1,25 (oh)2 vitamin d3 modulates intracellular ca2+ and force generation in resistance arteries. Bian, Ka, Katsuhiko Ishibashi, and Richard D. Bukoski. Hypertension and Vascular Research Laboratories, Departments of Internal Medicine and Physiology and Biophysics, University of Texas Medical Branch, Galveston Island, Texas
APStracts 2:0295H, 1995.
The mechanism by which 1,25 (OH)2 vitamin D3 (1,25 vitD) enhances smooth muscle force generation was examined. Rats were injected on 3 mornings with 35 ng/100 g 1,25 vitD or vehicle and on the 4th morning mesenteric resistance arteries were isolated and used for simul taneous measurement of intracellular Ca2+ and force generation, or determination of myosin light chain phosphorylation. 1,25 vitD was without effect on media thickness and wall:lumen ratio, but increased the resting level of free intracellular Ca2+ (vehicle= 49.2+2.2 nmol/L vs 1,25 vitD=65.9+/-4.0 nmol/L, p&LT0.05, n=24-26). 1,25 vitD enhanced the active stress and intracell ular Ca2+ responses to cumulative addition of norepinephrine; the increases were normalized by pre-treatment with 10 [mu]mol/L verapamil. The effect of treatment with 1,25 vitD on the time course and magnitude of the active stress, intracellular Ca2+, and myosin light chain phosphoryl ation responses to challenge with 10 [mu]mol/L norepinephrine determined in another group of ani mals showed that 1,25 vitD significantly increased the basal intracellular Ca2+ and light chain phosphorylation, and the magnitude of norepinephrine-induced stress generation and Ca2+ mobili zation. The hormone did not affect the peak or steady state light chain phosphorylation response. Myofilament Ca2+ sensitivity, determined in non-permeabilized vessels during stimulation with 2 [mu]mol/L norepinephrine, was depressed in vessels isolated from rats treated with 1,25 vitD (vehicle Ca2+-ED50=82.7+3.8 nmol/L vs 1,25 vitD=104.8+ 4.9 nmol/L, p=0.002). We con clude that 1,25 vitD enhances resistance artery force generation by altering smooth muscle Ca2+ homeostasis; with effects on basal and verapamil sensitive, agonist-induced Ca2+ mobilization. 

Received 16 March 1995; accepted in final form 20 June 1995.
APS Manuscript Number H258-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.