Abstract 622: Role of Endothelial Nitric Oxide Synthase in a Capsaicin Diet-Induced Alleviation of Blood Pressure-Elevation in 2-Kidney, 1-Clip Hypertensive Rats

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Abstract

Objective: Capsaicin directly acts on the sensory nerve ending and releases neuropeptides, which activate a vasodilator, nitric oxide (NO) and decrease blood pressure (BP). We demonstrated that BP elevation was alleviated by consuming a low concentration of capsaicin diet in 2-kidney, 1-clip (2K1C) hypertensive rats. We also observed that when 2K1C rats took the NO synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester, during the protocol, the effect of alleviating hypertension by dietary capsaicin was diminished. Thus, we hypothesized that NO is involved in the effect of capsaicin in 2K1C rats. In this study, to test the hypothesis, we observed endothelial NOS (eNOS) expression in 2K1C rats fed a diet containing capsaicin.

Methods: Six-week old male Sprague-Dawley rats were treated with sham operation (SHAM) or clipping the left renal artery (2K1C). One week after the surgery, each group of rats were further divided into 2 groups randomly, which received either a control diet (CTL) or a diet containing 0.006% capsaicin (CAP) for 6 weeks. The systolic BP (SBP) was measured by a tail-cuff method once per week throughout the protocol. At the end of the protocol, MAP was measured in each rat under anesthesia. After euthanasia, the thoracic aortas were collected for extracting mRNA. Then, eNOS mRNA expression in aorta was evaluated in each group of rats by reverse transcriptase PCR.

Results and Discussion: The present data of BP confirmed that capsaicin diet alleviates BP elevation in 2K1C rats. At six weeks after the surgery, SBP in 2K1C-CTL rats (183 ± 6 mmHg) was significantly higher than SHAM-CTL (124 ± 6 mmHg, p < 0.05), but SBP in 2K1C-CAP (140 ± 4 mmHg) was significantly lower than that in 2K1C-CTL. SHAM-CAP (129 ± 8 mmHg) did not show a significant difference in SBP with SHAM-CTL. MAP at the end of the protocol showed the same tendency as SBP. Moreover, eNOS mRNA expression was enhanced in 2K1C-CTL (0.39 ± 0.06) compared to SHAM-CTL (0.31 ± 0.04, p < 0.05). Although it was not enhanced in SHAM-CAP (0.30 ± 0.01) compared to SHAM-CTL, it was tended to be enhanced in 2K1C-CAP (0.43 ± 0.02) compared to 2K1C-CTL. These data suggested that dietary capsaicin decreased BP with elevation of eNOS mRNA expression in 2K1C rats, but did not change eNOS mRNA nor BP in SHAM normotensive rats.

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