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Biomedical subjects

A Goulding

Publications and source records attributed to A Goulding.

At least 73 records · Page 4Linked to original sources
PubMed1988

Effects of dietary NaCl supplementation on bone synthesis of hydroxyproline, urinary hydroxyproline excretion and bone 45Ca uptake in the rat.

High sodium chloride intakes are regarded as a risk factor for osteoporosis because they increase the obligatory urinary calcium loss and stimulate parathyroid activity. Sodium chloride loads induce osteopenia in the rat. The effect could be due to a decrease in bone formation or a rise in bone resorption. Two experiments were undertaken to study the effects of dietary NaCl supplementation on 3H-hydroxyproline synthesis and 45Ca uptake in femoral bone. Salt-treated rats excreted 1.7 times more total urinary hydroxyproline (P less than 0.001) and 2.1 times more recently labelled 3H-hydroxyproline than controls (P less than 0.02) but they did not accumulate less 3H-hydroxyproline or less 45Ca in their bones than controls. These results indicate that salt-mediated osteopenia is due to an increase in bone resorption, rather than to a decrease in bone formation.

Animals↗
PubMed1988

Effects of chronic prednisolone treatment on bone resorption and bone composition in intact and ovariectomized rats and in ovariectomized rats receiving beta-estradiol.

To examine the interactions between estrogen deficiency and glucocorticoid excess on bone metabolism the osteopenic effects of a standard dose of prednisolone (2 mg/kg BW.day) were studied in sham-ovariectomized (Sham-OVX), ovariectomized (OVX), and OVX rats given replacement beta-estradiol (OVX + E2). For 12 weeks six groups of female albino rats aged 4 months which had their skeletons labeled with 45Ca were fed matched amounts of low-calcium (0.1% Ca) hydroxyproline-free diet. The six treatment groups were: group 1, Sham-OVX; group 2, Sham-OVX + prednisolone; group 3, OVX; group 4, OVX + prednisolone; group 5, OVX + E2; group 6, OVX + E2 + prednisolone. Bone resorption was estimated by studying the urinary excretion of hydroxyproline and 45Ca. Parathyroid function was assessed indirectly from urinary cAMP excretion. Treatments did not influence parathyroid activity or serum levels of calcium or 1,25-dihydroxyvitamin D. However, ovariectomy increased bone resorption and induced osteopenia whereas prednisolone decreased bone resorption and formation and caused osteopenia. Ovariectomy increased the rate of bone resorption in prednisolone-treated rats; prednisolone lowered the rates of bone resorption and formation in OVX rats. The osteopenic effects of prednisolone and ovariectomy were additive and independent. E2 protected bone from the osteopenic effects of ovariectomy but did not affect bone loss induced by prednisolone. These results suggest prophylactic estrogen should help to avoid bone loss from estrogen deficiency in patients requiring chronic high dose glucocorticoid treatment.

Animals↗
PubMed1986

Effects of NaCl on calcium balance, parathyroid function and hydroxyproline excretion in prednisolone-treated rats consuming low calcium diet.

The short-term effects of dietary sodium chloride supplementation on calcium balance were examined in an animal model of corticosteroid-mediated osteoporosis. Changes in calcium and phosphate balance, parathyroid function and bone resorption elicited by salt supplements alone (8 g/100 g diet), prednisolone alone (2.2 mg/kg body wt per day) and both salt and prednisolone in combination were measured in rats consuming a low calcium diet (0.1% calcium) for 10 d. Parathyroid function was monitored by measuring urinary cyclic AMP excretion. Bone resorption was monitored by measuring urinary hydroxyproline excretion. Salt alone raised urinary calcium, cyclic AMP and hydroxyproline; prednisolone alone depressed net calcium absorption and urinary hydroxyproline but had no effect on urinary calcium. Salt and prednisolone each depressed calcium retention independently and together produced an additive adverse effect on calcium balance. Thus high dietary salt intakes augment urinary calcium loss, raise parathyroid activity, increase bone resorption and adversely affect calcium balance in prednisolone-treated growing rats with a restricted dietary calcium intake. These findings support the view that high salt intakes may exaggerate bone loss during chronic glucocorticoid therapy. Because people also develop osteoporosis during glucocorticoid therapy and respond to dietary salt supplements by increasing urinary calcium excretion and parathyroid hormone, high salt intakes may accelerate bone loss in patients receiving chronic glucocorticoid therapy. The beneficial effects of dietary salt restriction on the conservation of bone mass warrant investigation in these patients.

