Abstract
Objective:Periodontitis is associated with endothelial dysfunction, which is clinically characterized by a reduction in endothelium-dependent relaxation. However, we have previously shown that impairment in endothelium-dependent relaxation is transient. Therefore, we evaluated which mediators are involved in endothelium-dependent relaxation recovery.Material and methods:Rats were subjected to ligature-induced experimental periodontitis. Twenty-one days after the procedure, the animals were prepared for blood pressure recording, and the responses to acetylcholine or sodium nitroprusside were obtained before and 30 minutes after injection of a nitric oxide synthase inhibitor (L-NAME), cyclooxygenase inhibitor (Indomethacin, SC-550 and NS- 398), or calcium-dependent potassium channel blockers (apamin plus TRAM- 34). The maxilla and mandible were removed for bone loss analysis. Blood and gingivae were obtained for C-reactive protein (CRP) and myeloperoxidase (MPO) measurement, respectively.Results:Experimental periodontitis induces bone loss and an increase in the gingival MPO and plasmatic CRP. Periodontitis also reduced endothelium-dependent vasodilation, a hallmark of endothelial dysfunction, 14 days after the procedure. However, the response was restored at day 21. We found that endothelium-dependent vasodilation at day 21 in ligature animals was mediated, at least in part, by the activation of endothelial calcium-activated potassium channels.Conclusions:Periodontitis induces impairment in endothelial-dependent relaxation; this impairment recovers, even in the presence of periodontitis. The recovery is mediated by the activation of endothelial calcium-activated potassium channels in ligature animals. Although important for maintenance of vascular homeostasis, this effect could mask the lack of NO, which has other beneficial properties.
Highlights
Periodontitis is a chronic inflammatory disease that compromises the integrity of tooth-supporting tissues
We found that endothelium-dependent vasodilation at day 21 in ligature animals was mediated, at least in part, by the activation of endothelial calcium-activated potassium channels
To evaluate endothelial function in rats with experimental periodontitis, we evaluated the effects of endothelium-dependent and endothelium-independent vasodilators
Summary
Periodontitis is a chronic inflammatory disease that compromises the integrity of tooth-supporting tissues. In addition to the local effects of this disease, periodontitis is associated with systemic inflammation.. Periodontitis has been associated with endothelial dysfunction, which is an early event in the development of cardiovascular diseases, especially atherosclerosis.. Acetylcholine stimulates endothelial nitric oxide synthase (NOS-3) to generate nitric oxide (NO), which diffuses to the underlying smooth muscle cells, inducing relaxation by increasing the production of cGMP, leading to a transient reduction in blood pressure in vivo.. Endothelial dysfunction is broadly defined as an impairment in vascular relaxation, due to decreased NO production by the endothelium and/or increased inactivation of NO.. Besides being a potent vasodilator, NO has antithrombotic, anti-inflammatory, and antimitogenic properties, which explains why the reduction in NO levels is associated with increased cardiovascular disease risk. Acetylcholine stimulates endothelial nitric oxide synthase (NOS-3) to generate nitric oxide (NO), which diffuses to the underlying smooth muscle cells, inducing relaxation by increasing the production of cGMP, leading to a transient reduction in blood pressure in vivo. endothelial dysfunction is broadly defined as an impairment in vascular relaxation, due to decreased NO production by the endothelium and/or increased inactivation of NO. Besides being a potent vasodilator, NO has antithrombotic, anti-inflammatory, and antimitogenic properties, which explains why the reduction in NO levels is associated with increased cardiovascular disease risk.
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