Mechanical, Biochemical, and Structural Effects of Vitamin D Deficiency on the Chick Heart

Abstract

The effects of vitamin D depriva tion on the chick heart were investi gated from three aspects: cardiac contractility (±dP/dT), intracellular high-energy phosphorus compounds, and structural differences. Four- week-old vitamin D-deficient chicks were divided into four groups: Group A served as the normal group and re ceived subcutaneous injections of cholecalciferol; Groups B and C were vitamin D-deficient hearts but per fused differently; Group D received daily subcutaneous injections of 5 μg of 1,25(OH) 2D3. When the isolated spontaneously beating hearts (modi fied Langendorff preparation) were perfused with Krebs-Henseleit (KH) solution containing a calcium concen tration of 2.5mM, the myocardial contractility of the vitamin D-defi cient hearts was significantly in creased when compared with group A. After the isolated heart had beaten for one hour, the myocardial contractility in the vitamin D-defi cient hearts was found to decline to significantly lower values. Presacri fice administration of 1,25(OH) 2D3 improved cardiac performance. Vita min D deficiency resulted in an en hanced rate of decline of the intracellular high-energy phosphorus compounds. No differences were found in the microscopic study. These observations suggest that vitamin D has a role in cardiac function.

Poor outcome in end‐stage heart failure patients with low circulating calcitriol levels

“…Third, calcitriol therapy significantly reduces left ventricular mass in haemodialysis patients [16]. Finally, calcitriol administration can normalize the impaired contractility of the myocardium that is observed under experimental vitamin D deficiency [17]. Our results of an inverse association between calcitriol and TIMP‐1 may offer insights into mechanisms of cardiac hypertrophy under calcitriol deficiency.…”

Calciotropic and Phosphaturic Hormones in End-Stage Heart Failure Patients Supported by a Left-Ventricular Assist Device

“…As mentioned before, 1,25(OH) 2 D plays a pivotal role in the intracellular handling of ionized calcium [5,6] and 1,25(OH) 2 D administration can normalize the impaired contractility of the myocardium that is observed under experimental vitamin D deficiency [7]. Although cardiomyocytes possess 1-α-hydroxylase activity [28], the heart muscle probably depends at least in part on circulating 1,25(OH) 2 D levels.…”

“…In addition, a 1,25(OH) 2 D-mediated rapid activation of voltage-dependent Ca channels exists in cardiac muscle cells [6]. Consequently, 1,25(OH) 2 D administration can normalize the impaired contractility of the myocardium that is observed under experimental vitamin D deficiency [7]. Renal synthesis of 1,25(OH) 2 D is suppressed by the phosphaturic hormone fibroblast growth factor-23 (FGF-23).…”

Cardiovascular Risk Factors: The Old Ones and a Closer Look to the Mineral Metabolism

“…The role played by vitamin D and PTH in cardiovascular function appears to be much more important than was originally thought. The discovery of a protein that binds to calcium, which is calcitriol-dependent and which is present in the myocardium, the vascular smooth muscle, and the endothelium, offered a clearer view on this subject [93][94][95][96][97][98].…”

“…The recent discovery of the 25(OH)D-1 hydroxylase enzyme-whose activity is regulated by the action of PTH and by estrogenic compounds-in the vascular smooth muscle cell has also contributed to the growing importance of vitamin D in vascular function [93,96]. Cardiac tissue cells have receptors for both PTH and PTH-related peptides, which affect the physiology of the cardiovascular cell in a different way from the action they exert on classic bone tissue [100].…”