Absorption↗
PubMed1986

Effects of dietary sodium chloride loading on parathyroid function, 1,25-dihydroxyvitamin D, calcium balance, and bone metabolism in female rats during chronic prednisolone administration.

The effects of dietary sodium chloride supplements (8 g/100 g diet) on parathyroid function, serum 1,25-dihydroxyvitamin D [1,25-(OH)2D], calcium balance, bone metabolism, and bone composition were studied in rats treated with prednisolone (2 mg/kg w X day) for 12 weeks. Animals on a low calcium diet (0.1% Ca) received the following treatments: group 1, control; group 2, NaCl; group 3, prednisolone; group 4, NaCl plus prednisolone. Parathyroid function was assessed indirectly from urinary cAMP excretion: bone resorption was estimated by studying urinary hydroxyproline excretion and mobilization of 45Ca from bone. Dietary salt loading increased the urinary excretion of calcium, 45Ca, cAMP, and hydroxyproline and raised serum 1,25-(OH)2D and net calcium absorption, but lowered calcium retention, femoral calcium, and total body calcium. Prednisolone slowed body growth and lowered net calcium absorption, calcium retention, femoral calcium, and total body calcium. Urinary calcium excretion was higher in rats receiving salt and prednisolone in combination than in animals taking salt without prednisolone, but other responses to salt and prednisolone were independent. Thus, salt and prednisolone each elicit osteopenia, and salt causes bone loss in rats receiving prednisolone. The osteopenic effect of salt is attributed to primary augmentation of urinary calcium excretion and secondary increases in PTH-medicated bone resorption. Although salt-treated rats have higher blood levels of 1,25-(OH)2D, bone loss occurs because alimentary calcium absorption is not elevated sufficiently to offset urinary calcium losses. Prednisolone lowers bone formation and net calcium absorption without lowering serum 1,25-(OH)2D values. The parathyroid-vitamin D axis remains intact in prednisolone-treated rats, as they show increases in PTH and 1,25-(OH)2D after salt treatment.

Animals↗
PubMed1985

Renal calcium conservation in recurrent stone-formers with idiopathic hypercalciuria.

Urinary excretions of calcium and cyclic AMP were studied in male recurrent stone-formers after an overnight fast and following an oral calcium load. The results from eight patients with established hypercalciuria (greater than 7.5 mmol Ca/24 h) were compared with those from eight age matched normocalciuric stone-formers. The urinary calcium/creatinine ratio was higher in the hypercalciuric group both when fasting and calcium loaded whilst their urinary cyclic AMP was lower in both 24-h and calcium-loaded collections. Five of the eight hypercalciuric patients exhibited an increased urinary calcium/creatinine ratio whilst fasting. These findings support the view that renal calcium wasting, in association with suppression of parathyroid activity, is common among men with idiopathic hypercalciuria. Dietary calcium restriction may lead to bone loss in patients with obligatory renal calcium wasting and enteric adsorption is rarely applicable to the treatment of stone disease. Therefore, the demonstration of a high fasting urinary calcium/creatinine ratio is a strong indication for therapeutic agents which act to suppress renal calcium loss to treat hypercalciuria.

Adult↗
PubMed1985

Potassium bicarbonate supplementation blocks the hypocalciuric response to hydrochlorothiazide in rats.

Bicarbonate salts and thiazide diuretics each lower urinary calcium excretion. This study was undertaken to compare the effects of administering oral sodium or potassium bicarbonate supplements (4.5 mmol./day of each salt) each with or without hydrochlorothiazide (10 mg./kg. body weight/day) on urinary calcium excretion in rats. Urinary calcium decreased (p less than 0.01) by about 50 per cent after sodium bicarbonate supplementation and potassium bicarbonate supplementation. The hypocalciuric response to each bicarbonate salt was similar. However, although hydrochlorothiazide depressed urinary calcium in rats consuming sodium bicarbonate, rats receiving equimolar supplements of potassium bicarbonate did not lower urinary calcium when given hydrochlorothiazide, despite evidence of the expected thiazide-mediated diuresis. It is concluded that in the rat potassium bicarbonate loading blocks the ability of hydrochlorothiazide to lower urinary calcium excretion.

Animals↗
PubMed1985

Hydrochlorothiazide lowers urinary hydroxyproline in parathyroidectomized rats.

