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.
Subject(s)
Nitric Oxide/metabolism , Periodontitis/metabolism , Periodontitis/physiopathology , Potassium Channels/metabolism , Prostaglandin-Endoperoxide Synthases/metabolism , Vasodilation/physiology , Acetylcholine/pharmacology , Alveolar Bone Loss/metabolism , Alveolar Bone Loss/physiopathology , Animals , Arterial Pressure/drug effects , Arterial Pressure/physiology , C-Reactive Protein/analysis , Cyclooxygenase Inhibitors/pharmacology , Ligation , Male , NG-Nitroarginine Methyl Ester/pharmacology , Nitroprusside/pharmacology , Peroxidase/analysis , Potassium Channel Blockers/pharmacology , Potassium Channels/drug effects , Prostaglandin-Endoperoxide Synthases/drug effects , Random Allocation , Rats, Wistar , Time Factors , Vasodilation/drug effects , Vasodilator Agents/pharmacologyABSTRACT
Psoriasis is a complex inflammatory and hyperproliferative skin disease. The pathogenesis and mechanisms involved are not completely understood, which makes treatment a difficult issue. Angiotensin II, the most active peptide of the renin-angiotensin system, seems to be involved in processes related to psoriasis pathogenesis, such as inflammation and cell proliferation. The aim of this study was to investigate the influence of renin inhibition on inflammation parameters and keratinocyte proliferation in a mouse model of chronic skin inflammation induced by croton oil. Aliskiren had anti-inflammatory effects by reducing levels of tumor necrosis factor-α and interleukin -6, and by inhibiting myeloperoxidase activity. Aliskiren also showed antiproliferative activity by reducing epidermal hyperplasia and proliferating cell nuclear antigen levels. Aliskiren treatment did not induce alterations in the cardiovascular system, normal skin thickness, and organ weight. These results suggest that aliskiren could be a valuable tool to be incorporated in the treatment of hyperproliferative and inflammatory skin disorders such as psoriasis.
Subject(s)
Amides/pharmacology , Antihypertensive Agents/pharmacology , Fumarates/pharmacology , Skin Diseases/drug therapy , Angiotensin II/pharmacology , Animals , Anti-Inflammatory Agents/pharmacology , Cardiovascular System/drug effects , Cardiovascular System/metabolism , Disease Models, Animal , Female , Inflammation/drug therapy , Inflammation/metabolism , Keratinocytes/drug effects , Keratinocytes/metabolism , Mice , Psoriasis/drug therapy , Psoriasis/metabolism , Renin/metabolism , Renin-Angiotensin System/drug effects , Skin Diseases/metabolismSubject(s)
Edema/etiology , Inflammation/etiology , Periodontitis/complications , Receptor, Bradykinin B1/immunology , Alveolar Bone Loss/etiology , Alveolar Bone Loss/immunology , Alveolar Bone Loss/pathology , Animals , Chondrus , Disease Models, Animal , Edema/chemically induced , Edema/immunology , Edema/pathology , Extremities/pathology , Inflammation/immunology , Inflammation/pathology , Interleukin-1beta/immunology , Male , Periodontitis/immunology , Periodontitis/pathology , Rats , Rats, Wistar , Receptor, Bradykinin B1/analysis , Tumor Necrosis Factor-alpha/immunologyABSTRACT
PURPOSE: Evaluation of colonic healing in spontaneously hypertensive rats. METHODS: Fifty male, young and inbred rats were used. Twenty-five Wistar Kyoto rats (WKY) as control and twenty-five spontaneously hypertensive rats (SHR) as an experimental group. Colotomy and bowel suture at 2.5 cm from the peritoneal reflection were performed. All animals were allocated randomly into sub-groups for review at the third, seventh and fourteenth days after surgery. We evaluated the concentration of angiotensin II, the burst pressure, epithelialization, the organization of the tunics of the bowel wall, inflammatory response and collagen deposition. RESULTS: The burst pressure, epithelialization, organization of the tunics and collagen deposition was not significant between groups. The inflammatory reaction was more intense in the control group on the third postoperative day (p=0.023) as the experimental group on the remaining time. CONCLUSION: Systemic arterial hypertension in rats did not influence significantly the healing process of colonic anastomoses.
