How is calcium regulated

Blood levels of calcium are regulated by the parathyroid hormone, which acts on the bones, kidneys, and intestines to keep levels constant. Regulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive. If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms may result.

Blood calcium levels are regulated by parathyroid hormone PTH , which is produced by the parathyroid glands. PTH is released in response to low blood calcium levels.

It increases calcium levels by targeting the skeleton, the kidneys, and the intestine. What Is Secondary Prevention of Osteoporosis? July 21, Understanding Bone Density Results January 13, American Bone Health and Susan G. Cancer and Bone Health February 26, Subscribe to our mailing list.

Facebook-f Twitter Youtube. About Us. Quick Links. Systemic hormones such as growth hormone and somatomedins, glucocorticoids, sex hormones and thyroid hormone are essential for skeletal growth and development and interact with calcium regulators. Prostaglandins and osteoclast activating factor may be important in local regulation of bone. Under certain conditions, prolactin, estradiol, placental lactogen, and possibly somatotropin have a similar enhancing effect.

Increased secretion of these hormones, either alone or in combination, appears to be important in the efficient adaptation to the major calcium demands of pregnancy, lactation, and growth. Calcitonin is a amino acid polypeptide hormone secreted by the parafollicular cells C-cells of the thyroid gland in mammals and by ultimobranchial tissue in avian and other nonmammalian species.

The concentration of calcium ion in extracellular fluids is the principal stimulus for the secretion of calcitonin by C-cells. In hypercalcemia, the rate of secretion of calcitonin is increased greatly by rapid discharge of stored hormone from C-cells into interfollicular capillaries. Hyperplasia of C-cells occurs in response to longterm hypercalcemia.

When blood calcium is lowered, the stimulus for calcitonin secretion is diminished. Calcitonin exerts its effects by interacting with target cells, primarily in bone and kidney. The actions of PTH and calcitonin are antagonistic on bone resorption but synergistic on decreasing the renal tubular reabsorption of phosphorus. The hypocalcemic effects of calcitonin are primarily the result of decreased entry of calcium from the skeleton into plasma, resulting from a temporary inhibition of PTH-stimulated bone resorption.

The hypophosphatemia develops from a direct action of calcitonin, which increases the rate of movement of phosphorus out of plasma into soft tissue and bone and inhibits the bone resorption stimulated by PTH and other factors. Although many effects have been attributed to calcitonin at pharmacologic doses, their physiologic relevance is suspect.