Parathyroid Hormone's Acute Effect on Vasodilatory Function

Abstract

Parathyroid hormone (PTH) seems to affect the risk of cardiovascular disease. The aim of the present study was to investigate PTH's acute effect on endothelial vasodilatory function in forearm resistance vessels. Ten healthy subjects underwent forearm venous occlusion plethysmography. We measured forearm blood flow at baseline and at a stable, locally increased PTH level after intra-arterial infusion of metacholine and nitroprusside. The contralateral arm served as a control. Ionized calcium (Ca++) and PTH values were normal in all subjects at baseline (1.26 ± 0.02 mM/L, 3.6 ± 1.2 pM/L). After 30 minutes of PTH infusion, the PTH level increased in the active arm (13.8 ± 4.0 pM/L P < 0.01), while the Ca++ level was unchanged (1.25 ± 0.04; mM/L). Both the PTH and the Ca++ level in the contralateral arm remained unchanged, which indicates no systemic influence. The endothelial-dependent vasodilation was inversely correlated to the Ca++ level at baseline (r = -0.75, P < 0.05) and after PTH infusion (r = -0.68, P < 0.05). The vasodilatory function was not affected during PTH-infusion.

Keywords: endothelial function; forearm venous occlusion plethysmography; parathyroid hormone.

Figure 1.

Forearm blood flow (FBF), endothelium-dependent vasodilation (metacholine, MCh 2 and 4 μg/min, Fig 1a) and endothelium-independent vasodilation (sodium nitroprusside, SNP 5 and 10 μg/min, Fig 1b) before and at steady state of local intra-arterial administration of parathyroid hormone (PTH).

Figure 2.

Forearm blood flow, endothelium-dependent vasodilation (EDV), during metacholine infusion (MCh 4 μg/min) before and at steady state of local intra-arterial administration of parathyroid hormone (PTH) correlated inversely to the ionized calcium level (baseline, r = −0.75, P < 0.05 and after PTH infusion, r = −0.68, P < 0.05).