Tissue (65)Zinc translocation in a rat model of chronic aldosteronism

Zinc, an essential micronutrient, is involved in wound healing. The hypozincemia seen with chronic aldosteronism is associated with enhanced fecal and urinary excretory Zn losses, and its tissue distribution is less certain. This study monitored tissue Zn-65 distribution in uninephrectornized rats at weeks I and 4 of aldosterone/salt treatment (ALDOST). Plasma and tissue total radio-nucleotide uptake was determined by calculating its mean radioactivity at 1, 4, 8, 24, and 4 3 hours after intravenous Zn-65 administration and where respective area under the concentration-time curves (AUC) were determined by the linear trapezoidal rule and expressed as a tissue:plasma AUC ratio. Examined tissues included: (1) injured heart and kidney in response I D ALDOST and incised skin; (2) noninjured liver, skeletal muscle, an] spleen sites of stress-linked Zn uptake; and (3) bone, a major storage and release site when Zn homeostasis is threatened. In comparison with age-matched and gender-matched controls, the following were found with week I and 4 ALDOST: (1) reduced plasma (65)Zi; (2) an accumulation of Zn-65 in heart and kidneys, where a well-known vasculopathy involves intramural vessels, and in incised skin at week 1; (3) an organ-specific increase in tissue Zn-65 in liver, in keeping with upregulated metallothionein expression, skeletal muscle, and spleen; and (4) a fall in bone and healed skin Zn-65 at week 4. Thus a wide-ranging disturbance in Zn homeostasis appears during ALDOST to include its translocation from plasma to injured heart, kidneys, and skin and noninjured liver, skeletal muscle, and spleen together with a resorption of stored Zn in bone at week 4. Zinc dysborneostasis is an integral feature of chronic aldosteronism.