Advances in Dentistry and Oral Health Research Article Volume 1 Issue 2 - November 2015 Adv Dent & Oral Health Copyright © All rights are reserved by Ahmed Alsaadi PGE 2 and 6-Keto-PGF 1α Generation and Cyclic AMP in the Atria of Rats during Normoxia and Hypoxia Sabrina Ganzinelli and Enri Borda* Department of Pharmacology, University of Buenos Aires, USA Submission: October 22, 2015; Published: November 24, 2015 *Corresponding author: Prof. Dr. Enri Borda, Pharmacology Unit-School of Dentistry, University of Buenos Aires, M. T. de Alvear 2142 – 4ºFloor “B”, 1122AAH Ciudad Autónoma de Buenos Aires Argentina, USA, Email: Abstract Circulating antibodies can be detected in chronic periodontitis patients given the presence of serum auto antibodies against β 1 -adrenoceptor (β 1 -AR) in periodontitis patients by using cardiac membranes or a synthetic β 1 -AR peptide corresponding to the second extracellular loop of human β 1 -AR as antigens. Periodontitis patients also exhibit enhanced atria contractility in normoxia and tonic contraction in hypoxia. Atenolol, synthetic β 1 peptide and nifedipine abrogate the action of both Isoproterenol and β 1 IgG on atria contractility in both experimental conditions. In turn, β 1 IgG display a partial agonist-like activity and modifies the contractility of isolated atria, accompanied by an accumulation of cyclic AMP nucleotide in normoxia and hypoxia. The autoantibody is able to provoke an increment in the concentrations of PGE 2 and 6-keto- PGF 1α , which is abrogated by preincubating atria with adrenergic antagonist, synthetic β 1 peptide and prostanoid receptor antagonists. On this basis this study seeks to correlate the periodontitis infection to an increased risk of cardiac disease high lightening the role of β 1 IgG in the alteration of myocardial contractility and the subsequent increment of prostaglandins (PGE 2 and 6-keto-PGF 1α ,) accompanied by an increment in the production of cyclic AMP, resulting in an effective adaptation of myocardium function in acute ischemia. Keywords: Myocardium; Hypoxia; Periodontitis; Prostanoids; cAMP; Contractility Abbreviations: AR: Adreno Receptors; COX-2: Cyclooxygenase-2; PKC: Protein Kinase C; PTKs: Protein Tyrosine Kinases; ROS: Reactive Oxygen Species; NO: Nitric Oxide; CAL: Clinical Attachment Loss; cAMP: Cyclic Adenosine Monophosphate; ANOVA: Analysis of Variance; ISO: Isoproterenol; KRB: Krebs Ringer bicarbonate; HRV: Heart Rate Variability Introduction Intermittent hypoxia has been demonstrated to have powerful cardiovascular protective capabilities [1]. These effects can be grouped into three major categories: 1: adaptation of organs and tissues responsible for oxygen uptake and transport [2], 2: proliferation and increased density of vascular networks [3], and 3: increased mitochondrial density in the brain, the liver and the heart [4]. Consequently, adaptation to intermittent hypoxia has been used to treat patients with ischemic heart disease [5] and with post myocardial infarction heart failure [6]. Periodontitis is on its part characterized by a gingival inflammation in which periodontopathic bacteria generate immunological inflammatory responses and is seen as a key risk factor for the onset of cardiovascular disease [7-9]. In this connection it is important to mention, that autoantibodies against atria cardiac β 1 -adrenoreceptors (AR) are able to mimic the effect of an authentic β 1 -AR agonist acting on atria β 1 -AR [10] in the sera of patients with periodontitis. The joined release of host-derived inflammatory mediators (such as cytokines) and serum anti-β 1 -AR IgG into the circulation of chronically-inflamed periodontal tissues may thus provide a link between periodontal disease and cardiovascular disease [8,9]. Other studies state that the exposure of the heart to a sub lethal ischemic stress induces a phenotypic change that renders the myocardium relatively resistant to a subsequent ischemic insult occurring 24 to 72 hours later, corresponding to late phase of ischemic preconditioning [11,12]. Late phase of ischemic preconditioning is itself associated with the up regulation of cyclooxygenase-2 (COX-2) expression; the COX-2–dependent synthesis of prostanoids (ie, prostaglandin E 2 and prostaglandin I 2 ) is viewed as essential for the observed cardio protective effects [13]. Prostanoids have been shown to alleviate myocardial ischemia/reperfusion injury [14]. What remains unknown on the one hand is which are the signaling pathways whereby a sub lethal ischemic stress leads to an increased expression of prostanoids in the heart; on the other, how the modulation of COX-2 in adult myocardium takes place. Adv Dent & Oral Health 1(2): ADOH.MS.ID.555557 (2015) 001