科研之友
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摘要
Exogenous administration of nitric oxide (NO) markedly decreases neointimal hyperplasia following arterial injury in several animal models. However, the effect of NO on neointimal hyperplasia in hypertension remains unknown. Here, we employ the spontaneously hypertensive rat (SHR) strain, inbred from Wistar Kyoto (WRY) rats, and the carotid artery balloon injury model to assess the effects of NO on neointimal hyperplasia development. 2 weeks after arterial injury, we showed that both rat strains developed similar levels of neointimal hyperplasia, but local administration of NO was less effective at inhibiting neointimal hyperplasia in the SHR compared to WRY rats (58% vs. 79%, P < 0.001). Interestingly, local administration of NO did not affect systemic blood pressure in either rat strain. Compared to WRY, the SHR displayed more proliferation in the media and adventitia following balloon injury, as measured by BrdU incorporation. The SHR also showed more inflammation in the adventitia after injury, as well as more vasa vasorum, than WRY rats. NO treatment reduced the vasa vasorum in the SHR but not WRY rats. Finally, while NO decreased both injury-induced proliferation and inflammation in the SHR, it did not return these parameters to levels seen in WRY rats. We conclude that NO is less effective at inhibiting neointimal hyperplasia in the SHR than WRY rats. This may be due to increased scavenging of NO in the SHR, leading to diminished bioavailability of NO. These data will help to develop novel NO-based therapies that will be equally effective in both normotensive and hypertensive patient populations. Published by Elsevier Inc.
- 出版日期2013-11-30
- 单位西北大学
