Control of Renal Calcium Excretion and Extracellular Calcium Ion Concentration

The mechanisms for regulating calcium ion concentration are discussed in detail in Chapter 79, along with the endocrinology of the calcium-regulating hormones parathyroid hormone (PTH) and calcitonin. Therefore, calcium ion regulation is discussed only briefly in this chapter.

Extracellular fluid calcium ion concentration normally remains tightly controlled within a few percentage points of its normal level, 2.4mEq/L. When calcium ion concentration falls to low levels (hypocalcemia), the excitability of nerve and muscle cells increases markedly and can in extreme cases result in hypocalcemic tetany. This is characterized by spastic skeletal muscle contractions. Hypercalcemia (increased calcium concentration) depresses neuromus-cular excitability and can lead to cardiac arrhythmias.

About 50 per cent of the total calcium in the plasma (5 mEq/L) exists in the ionized form, which is the form that has biological activity at cell membranes. The remainder is either bound to the plasma proteins (about 40 per cent) or complexed in the non-ionized form with anions such as phosphate and citrate (about 10 per cent).

Changes in plasma hydrogen ion concentration can influence the degree of calcium binding to plasma proteins. With acidosis, less calcium is bound to the plasma proteins. Conversely, in alkalosis, a greater amount of calcium is bound to the plasma proteins. Therefore, patients with alkalosis are more susceptible to hypocalcemic tetany.

As with other substances in the body, the intake of calcium must be balanced with the net loss of calcium over the long term. Unlike ions such as sodium and chloride, however, a large share of calcium excretion occurs in the feces. The usual rate of dietary calcium intake is about 1000 mg/day, with about 900 mg/day of calcium excreted in the feces. Under certain conditions, fecal calcium excretion can exceed calcium ingestion because calcium can also be secreted into the intestinal lumen. Therefore, the gastrointestinal tract and the regulatory mechanisms that influence intestinal calcium absorption and secretion play a major role in calcium homeostasis, as discussed in Chapter 79.

Almost all the calcium in the body (99 per cent) is stored in the bone, with only about 1 per cent in the extracellular fluid and 0.1 per cent in the intracellular fluid. The bone, therefore, acts as a large reservoir for storing calcium and as a source of calcium when extracellular fluid calcium concentration tends to decrease.

One of the most important regulators of bone uptake and release of calcium is PTH.When extracellular fluid


Vitamin And Pth Physiology
Compensatory responses to decreased plasma ionized calcium concentration mediated by parathyroid hormone (PTH) and vitamin D.

calcium concentration falls below normal, the parathyroid glands are directly stimulated by the low calcium levels to promote increased secretion of PTH. This hormone then acts directly on the bones to increase the resorption of bone salts (release of salts from the bones) and, therefore, to release large amounts of calcium into the extracellular fluid, thereby returning calcium levels back toward normal. When calcium ion concentration is elevated, PTH secretion decreases, so that almost no bone resorption now occurs; instead, excess calcium is deposited in the bones because of new bone formation. Thus, the day-to-day regulation of calcium ion concentration is mediated in large part by the effect of PTH on bone resorption.

The bones, however, do not have an inexhaustible supply of calcium. Therefore, over the long term, the intake of calcium must be balanced with calcium excretion by the gastrointestinal tract and the kidneys. The most important regulator of calcium reabsorption at both of these sites is PTH. Thus, PTH regulates plasma calcium concentration through three main effects: (1) by stimulating bone resorption; (2) by stimulating activation of vitamin D, which then increases intestinal reabsorption of calcium; and (3) by directly increasing renal tubular calcium reabsorption (Figure 29-10). The control of gastrointestinal calcium reabsorption and calcium exchange in the bones is discussed elsewhere, and the remainder of this section focuses on the mechanisms that control renal calcium excretion.

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