Abstract 111: Blood Lipoproteins May Be Implicated in Blood Pressure Regulation

Abstract

Background: An increase in triglycerides, which comprise the main component of VLDL, belongs to definition criteria of the metabolic syndrome. We investigated the influence of VLDL (30 mg/dL) on flow-dilatation without and with α- (10 -7 mol/L) and β-blockers (10 -7 mol/L) to find out whether the VLDL effect is partly due to a possible α- and β-receptor interaction. Methods: Isometric tension, membrane potential and cAMP-cGMP were measured in 16 coronaries from heart transplantations. Results: Flow-dependent relaxation of 0.432 g in Krebs solution (T 3 - T 100 ) was reduced under VLDL by 15.3% to 0.366 g, and under VLDL + α/β-blockers by 20.1% to 0.345 g, thus practically no change. However, calculation of the difference in tension for the individual flow rates between Krebs and VLDL on the one hand, and Krebs and VLDL + α/β-blockers on the other, results in significant differences (Table). Setting the difference between Krebs and VLDL equal to 100%, leads to a 12.2% to 45.4% change in difference under α/β-blockers. Experiments under blockers yielded that α-receptor blockade alone is sufficient to explain the reduction of the VLDL-effect. β-effects were reflected by variation in [cAMP], α-effects in [cGMP]. Conclusion: About one third of the constricting VLDL-effect is due to a direct VLDL-inhibition of the β- receptor and/or stimulation of the α- receptor. We prove for the first time that blood lipoproteins exert their influence on arterial tone also via an interaction with the autonomic nervous system. We conclude that blood lipids may be implicated in blood pressure regulation. This unveiling could help in navigating the treatment options of both hypertension and hypercholesterolemia.