Alterations of dietary calcium intake as a therapeutic modality in essential hypertension

1986 ◽  
Vol 64 (6) ◽  
pp. 803-807 ◽  
Author(s):  
Lawrence M. Resnick
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Calcium Metabolism ◽  
Calcium Supplementation ◽  
Ionized Calcium ◽  
Therapeutic Modality ◽  
Dietary Calcium Intake ◽  
Vitamin D Metabolites ◽  
Dietary Salt ◽  
Hypertensive Disease

Alterations of calcium metabolism in hypertensive disease have been increasingly observed, although the specific manner in which these alterations contribute to the increased blood pressure remains unclear. We have studied calcium metabolism in essential hypertension and have adopted an approach based on analysis of renin system activity, which emphasizes the heterogeneity of human hypertensive disease. With this approach we have defined parallel deviations of plasma renin activity, circulating ionized calcium, and calcium-regulating hormones, which suggest a calcium deficiency in some hypertensives and, an excess of calcium in others. These deviations can be used to predict and may mediate the blood pressure sensitivity of hypertensives to dietary salt, and may also target those individuals most likely to benefit from oral calcium supplementation. Calcium itself has enhanced antihypertensive effects in low renin subjects, having lower ionized calcium and higher endogenous 1,25-dihydroxyvitamin D values, and in subjects on higher dietary salt intakes. Calcium may alter pressure, at least in part, by suppressing endogenous vitamin D metabolites and by stimulating calcitonin secretion. We hypothesize that calcium-regulating hormones participate in the physiology of the renin–angiotensin system and in the pathophysiology of human hypertension.

Changes in calcium metabolic indices during long-term treatment of patients with essential hypertension

1988 ◽  
Vol 75 (5) ◽  
pp. 543-549 ◽  
Author(s):  
Andreas Hvarfner ◽  
Reinhold Bergström ◽  
Hans Lithell ◽  
Claes Mörlin ◽  
Leif Wide ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Essential Hypertension ◽  
Parathyroid Hormone ◽  
Free Fatty Acids ◽  
Calcium Metabolism ◽  
Elevated Blood Pressure ◽  
Ionized Calcium ◽  
Elevated Blood ◽  
Metabolic Indices

1. Disturbances of calcium metabolism, mimicking mild, compensated secondary hyperparathyroidism, accompany essential hypertension, but it is not known whether these alterations are primary or only secondary to the elevated blood pressure. 2. Indices of systemic calcium metabolism were followed prospectively during 6 months' treatment with either propranolol, bendroflumethiazide or verapamil in 35 patients with essential hypertension. Multivariate statistical methods were employed to study the effects of blood pressure reduction upon the metabolic indices with adjustment for the effects of the different antihypertensive agents. 3. Propranolol treatment increased the plasma ionized calcium and serum phosphate concentrations, and reduced the serum levels of parathyroid hormone, free fatty acids and glycerol. Neither the total nor the total albumin-modified serum calcium concentration was significantly affected. Thus, presumably the decrease in free fatty acids reduced the calcium complex and the calcium binding to albumin, and consequently increased the plasma ionized calcium, thereby suppressing the secretion of parathyroid hormone. 4. Bendroflumethiazide caused a reduction of the fasting renal calcium excretion to half the pretreatment level, but produced no other significant changes in the various indices of calcium metabolism. 5. During verapamil treatment, the fasting renal excretion of calcium and magnesium increased, whereas the free fatty acids and glycerol concentrations in serum were reduced. These two changes presumably balanced each other, as the plasma ionized calcium and serum parathyroid hormone concentrations were not significantly altered. 6. There were no consistent relationships between the decrease in blood pressure and the changes in the metabolic indices, either in the total sample or within any subgroup. These findings indicate that disturbances of calcium metabolism in essential hypertension are primary to, and not induced by, the elevated blood pressure per se.

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.

scholarly journals Effects of dietary salt intake on nocturnal blood pressure fall in essential hypertension

2005 ◽  
Vol 18 (5) ◽  
pp. A216-A217 ◽  
Author(s):  
G VYSSOULIS ◽  
E KARPANOU ◽  
A TRIANTAFYLLOU ◽  
A DELIGEORGIS ◽  
K AZNAOURIDIS ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Salt Intake ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
Nocturnal Blood Pressure ◽  
Blood Pressure Fall ◽  
Pressure Fall

The Evaluation of Therapeutic Procedures used in the Management of Essential Hypertension

1962 ◽  
Vol 1 (03) ◽  
pp. 82-86
Author(s):  
A. Grollman
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Small Group ◽  
Experimental Evaluation ◽  
Surgical Correction ◽  
Hypertensive Disease ◽  
Common Disorder ◽  
Sources Of Error ◽  
Therapeutic Procedures ◽  
Therapeutic Measures

The nature of essential hypertension, its pathogenesis and the disturbances which it induces are reviewed as a basis for an evaluation of the procedures and drugs used in the treatment of this common disorder. The therapeutic measures now available aim at lowering the blood pressure which is only one manifestation of hypertensive disease but fail to counteract the fundamental disturbance responsible for the disorder except in the small group of patients amenable to surgical correction. The procedures used in the experimental evaluation of the blood-pressure-reducing effects of drugs and other measures are outlined and the sources of error in such evaluations are emphasized. The methods now available for the management of essential hypertensionare outlined and their inadequacies discussed.

Abnormalities of Calcium Metabolism in Essential Hypertension

1983 ◽  
Vol 65 (2) ◽  
pp. 137-141 ◽  
Author(s):  
P. Strazzullo ◽  
V. Nunziata ◽  
M. Cirillo ◽  
R. Giannattasio ◽  
L. A. Ferrara ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Parathyroid Hormone ◽  
Calcium Metabolism ◽  
Excretion Rate ◽  
Urinary Calcium ◽  
Calcium Handling ◽  
Ionized Calcium ◽  
Calcium Excretion ◽  
Hypertensive Patients ◽  
Excretion Rates

1. Calcium metabolism has been investigated in patients with essential hypertension and normal renal function to evaluate the renal calcium handling and the reported increase in renal calcium loss. 2. In 55 hypertensive and 55 sex- and age-matched healthy normotensive subjects creatinine clearance, serum total and ionized calcium, plasma parathyroid hormone and 24 h urinary excretion of calcium, sodium and cAMP were measured. In a subgroup of 20 hypertensive patients and 20 controls the fasting calcium excretion rate was also measured. 3. Both 24 h and fasting calcium excretion rates were higher in the hypertensive group; so also were plasma parathyroid hormone and urinary cAMP. Serum total and ionized calcium levels were not different in the two groups. 4. After intravenous calcium infusion (15 mg 3 h−1 kg−1) in seven hypertensive patients and controls, the hypertensive patients excreted more calcium at all serum calcium concentrations. 5. These results support the hypothesis of primary renal calcium leak in essential hypertension. Enhanced urinary calcium excretion rate may cause compensatory parathyroid overactivity.

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