Presence of dysfunctional soluble guanylate cyclase in mesenteric resistance arteries from rats with mild ligature-induced periodontitis.

Periodontitis is notable for its high prevalence in the oral cavity and its association with systemic diseases. Functional alterations in vasomotor activity occur in the arteries of rats with mild periodontitis, primarily due to decreased soluble guanylate cyclase (sGC) enzyme activity. This study aims to investigate the functional response of mesenteric resistance arteries (MRA) obtained from rats with mild periodontitis. Vascular reactivity of MRAs from rats in the ligature (L) or sham (S) groups was assessed using a wire myograph. Additionally, antioxidant enzyme activity, the presence of nitrated proteins, cyclic guanosine monophosphate (cGMP) levels, and electron paramagnetic resonance (EPR) spectroscopy were analyzed. The MRAs from the L group showed lower pD2 values in response to sodium nitroprusside or sildenafil and decreased Emax to the sGC stimulator Bay 41-2271 compared to the S group. However, no differences were observed between the groups with respect to the sGC activator Bay 60-2770. The L group exhibited increased nitrotyrosine protein expression, enhanced catalase activity, and reduced superoxide dismutase activity, along with decreased cGMP content after SNP stimulation. The EPR spectrum of the L group showed a weak peak at g 6.00, compared to the S group, confirming the oxidation of sGC heme-iron (Fe+2) to heme-Fe+3. In the early phase of bilateral ligature-induced periodontitis in rats, functional changes in the nitric oxide (NO)-cGMP pathway occur in the MRA due to reduced sGC activity and excessive production of iNOS-derived NO, superoxide anion, or a combination of both.