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Treatment of pregnant mothers with an antidiuretic may correct the lack of amniotic fluid known as oligohydramnios. Researchers administered the antidiuretic vasopressin to pregnant sheep after they had been given lots of water to drink. Mothers experienced a decrease in plasma volume, and fetuses swallowed less fluid and excreted more urine, all of which raised the amount of amniotic fluid by 70% within two days. Vasopressin did not cause maternal blood pressure to drop. Instead maternal systolic pressure increased. Vasopressin was not found to cross the placenta. Red blood cell counts and systolic blood pressure were normal in the fetuses and no swelling was observed, indicating that the fetuses were well hydrated.

We examined the ontogeny of relaxation responses to three categories of calcium channel antagonists, represented by verapamil, diltiazem, and nifedipine, for both potential-operated (KCl-mediated) and receptor-operated channels [norepinephrine (NE)-mediated] in rat thoracic aorta. Aortic rings from 2− to 3-d, 1-wk, and 12-wk-old Sprague Dawley rats were mounted in an organ bath, bathed in Krebs' solution, and connected to a force-displacement transducer to measure isometric tension. Endothelium intact vessels at optimal passive force were exposed to a single ED50of isotonic KCl or NE, equilibrium contraction was measured, then vessels were washed and exposed for 30 min to 1 $mUM verapamil, 1 $mUM diltiazem, or 0.1 $mUM nifedipine, followed by another dose of KCl or NE. Verapamil and diltiazem demonstrated significant (p< 0.05) age-related increases in effectiveness for blocking KCl-mediated contraction [( reduction of control contraction $$ SEM) (Verapamil: 2–3 d, 67.7 $$ 4.2; 1 wk, 72.5 $$ 1.8; 12 wk, 89.5 $$ 1.0. Diltiazem: 2–3 d, 64.6 $$ 2.9; 1 wk, 73.5 $$ 3.0; 12 wk, 83.1 $$ 1.8]. Nifedipine was equally effective at all ages: 2–3 d, 85.6 $$ 1 1.3; wk, 90.0 $$ 1.6; and 12 wk, 91.3 $$ 1.4. Verapamil and diltiazem also showed significant age-related increases in effectiveness for blocking NE-mediated contraction (Verapamil: 2–3 d, 6.2 $$ 3.9; 1 wk, 28.0 $$ 4.8; 12 wk, 44.1 $$ 6.0. Diltiazem: 2–3 d, 8.0 $$ 3.1; 1 wk, 20.5 $$ 3.9; 12 wk, 46.5 $$ 4.8). Again, nifedipine was equally effective at all ages: 2–3 d, 42.0 $$ 6.8; 1 wk, 35.8 $$ 3.9; and 12 wk, 37.5 $$ 3.2. In summary, for the categories of calcium channel antagonists that interact at the phenylalkytomine (verapamil) and benzothiazepine (diltiazem) binding sites, there were age-related increases in effectiveness for blocking both potential-operated and receptor-operated channels. However, for nifedipine, which binds to the 1,4-dihydropyridine binding site, no maturational change was observed. These results suggest that the ontogeny of calcium channel antagonists' function may vary depending on the site of binding within the calcium channel. (Pediatr Res29: 278–281, 1991)