Effect of High Calcium Diet on Magnesium, Catecholamines, and Blood Pressure of Stroke-Prone Spontaneously Hypertensive Rats

Luft, Friedrich C.; Ganten, Ursula; Meyer, Dieter; Steinberg, Harry R.; Gless, K.-H.; Unger, Th.; Ganten, D

doi:10.3181/00379727-187-42691

Cited by 9 publications

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“…A high calcium diet may influence blood pressure by affecting the sympathetic tone. Calcium supplementation has been found to attenuate stress-induced blood pressure responses (Hatton et al 1987) and to reduce plasma adrenaline levels both at rest and in response to cold stress in SHR (Luft et al 1988). However, we found no differences either in urinary excretion of catecholamines or adrenergic nerve density of the mesenteric artery between the four treatment groups.…”

Section: Discussionmentioning

confidence: 99%

“…A high calcium diet also prevents the development of mineralocorticoid hypertension in rats (DiPette et al 1989). However, contradictory results have been published (Capuccio et al 1987, Luft et al 1988.…”

mentioning

confidence: 99%

“…(1989) have suggested that dietary calcium provides a membrane stabilizing effect in vascular smooth muscle, resulting in attenuated smooth muscle reactivity. Calcium supplementation has also been found to enhance natriuresis (Ayachi 1979), and to decrease sympathetic nerve activity in spontaneously hypertensive rats (SHR) (Luft et al 1988). McCarron et al (1985) have suggested that increasing dietary sodium amplifies the hypotensive effect of calcium, and Resnick et a.1.…”

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Effects of calcium supplementation and deoxycorticosterone on plasma atrial natriuretic peptide and electrolyte excretion in spontaneously hypertensive rats

Pörsti¹,

Wuorela²,

Arvola³

et al. 1991

Acta Physiologica Scandinavica

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The effects of calcium and the mineralocorticoid deoxycorticosterone (DOC) on blood pressure were studied in four groups of spontaneously hypertensive rats (SHR): (1) control; (2) calcium; (3) deoxycorticosterone and; (4) deoxycorticosterone + calcium. Calcium was given as 1.5% calcium chloride in drinking fluid and deoxycorticosterone by weekly subcutaneous injections (25 mg kg-1). During the nine weeks of treatment the increase in systolic blood pressure was enhanced in the deoxycorticosterone and attenuated in the calcium group, whereas the deoxycorticosterone + calcium group did not deviate from control. Total plasma calcium was elevated in the calcium group. Plasma concentrations of sodium and atrial natriuretic peptide (ANP) were increased by deoxycorticosterone while neither of the calcium-treated groups differed from control in these respects. Urinary excretions of calcium and sodium were increased in both groups receiving calcium, and also the deoxycorticosterone group excreted more calcium into urine than the control. Adrenergic nerve density in a section of the mesenteric artery and the urinary excretion of noradrenaline and adrenaline were similar in all study groups. The results indicate that calcium supplementation can attenuate the development of hypertension and prevent the deoxycorticosterone-induced blood pressure rise in SHR, possibly by influencing sodium metabolism as seen in increased natriuresis, and by preventing the actions of deoxycorticosterone on sodium balance.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Effects of calcium supplementation and deoxycorticosterone on plasma atrial natriuretic peptide and electrolyte excretion in spontaneously hypertensive rats

Pörsti¹,

Wuorela²,

Arvola³

et al. 1991

Acta Physiologica Scandinavica

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“…Increased dietary calcium reduces circulating hypertensive factor, whereas restricted calcium increases it. 167 Calcitriol. As mentioned previously, low calcium diets provoke an increase in the synthesis and release of 1,25(OH) 2 2 vitamin D 3 in SHR produced only a transient elevation in blood pressure after 5 weeks of treatment, suggesting a modest effect of the hormone on blood pressure.…”

Section: Calmodulinmentioning

confidence: 99%

“…Restricted dietary calcium has also been reported to alter peripheral catecholamine levels. Baksi and Hughes 283 and Hagihara et al 284 reported altered adrenal catecholamine levels with reduced calcium diets, and Luft et al 167 observed reduced epinephrine levels and epinephrine responses to stress in stroke-prone SHR on high calcium diets. Scrogin et al 188 also observed diminished circulating epinephrine in calcium-supplemented SHR.…”

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Dietary calcium and blood pressure in experimental models of hypertension. A review.