This study was undertaken to examine the effects of hydrochlorothiazide treatment on urinary hydroxyproline excretion in parathyroidectomized rats. Urinary hydroxyproline (mumol/24 hr) fell significantly in thiazide-treated rats compared with control animals (5.66 +/- 0.37 versus 7.30 +/- 0.6, P less than 0.05, means +/- SEM). This fall in hydroxyproline excretion occurred without a decrease in glomerular filtration rate. It is concluded that the ability of thiazide diuretics to reduce urinary hydroxyproline excretion is not dependent upon suppression of parathyroid hormone-mediated bone turnover.

Animals↗
PubMed1984

Effects of sodium bicarbonate and hydrochlorothiazide on the hypercalciuric action of 1,25(OH)2D3 in the rat.

The hypercalcaemic and hypercalciuric effects of high doses of 1,25(OH)2D3 (50 nanograms per day for 7 days) were studied in rats taking a standard basal diet, with or without supplements of NaHCO3 (4.5 mmoles per day), hydrochlorothiazide (10 milligrams per kilogram body weight per day), or both NaHCO3 and hydrochlorothiazide. 1,25(OH)2D3 elevated plasma and urinary calcium values. The degree of hypercalcaemia elicited was similar in all groups but hypercalciuria was less in groups given NaHCO3 or hydrochlorothiazide. It is suggested that NaHCO3, like thiazide diuretics, might be useful in limiting hypercalciuria in stone-formers with elevated plasma levels of 1,25(OH)2D3.

Animals↗
PubMed1984

Effects of sodium bicarbonate and 1,25-dihydroxy-cholecalciferol on calcium and phosphorus balances in the rat.

Metabolic balance studies were undertaken to determine whether sodium bicarbonate (NaHCO3) supplements (4.5 mmol/day) altered 7-day cumulative calcium (Ca) phosphorus (P) balances in growing rats consuming either a basal diet providing 0.6% Ca and 0.3% P, or this diet plus 1,25-dihydroxycholecalciferol [40 ng 1,25(OH)2D3/day]. Feeding bicarbonate lowered urinary Ca but raised fecal Ca so that Ca balance became less positive. However, 1,25(OH)2D3 increased net absorption of Ca and P to the same degree when given to control rats and rats consuming bicarbonate. Nevertheless, bicarbonate-fed rats had lower net Ca absorption than controls, even when treated with high doses of 1,25(OH)2D3. Changes in net Ca absorption induced by bicarbonate may occur at a point in the gut distal to the duodenum since duodenal 45Ca absorption was decreased by bicarbonate feeding. The present results show that bicarbonate consumption depressed net Ca absorption in the rat. The effect appears to be independent of changes in 1,25(OH)2D3 metabolism because it is manifest in animals receiving high doses of 1,25(OH)2D3, which stimulate alimentary Ca absorption maximally, and because bicarbonate-fed rats are able to respond normally to exogenous 1,25(OH)2D3 by increasing their net absorption of Ca and P. In view of this demonstration that NaHCO3 supplements elevate fecal Ca loss in the rat, it is suggested that studies should be undertaken to determine whether bicarbonate exerts similar adverse effects on Ca balance in humans.

Absorption↗
PubMed1984

Thyroparathyroidectomy exaggerates calciuric action of ammonium chloride in rats.

The effects of chronic ammonium chloride (NH4Cl) administration on urinary calcium, urinary hydroxyproline, and calcium and phosphate balances were studied in intact and thyroparathyroidectomized (TPTX) rats. NH4Cl (2 g/100 g diet) was administered for 16 days to growing rats consuming a low calcium (0.1% Ca) diet. NH4Cl increased urinary calcium and hydroxyproline. NH4Cl caused greater urinary calcium loss in TPTX than in intact rats, but hydroxyproline excretion in these groups was similar. Compensatory increases in net alimentary absorption of calcium and phosphate occurred in intact but not in TPTX rats. Urinary cAMP was depressed by thyroparathyroidectomy but was unaffected by NH4Cl. It is concluded that NH4Cl depresses renal tubular reabsorption of calcium and increases bone resorption in the presence and absence of the thyroid and parathyroid glands. However, our results suggest that parathyroid hormone plays an important calcium-sparing role, while calcitonin may act to limit the rate of bone resorption, in intact rats during chronic administration of NH4Cl.

Ammonium Chloride↗
PubMed1984

Effects of oral loads of sodium chloride on bone composition in growing rats consuming ample dietary calcium.

