RESUMEN
Sphingolipids are a structural component of the cell membrane, derived from sphingosine, an amino alcohol. Its sphingoid base undergoes various types of enzymatic transformations that lead to the formation of biologically active compounds, which play a crucial role in the essential pathways of cellular signaling, proliferation, maturation, and death. The constantly growing number of experimental and clinical studies emphasizes the pivotal role of sphingolipids in the pathophysiology of cardiovascular diseases, including, in particular, ischemic heart disease, hypertension, heart failure, and stroke. It has also been proven that altering the sphingolipid metabolism has cardioprotective properties in cardiac pathologies, including myocardial infarction. Recent studies suggest that selected sphingolipids may serve as valuable biomarkers useful in the prognosis of cardiovascular disorders in clinical practice. This review aims to provide an overview of the current knowledge of sphingolipid metabolism and signaling in cardiovascular diseases.
RESUMEN
The present study was aimed at determining the role of centrally released oxytocin in regulation of blood pressure and heart rate (HR) under resting conditions and during an acute air-jet stress in rats with a myocardial infarction and controls infarcted. Four weeks after ligation of a coronary artery or sham surgery, conscious Sprague Dawley rats were subjected to one of the following intracerebroventricular (ICV) infusions: (1) 0.9% NaCl (control), (2) oxytocin, (3) oxytocin receptor antagonist {desGly-NH(2)-d(CH(2))(5)[D-Tyr(2)Thr(4)]OVT}(OXYANT). Resting arterial blood pressure and HR were not affected by any of the ICV infusions either in the infarcted or sham-operated rats. In the control experiments, the pressor and tachycardic responses to the air jet of infarcted rats were significantly greater than in the sham-operated rats. OXYANT significantly enhanced the cardiovascular responses to stress only in the sham-operated rats whereas oxytocin significantly attenuated both responses in the infarcted but not in the sham-operated rats. The results suggest that centrally released endogenous oxytocin significantly reduces the cardiovascular responses to the acute stressor in control rats. This buffering function of the brain-oxytocin system is not efficient during the post-myocardial infarction state, however it may be restored by central administration of exogenous oxytocin.