artery were measured by natriuresis and vasoconstrictor response, respectively.

Results

Compared with vehicle-treated WKY rats, vehicle-treated SHRs exhibited higher blood pressure, increased oxidative stress, accompanied by exaggerated diuretic and natriuretic responses to candesartan (AT₁ receptor antagonist) and vasoconstrictor responses to angiotensin II (Ang II). Moreover, SHRs had higher ACE and AT₁R in the kidney and mesenteric artery, and higher Ang II and lower renin levels. Interestingly, paeonol treatment reduced the candesartan-induced increase in diuresis and natriuresis and vasoconstrictor responses to Ang II, and lowered blood pressure in SHRs, accompanied by reducing AT₁R protein expression in the kidney and mesenteric artery of SHR, and Ang II levels in plasma and increasing renin levels in renal cortex. In addition, these changes were associated with reducing oxidative stress.

Conclusions

The present study suggests that paeonol improves renal and vascular AT₁R functions by inhibition of oxidative stress, thus lowering blood pressure in SHRs.

KEYWORDS:

• Paeonol
• hypertension
• angiotensin II type 1 receptor
• oxidative stress
• kidney
• mesenteric artery

Data sharing statement

The data sets used and/or analyzed during the current study are available from the corresponding author on reasonable request

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author contribution

YW conceived and designed the experiments and wrote the manuscript; YZ performed the experiments and analyzed the data; QH contributed reagents analysis tools; ST approved the final version of the manuscript.

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.