Analysis of BP response and Ca2+ metabolism using the saturation kinetics model.

The provision of supplemental dietary calcium (dCa) lowers blood pressure (BP) in the spontaneously hypertensive rat (SHR). Whether calcium's antihypertensive effects can be expressed in the presence of potentially hypertensinogenic nutrients is not known. Furthermore, the amount of dCa required to attenuate hypertension in the SHR remains undetermined. Along with establishing the effects of dCa on BP under conditions of a high Na+ intake, we sought to define the lowest dose of dCa associated with the greatest attenuation in arterial pressure in the young SHR. Thirty-five 6-wk-old SHR were fed one of five diets containing either 0.1, 0.25, 0.5, 1.0, or 2.0% dCa. All diets contained 1.0% Na+. The rates of change (delta) in body weight, BP, and serum ionized calcium were determined between 6 and 20 wk of age. Bone density (BD) was measured only at 20 wk of age. The data were analyzed using the saturation kinetics model. Results indicate that the half-maximal dose (K50) of dCa needed to lower pressure is 0.67 +/- 0.18%, which is higher than the K50 for weight (0.23 +/- 0.18) and BD (0.36 +/- 0.22). It is concluded that supplemental dCa lowers BP despite a high Na+ intake. Furthermore, a dose of approximately 1.5 dCa is sufficient to attenuate the rate of hypertension in the young growing SHR.

Parathyroid hormone in sodium-dependent hypertension.

Plasma parathyroid hormone (pPTH) levels have been assessed in three separate radioimmunoassay systems in samples from Wistar-Kyoto rats. The animals were subjected to one of three dietary regimens throughout the study period: Group 1 animals consumed normal rat chow and drank tap water; Group 2 animals consumed normal rat chow and tap water was replaced with 0.5% saline solution; Group 3 animals consumed normal rat chow to which 2.5% CaCO3 (by weight) had been added and also drank 0.5% saline solution. Animals had consumed these diets for approximately 7 months prior to sacrifice for blood collection. Blood pressure was measured by tail cuff plethysmography in these animals and, as previously reported, saline consuming animals showed a moderate hypertension (Gp 2) only when diets did not contain added calcium (Gp 3). In the week prior to sacrifice, mean blood pressures were: Gp 1: 128.0 +/- 3.46 mmHg; Gp 2: 140.2 +/- 3.15 mmHg; and Gp 3: 133.5 +/- 2.90 mmHg. Three assay systems were used to measure pPTH levels from trunk blood samples obtained by guillotine decapitation. One assay used an antiserum directed toward the vasoactive N terminal fragment 1-34 and produced pPTH measurements of 0.74 +/- 0.05 ng/ml in Gp 1 animals, 1.04 +/- 0.07 ng/ml in Gp 2 animals and 1.12 +/- 0.08 ng/ml in Gp 3 animals. This pattern was consistent with that obtained by another antiserum which had been raised against the intact 1-84 PTH molecule and produced values of 0.25 +/- 0.03 ng/ml in Gp 1 animals, 0.55 +/- 0.07 ng/ml in Gp 2 animals and 0.74 +/- 0.04 ng/ml in Gp 3 animals. Antiserum raised against the C-terminal did not show any difference in pPTH across groups. We conclude that saline consumption may increase some portions of circulating PTH. Such elevation of pPTH may not be a pathophysiological component in the sodium dependent elevation of blood pressure since animals concurrently consuming both saline and calcium supplemented diets retained elevated pPTH levels even though blood pressures did not differ from controls. Rather, elevation of circulating PTH levels may be a response to prolonged increases in sodium consumption.

Calcium metabolism in pregnancy and the perinatal period: a review.

Calcium homeostasis is a complex process involving calcium, other involved ions, and three calcitropic hormones, parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D3. The principal maternal adjustment during pregnancy is an increasing parathyroid hormone secretion which maintains the serum calcium concentration in the face of a falling albumin level, an expanding extracellular fluid volume, an increasing renal excretion, and placental calcium transfer. The placenta transports calcium ions actively, making the fetus hypercalcemic relative to its mother, which in turn stimulates calcitonin release and perhaps suppresses parathyroid hormone secretion by the fetus. A unique extrarenal system for 1 alpha-hydroxylation of 25-hydroxyvitamin D3 exists in the placenta and/or decidua, providing a source of 1,25-dihydroxyvitamin D3 for the fetus. With the abrupt cessation of the placental source of calcium at birth, the neonate's serum calcium level falls for 24 to 48 hours, then stabilizes and rises slightly. Hyperparathyroidism during pregnancy causes complications in both mother and infant and should usually be treated surgically as soon as diagnosed. Maternal hypoparathyroidism can be treated satisfactorily with high doses of supplemental calcium and vitamin D. Osteopenia accompanying long-term heparin administration may respond to 1,25-dihydroxyvitamin D3 (calcitriol) therapy. Diabetes in pregnancy is associated with disturbed neonatal calcium homeostasis, perhaps due to chronic hypomagnesemia. A possible etiologic role of calcium deficiency in pregnancy-related hypertension has been suggested. Dietary deficiency of calcium and/or vitamin D during gestation may lead to several adverse effects in the newborn infant.

Milk, serum cholesterol, and the Maasai. A hypothesis.

The Maasai of East Africa have been found to have low serum concentrations of cholesterol and a low incidence of cardiovascular disease in spite of apparently very high milk intakes. On that basis it has been frequently suggested that milk contains a "hypocholesterolaemic factor". The hypocholesterolaemia of the Maasai had also been attributed to a genetic adaptation. We feel that the milk intakes reported for the Maasai are excessively high and that the low incidence of cardiovascular diseases and low levels of serum cholesterol may be adequately explained by their variable and generally low energy intakes.