Description:
Introduction: HDL is known for its anti-atherogenic qualities and serves as an important protective factor against cardiovascular disease. Recent studies suggested that this vasoprotective effect may not merely be based on reverse cholesterol transport. In fact, HDL has been proven to have vasodilatative properties of its own, a significant mechanism we investigated. Materials and Methods: Flow-dependent isometric tension, intracellularly recorded membrane potential and cAMP-cGMP were measured in segments of 20 coronaries from heart transplantations. Results: Flow-dependent vasodilatation was elevated by HDL administration [50 mg/dL] causing a mean relaxing effect of -0.236 g (Table). Application of phentolamine (10 -7 mol/L) and propranolol (10 -7 mol/L) resulted in a reduction of HDL induced vasorelaxation. This reduction was also flow-dependently progressing as flow increased. Interestingly, simultaneous α- and β-blockade did not follow an additive interaction pattern. The interaction seemed to be flow-dependent as well, with β-receptors contributing more to the combined effect at low flow rates and α-receptors to a greater proportion at high flows. Discussion: For the first time, we describe a potential mechanism of HDL-induced vasodilatation. Blood pressure and lipid profile - two independent risk factors of arteriosclerosis - may be linked by multiple HDL effects. We suggest that this vasorelaxation is in part mediated by activation of β-adrenoreceptors and inactivation of α-adrenoreceptors. This may have crucial implications in the clinical management of both hypertension and hyperlipidemia.