Effect of dietary calcium intake and protein source on calcium utilization and bone biomechanics in the spontaneously hypertensive rat

1992 ◽  
Vol 3 (9) ◽  
pp. 452-460 ◽  
Author(s):  
Y Yuan
Keyword(s):  
Calcium Intake ◽  
Spontaneously Hypertensive Rat ◽  
Dietary Calcium ◽  
Protein Source ◽  
Bone Biomechanics ◽  
Dietary Calcium Intake ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Calcium Utilization

Dietary calcium, defective cellular Ca2+ handling, and arterial pressure control

1994 ◽  
Vol 72 (8) ◽  
pp. 937-944 ◽  
Author(s):  
David A. McCarron ◽  
Daniel Hatton ◽  
Jean-Baptiste Roullet ◽  
Chantal Roullet
Keyword(s):  
Blood Pressure ◽  
Clinical Trials ◽  
Calcium Intake ◽  
Inverse Relationship ◽  
Spontaneously Hypertensive Rat ◽  
Calcium Supplementation ◽  
Dietary Calcium ◽  
Calcium Handling ◽  
Dietary Calcium Intake ◽  
Experimental Hypertension

The association between dietary calcium intake, calcium metabolism, and blood pressure form the basis of this review. Epidemiologic data consistently show an inverse relationship between dietary calcium and blood pressure. Clinical trials of calcium supplementation have not been as consistent in outcome. Approximately two-thirds of the supplementation studies have found a beneficial effect of calcium on blood pressure. The lack of consistency in outcome from the clinical trials relative to the epidemiological literature may be related to calcium intake. The epidemiological literature indicates an inverse relationship between calcium intake and blood pressure, with those individuals with the lowest calcium intake (< 700 mg/day) having the highest blood pressure. Clinical studies utilizing patients with high baseline calcium levels (> 700 mg/day) may not see an effect of calcium supplementation on blood pressure because of a ceiling effect. Supplemental calcium appears to correct a defect in calcium handling characterized by a renal calcium leak, increased circulating parathroid hormone, and increased intracellular calcium levels. In part, the deficit in cellular calcium homeostasis may be a consequence of abnormal calmodulin activity. Specifically, it appears that calmodulin activity is diminished in experimental hypertension and that increasing dietary calcium may improve calmodulin activity in the spontaneously hypertensive rat. The deficit in calmodulin activity has the potential to interfere with a number of cellular processes crucial to the regulation of cell function and maintenance of appropriate vascular tone. It is concluded that additional research should be directed toward understanding the ramifications of altered calmodulin activity in hypertension and the influence that dietary calcium can have on the activity of calmodulin.Key words: hypertension, dietary Ca2+, calmodulin, Ca2+ metabolism, calcium channel blockers.

Psychosocial stress, dietary calcium and hypertension in the spontaneously hypertensive rat

1987 ◽  
Vol 40 (4) ◽  
pp. 425-429 ◽  
Author(s):  
Paul E. Huie ◽  
Daniel C. Hatton ◽  
Martin S. Muntzel ◽  
Jill A. Metz ◽  
David A. McCarron
Keyword(s):  
Psychosocial Stress ◽  
Spontaneously Hypertensive Rat ◽  
Dietary Calcium ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

Mechanisms of the antihypertensive effects of dietary calcium and role of calcitonin gene related peptide in hypertension

1995 ◽  
Vol 73 (7) ◽  
pp. 981-985 ◽  
Author(s):  
Sunil J. Wimalawansa ◽  
Scott C. Supowit ◽  
Donald J. DiPette
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Calcium Supplementation ◽  
Dietary Calcium ◽  
Calcitonin Gene Related Peptide ◽  
Spontaneously Hypertensive ◽  
Oral Calcium ◽  
Related Peptide ◽  
Hypertensive Rat ◽  
Calcitonin Gene ◽  
Salt Hypertension

Alterations in calcium metabolism and calcium-regulating hormones have been described in essential hypertension. However, the mechanisms that mediate these responses are unknown. In previous studies, using the genetically spontaneously hypertensive rat and the mineralocorticoid-salt (DOC-salt) hypertensive rat model, we and others have observed that oral calcium supplementation attenuates the associated increase in peripheral vascular resistance and consequently lowers blood pressure (BP). When hypertensive patients (n = 8, diastolic BP 90–95 mmHg (1 mmHg = 133.3 Pa)) were given daily oral calcium supplementation (1.4 g elemental calcium), both systolic and diastolic BP were decreased (5–10 mmHg, p < 0.01). The only biochemical variables significantly changed were serum ionized calcium and intact parathyroid hormone (PTH, 1–84) (p < 0.05); furthermore, the levels of calcitonin gene related peptide (CGRP), measured by both radioimmunoassay and radioreceptor assay, showed a marked 75% increase (p < 0.001). The antihypertensive effects of Ca2+ and the increased levels of CGRP in the circulation returned to baseline levels immediately following cessation of calcium supplementation, suggesting that the effects of calcium on BP and CGRP are specific. On the basis of these observations we propose that the antihypertensive effect of dietary calcium supplementation, at least in part, is mediated through CGRP.Key words: calcium, calcitonin gene related peptide, human hypertension, mineralocorticoid-salt hypertension.

Higher Dietary Acidity is Associated with Lower Bone Mineral Density in Postmenopausal Iranian Women, Independent of Dietary Calcium Intake

2014 ◽  
Vol 84 (3-4) ◽  
pp. 0206-0217 ◽  
Author(s):  
Seyedeh-Elaheh Shariati-Bafghi ◽  
Elaheh Nosrat-Mirshekarlou ◽  
Mohsen Karamati ◽  
Bahram Rashidkhani
Keyword(s):  
Calcium Intake ◽  
Dietary Calcium ◽  
Dietary Calcium Intake ◽  
Dietary Intakes ◽  
Iranian Women ◽  
Acid Base Balance ◽  
Mineral Density ◽  
Acid Base ◽  
Base Balance ◽  
Dietary Acid

Findings of studies on the link between dietary acid-base balance and bone mass are relatively mixed. We examined the association between dietary acid-base balance and bone mineral density (BMD) in a sample of Iranian women, hypothesizing that a higher dietary acidity would be inversely associated with BMD, even when dietary calcium intake is adequate. In this cross-sectional study, lumbar spine and femoral neck BMDs of 151 postmenopausal women aged 50 - 85 years were measured using dual-energy x-ray absorptiometry. Dietary intakes were assessed using a validated food frequency questionnaire. Renal net acid excretion (RNAE), an estimate of acid-base balance, was then calculated indirectly from the diet using the formulae of Remer (based on dietary intakes of protein, phosphorus, potassium, and magnesium; RNAERemer) and Frassetto (based on dietary intakes of protein and potassium; RNAEFrassetto), and was energy adjusted by the residual method. After adjusting for potential confounders, multivariable adjusted means of the lumbar spine BMD of women in the highest tertiles of RNAERemer and RNAEFrassetto were significantly lower than those in the lowest tertiles (for RNAERemer: mean difference -0.084 g/cm2; P=0.007 and for RNAEFrassetto: mean difference - 0.088 g/cm2; P=0.004). Similar results were observed in a subgroup analysis of subjects with dietary calcium intake of >800 mg/day. In conclusion, a higher RNAE (i. e. more dietary acidity), which is associated with greater intake of acid-generating foods and lower intake of alkali-generating foods, may be involved in deteriorating the bone health of postmenopausal Iranian women, even in the context of adequate dietary calcium intake.

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