1994

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More than 80 studies have reported lowered blood pressure after dietary calcium enrichment in experimental models of hypertension. The evidence presented here suggests that dietary calcium may act concurrently through a number of physiological mechanisms to influence blood pressure. The importance of any given mechanism may vary depending on the experimental model under consideration. Supplemental dietary calcium is associated with reduced membrane permeability, increased Ca(2+)-ATPase and Na,K-ATPase, and reduced intracellular calcium. These results suggest that supplemental calcium may limit calcium influx into the cell and improve the ability of the VSMC to extrude calcium. This could be a direct effect of calcium on the VSMC or an indirect effect mediated hormonally. The calcium-regulating hormones have all been found to have vasoactive properties and therefore may influence blood pressure. Furthermore, CGRP and the proposed parathyroid hypertensive factor are both vasoactive substances that are responsive to dietary calcium. Therefore, diet-induced variations in calcium-regulating hormones may influence blood pressure. Modulation of the sympathetic nervous system is another important way that dietary calcium can influence blood pressure. There is evidence of altered norepinephrine levels in the hypothalamus as a consequence of manipulations of dietary calcium as well as changes in central sympathetic nervous system outflow. Dietary calcium has also been shown to specifically modify alpha 1-adrenergic receptor activity in the periphery. In some experimental models of hypertension, dietary calcium may alter blood pressure by changing the metabolism of other electrolytes. For example, the ability of calcium to prevent sodium chloride-induced elevations in blood pressure may be attributed to natriuresis. However, natriuresis does not account for all of the interactive effects of calcium and sodium chloride on blood pressure. Sodium chloride-induced hypertension may be due in part to calcium wasting and subsequent elevation of calcium-regulating hormones. Chloride is an important mediator of this effect because it appears that sodium does not cause calcium wasting when it is not combined with chloride. More attention to the central nervous system effects of dietary calcium is needed. Not only can calcium itself influence neural function, but many of the calcium-regulating hormones appear to affect the central nervous system. The influence of calcium and calcium-regulating hormones on central nervous system activity may have important implications for blood pressure regulation and also may extend to other aspects of physiology and behavior.

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High‐Calcium Diet in Spontaneously Hypertensive Rats: Intervention with Calcium Antagonist Verapamil

Saelens

Zawada

Peterson

et al. 1993

The Journal of Clinical Pharma

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A number of studies have shown an antihypertensive effect for high-calcium diets, but others have found no effect or, even a prohypertensive effect. Because of these disparate results, studies were conducted in spontaneously hypertensive rats (SHR) fed either a normal calcium diet (1.0% calcium) or a high-calcium diet (4.0% calcium) with or without verapamil HCl (50 mg/kg body weight) from ages 5 to 12 weeks. Systolic blood pressure (SBP) and heart rate (HR) were measured by indirect tail cuff method. During the analysis of the electrolytes and vasoactive hormones monitored in this study, it was found that rats fed high-calcium diet had significantly elevated serum ionized and total calcium and calcium excretion. Systolic blood pressure for the verapamil-normal calcium diet (week 5, 148 +/- 4 mm Hg; week 7, 162 +/- 4 mm Hg) did not differ significantly from that of normal calcium diet (week 5, 152 +/- 2 mm Hg; week 7, 160 +/- 1 mm Hg). The high-calcium diet potentiated the development of hypertension, i.e., SBP was (157 +/- 2 mm Hg) on the 5th week and (174 +/- 4 mm Hg) on the 7th week. Conversely, verapamil high-calcium diet prevented the development of hypertension (week 5, SBP was 139 +/- 4 mm Hg; week 7, SBP was 146 +/- 3 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of High Calcium Diet on Magnesium, Catecholamines, and Blood Pressure of Stroke-Prone Spontaneously Hypertensive Rats

Cited by 9 publications

References 0 publications

Effects of calcium supplementation and deoxycorticosterone on plasma atrial natriuretic peptide and electrolyte excretion in spontaneously hypertensive rats

Effects of calcium supplementation and deoxycorticosterone on plasma atrial natriuretic peptide and electrolyte excretion in spontaneously hypertensive rats

Dietary calcium and blood pressure in experimental models of hypertension. A review.

High‐Calcium Diet in Spontaneously Hypertensive Rats: Intervention with Calcium Antagonist Verapamil

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