Center for Physical Activity Research, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark.
Department of Anaesthesia and Intensive Care, Copenhagen University Hospital - Hvidovre Hospital, Copenhagen, Denmark.
Exp Physiol. 2024 May;109(5):779-790. doi: 10.1113/EP091645. Epub 2024 Mar 6.
Endothelial dysfunction develops with age and may precede cardiovascular disease. Animal data suggest that T-type calcium channels play an important role in endothelial function, but data from humans are lacking. This study included 15 healthy, sedentary, elderly males for a double blinded, randomized controlled trial. For 8 weeks, they were given 40 mg/day of either efonidipine (L- and T-type calcium channel blocker (CCB)) or nifedipine (L-type CCB). Vascular function was evaluated by graded femoral arterial infusions of acetylcholine (ACh; endothelium-dependent vasodilator) and sodium nitroprusside (endothelium-independent vasodilator) both with and without co-infusion of N-acetylcysteine (NAC; antioxidant). We measured leg blood flow and mean arterial pressure and calculated leg vascular conductance to evaluate the leg vascular responses. Despite no significant change in blood pressure in either group, we observed higher leg blood flow responses (Δ 0.43 ± 0.45 l/min, P = 0.006) and leg vascular conductance (Δ 5.38 ± 5.67 ml/min/mmHg, P = 0.005) to intra-arterial ACh after efonidipine, whereas there was no change in the nifedipine group, and no differences between groups. We found no upregulation of endothelial nitric oxide synthase in vastus lateralis muscle biopsies within or between groups. Smooth muscle cell responsiveness was unaltered by efonidipine or nifedipine. Intravenous co-infusion of NAC did not affect endothelium-dependent vasodilatation in either of the CCB groups. These results suggest that 8 weeks' inhibition of T- and L-type calcium channels augments endothelium-dependent vasodilatory function in healthy elderly males. Further studies are required to elucidate if T-type calcium channel inhibition can counteract endothelial dysfunction.
内皮功能障碍随年龄增长而发展,可能先于心血管疾病发生。动物数据表明 T 型钙通道在血管内皮功能中发挥重要作用,但缺乏人类的数据。这项研究纳入了 15 名健康、久坐的老年男性,进行了一项双盲、随机对照试验。8 周内,他们分别服用 40mg/天的依福地平(L 和 T 型钙通道阻滞剂(CCB))或硝苯地平(L 型 CCB)。通过股动脉输注乙酰胆碱(内皮依赖性血管扩张剂)和硝普钠(内皮非依赖性血管扩张剂),并同时输注 N-乙酰半胱氨酸(抗氧化剂),评估血管功能。我们测量了腿部血流量和平均动脉压,并计算了腿部血管传导率,以评估腿部血管反应。尽管两组的血压均无显著变化,但我们观察到依福地平组腿部血流反应(Δ 0.43±0.45l/min,P=0.006)和腿部血管传导率(Δ 5.38±5.67ml/min/mmHg,P=0.005)更高,而硝苯地平组无变化,两组之间也无差异。我们未发现依福地平或硝苯地平对内腓肌活检中内皮型一氧化氮合酶有上调作用。依福地平或硝苯地平均未改变平滑肌细胞的反应性。静脉输注 NAC 对两种 CCB 组的内皮依赖性血管舒张均无影响。这些结果表明,抑制 T 型和 L 型钙通道 8 周可增强健康老年男性的内皮依赖性血管舒张功能。需要进一步研究以阐明 T 型钙通道抑制是否可以对抗内皮功能障碍。