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Alcohol ingestion during pregnancy is known to cause fetal malformation and growth retardation. We investigated the effect of alcohol on mineral content and fetal development in rats fed 24% (v/v) alcohol eight weeks prior to and during pregnancy. Rats ingesting alcohol produced fewer fetuses (6.3 +/- 0.3 vs 9.6 +/- 0.3 in control) with lower fetal weight (3.48 +/- 0.09 vs 4.12 +/- 0.08 gm in control) and heavier placentas (0.66 +/- 0.05 vs 0.50 +/- 0.01 gm in control). The fetuses of alcoholic rats contained lower zinc (423.8 +/- 4.5 vs 459.9 +/- 5.4 microEq/100 gm dry weight in control) and magnesium (12.4 +/- 0.1 vs 12.7 +/- 0.1 mEq/100 gm dry weight in control) in the total carcass.

The effect of hypomagnesemia on renal concentrating ability was assessed in rats fed diets either low in magnesium or low in magnesium and calcium for 30 days. The rats fed a low-magnesium diet became hypomagnesemic (0.26 +/- 0.03 versus 1.53 +/- 0.04 mEq/L in controls), hypercalcemic (5.96 +/- 0.04 versus 5.22 +/- 0.11 mEq/L in controls), and hypokalemic (3.1 +/- 0.1 versus 4.2 +/- 0.4 mEq/L in controls) with decreased muscle content of potassium. Despite being hypomagnesemic, hypercalcemic, and potassium depleted, the rats had normal renal concentration ability (2499 +/- 65 versus 2415 +/- 119 mOsm/kg H2O in control). Those rats fed a diet low in both magnesium and calcium became hypomagnesemic (0.41 +/- 0.08 versus 1.53 +/- 0.04 mEq/L in controls) but were hypocalcemic. They also had normal renal concentrating ability (2399 +/- 109 versus 2415 +/- 119 mOsm/kg H2O in controls). It is concluded that hypomagnesemia does not decrease renal concentrating ability in rats. Furthermore, a normal concentrating ability demonstrated in hypomagnesemic rats, in spite of hypercalcemia and potassium depletion suggests that hypomagnesemia may ameliorate the deleterious effects of hypercalcemia and/or potassium depletion on renal concentrating ability.