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Biomedical subjects

R Hegstad

Publications and source records attributed to R Hegstad.

6 recordsLinked to original sources
PubMed1992

Cadmium effects on bone metabolism: accelerated resorption in ovariectomized, aged beagles.

The purpose of this study was to evaluate, in an animal whose skeleton is comparable to humans, the combined effects of estrogen depletion and Cd exposure on bone resorption by monitoring skeletal release of 45Ca and to determine whether Cd-induced bone resorption occurred independent of osteotropic hormone changes and renal dysfunction. Cd exposure following ovariectomy or sham surgery was for 7 months: 1 month by oral ingestion of capsules (1, 5, 15, 50 ppm) and 6 months via drinking water (15 ppm). Serum and fecal 45Ca were increased at 1 week following ovariectomy (OV) (54 +/- 9% and 122 +/- 40%, respectively), but this response was attenuated by 2 weeks. Five of seven exposed dogs had increased serum and fecal 45Ca during the 50-ppm Cd capsule period (15-40% and 15-190%, respectively). Serum 45Ca levels in OV/+Cd dogs showed a significant and consistent increase within 1 week of initiating each of three separate Cd.H2O exposure cycles. Blood Cd levels increased over time from 2 to 15 micrograms/l, coinciding with the elevated serum 45Ca concentrations. No correlation was observed between serum 45Ca increases and parathyroid hormone, 1,25-(OH)2-vitamin D, or calcitonin. No effects of ovariectomy and/or Cd were observed in total serum Ca, calciotropic hormone concentrations, serum or urinary phosphorus and creatinine, creatinine clearance, or urinary specific gravity. Urinary Cd concentrations ranged from 7 to 50 micrograms/l in exposed dogs but were not detectable in nonexposed dogs. Urinary protein concentrations showed no differences between groups. Cd increased bone resorption (skeletal 45Ca release) in ovariectomized and sham-operated dogs without renal dysfunction or calciotropic hormone interaction. Based on our results, Cd is an exogenous factor which exacerbates bone mineral loss in postmenopausal osteoporosis.

Aging↗
PubMed1983

Aging and aldosterone.

We measured urinary and plasma aldosterone in normal subjects, aged 20 to 59 years, during a period of unrestricted sodium intake and after sodium depletion, using furosemide or a 20 meq sodium diet. Before and after sodium depletion, the mean and the upper limit of the range of urinary aldosterone excretion were considerably lower in subjects over 50 years compared with subjects under 30 years. Aging had no effect on plasma aldosterone concentration when the subjects were on an unrestricted sodium diet and blood was sampled while they were recumbent. In contrast, when the subjects were upright, both before and after sodium depletion, the mean and the upper limit of the range of plasma aldosterone concentration were lower in the subjects over 50 years compared with those under 30 years. The metabolic clearance of aldosterone was the same in the younger and the older subjects. Of eight patients over 40 years of age with aldosterone-producing adenoma, four had normal aldosterone excretion rates when the normal range was not age adjusted, but with age adjustment, all of the patients had clearly elevated excretion rates. Similarly, six of seven patients over 40 years of age had normal upright plasma aldosterone concentrations if the normal range of plasma aldosterone concentration was not age adjusted. We conclude that aldosterone secretion declines with advancing age. The effect of age on aldosterone secretion is an important consideration when evaluating older hypertensive patients for primary aldosteronism.

Adenoma↗
PubMed1981

Effect of metoclopramide on the secretion and metabolism of aldosterone in man.

We performed this study to determine whether metoclopramide increases the concentration of plasma aldosterone in normal man by increasing the secretion rate of aldosterone or by decreasing aldosterone metabolic clearance. On the first day that metoclopramide was administered orally to seven normal subjects, the secretion rate of aldosterone increased significantly (P less than 0.05) from the rate during the preceding placebo period. By the fourth day of treatment, the secretion rate had returned to control values and remained there during an ensuing placebo period. The excretion rate of aldosterone followed a similar pattern. The increase in aldosterone secretion was accompanied by a transient but significant decrease in urinary sodium excretion. Metoclopramide administered iv had no effect on the metabolic clearance of aldosterone. Metoclopramide stimulated aldosterone-producing adenomas and nodular hyperplastic adrenal tissue resected from patients with primary aldosteronism to produce aldosterone in vitro. We conclude that metoclopramide increases the concentration of aldosterone in plasma by stimulating the secretion of aldosterone rather than by decreasing aldosterone metabolic clearance, and that metoclopramide probably stimulates aldosterone secretion by acting directly on adrenal tissue.

Adult↗