High dietary intakes of sodium chloride and protein are known to promote urinary calcium excretion. The aim of this work was to study the effects of bone composition, calcium balance and phosphorus balance, of administering oral salt supplements (8 g/100 g diet) to growing rats consuming moderate or high dietary levels of protein (25 and 60% casein) with ample calcium (0.6% Ca) and adequate vitamin D. Animals given salt supplements excreted more calcium and phosphate in their urine and had less calcium and phosphate in their bones than controls which did not receive supplementary salt. However, salt-loaded rats did not increase their intestinal absorption of calcium to compensate for urinary losses of calcium. Calciuria was greater at the high, than at the moderate, protein intake. Salt supplements raised urinary cyclic AMP and urinary hydroxyproline in rats consuming 25% casein but not in those receiving 60% casein. It is concluded that high dietary intakes of sodium chloride depress the accumulation of mineral in bone; the effect is attributed to increased excretion of calcium and phosphate. These findings raise the possibility that a high salt intake may adversely affect bone mass in man.

Animals↗
PubMed1983

Dietary NaCl loads promote calciuria and bone loss in adult oophorectomized rats consuming a low calcium diet.

This study was undertaken to determine whether dietary supplements of NaCl would exaggerate osteopenia in oophorectomized (OOPX) rats consuming a low calcium (0.01% Ca) diet. Thirty 300 g OOPX rats with 45Ca-labeled bones were studied. Animals in group 1 were killed at the start of the experiment, whereas those in groups 2 and 3 were fed a low calcium diet for 2 months. Group 3 rats received NaCl (8 g/100 g diet). Salt increased the urinary excretion of sodium, calcium, phosphate, cyclic AMP, 45Ca and hydroxyproline but did not augment fecal excretion of calcium or 45Ca. Salt caused bone loss. The femora of NaCl-treated rats contained less 45Ca, less calcium, less phosphate and less mineral ash than those of rats killed at the start of the experiment. It is suggested that in OOPX rats consuming a low calcium diet, increased NaCl intake causes decreased renal tubular reabsorption of calcium and consequently lowered plasma Ca++. This results in stimulation of parathyroid hormone secretion and thus increased bone resorption. We conclude that NaCl supplements exacerbate osteopenia in adult OOPX rats consuming a low calcium diet. The effects of high dietary salt intakes on bone loss in postmenopausal women deserve further study.

Animals↗
PubMed1982

Smoking, the menopause and biochemical parameters of bone loss and bone turnover.

It has been suggested that cigarette smoking may contribute to the pathogenesis of osteoporosis. A retrospective study of data obtained in a health survey was conducted to study the effects of smoking on the age of onset of menopause and parameter of bone loss and one turnover in a population of women living in a rural town in new Zealand. Smokers underwent menopause earlier than nonsmokers. However, smoking did not effect bone loss or bone turnover after the menopause. Thus, if smoking increases the propensity to osteoporosis, the effect is more likely to be related to early onset of menopause than to increased intensity of postmenopausal bone loss.

Age Factors↗
PubMed1981

Fasting urinary sodium/creatinine in relation to calcium/creatinine and hydroxyproline/creatinine in a general population of women.

The relationships between urinary sodium excretion and bone loss and bone turnover were studied by looking at sodium/creatinine (Na/creat) values in relation to: (a) calcium/creatinine (Ca/creat); and (b) hydroxyproline/creatinine (HP/creat) values in fasting urines obtained from 574 women over 16 years of age participating in a health survey. Na/creat was positively correlated with Ca/creat (r=0.567, p less than 0.001) and with HP/creat (r=0.341, p less than 0.001). Both young and old women showed these relationships. However, postmenopausal women had higher Na/creat, Ca/creat and HP/creat values than premenopausal women. It seems that subjects with a high sodium excretion show a higher net bone loss and a higher bone turnover than subjects with low sodium excretion. The results suggest that salt intake should be considered when evaluating bone loss and bone turnover from fasting urinary Ca/creat and HP/creat measurements.

Adolescent↗
PubMed1979

Effects of diphosphonate and colchicine administration upon acid-base changes induced in rats by bilateral nephrectomy.

1. The effects of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) and colchicine on acid--base balance were examined in intact and nephrectomized rats. 2. Both drugs increased extracellular hydrogen ion concentrations and depressed extracellular bicarbonate concentrations in nephrectomized rats compared with controls but did not alter these parameters in intact animals. 3. Intracellular hydrogen ion concentrations in the skeletal muscle of nephrectomized rats given EHDP were higher than those of control animals. 4. It is postulated that colchicine and EHDP inhibit skeletal buffering of non-volatile acids produced endogenously in nephrectomized rats.

Acid-Base Equilibrium↗