Evidence against the role of calcium deficiency in genetic hypertension.

Lau, Kai; Gafter, Uzi; Rydell, D; Eby, B.; Pesigan, M; Tropp, I; Garno, J; Zikos, D.

doi:10.1161/01.hyp.8.1.45

Cited by 18 publications

(3 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The increase in BP in a high PTH state, such as that seen following a low Ca diet, and the decrease in BP following a high Ca diet agree with this hypothesis. The reduction in PTH, coupled with hypocalcemia, would produce the opposite effect, 27 which is what we found in our study. At 4 weeks of age rats underwent sham operation or thyroparathyroidectomy (TPTX) and were treated with thyroxine (T 4 ; 10 jig/kg/day) in drinking water.…”

Section: Figure 2 Depressor Response To Parathyroid Hormone (Pth-[1 supporting

confidence: 83%

Hypotensive action of parathyroid hormone in hypoparathyroid and hyperparathyroid rats.

Baksi

1988

Hypertension

View full text Add to dashboard Cite

SUMMARY Experimental and clinical data suggest an association between chronic hyperparathyroidism and hypertension, but acute infusion of parathyroid hormone causes vasodilation and hypotension. These observations imply that chronic and acute parathyroid states affect blood pressure through different mechanism(s), either by modification of vascular receptors or by an ionophoretic effect of parathyroid hormone. The effect of parathyroid status induced by dietary calcium manipulations or by surgical ablation of the parathyroid gland on the hypotensive response of parathyroid hormone infusion was studied in rats. At 4 weeks of age 24 male rats were divided into four equal groups. Three groups were sham-operated, and one group was thyroparathyroidectomized. Only the thyroparathyroidectomized group was treated with thyroxine, 10 /xg/kg/day. The control and thyroparathyroidectomized groups were raised on a 1.4% calcium diet; the other two groups were raised on 0.005% and 2.8% calcium diets. After 8 weeks on the diets, parathyroid hormone was infused through a venous cannula at 5 and 10 ng/kg doses and blood pressure was measured through arterial cannulas. The results indicate that hyperparathyroidism and hypocalcemia induced by the low calcium diet attenuated the hypotensive response to parathyroid hormone compared with responses in rats raised on a 1.4% calcium diet. In hypoparathyroid rats (2.8% Ca diet) with hypercalcemia, the hypotensive response was also reduced. However, in hypoparathyroid (thyroparathyroidectomized) rats with hypocalcemia, the hypotensive response was enhanced. The data suggest that chronic parathyroid status, as well as hypercalcemia, alters the hypotensive response to parathyroid hormone infusion, presumably by altering the vascular parathyroid hormone receptors or by some other mechanism. (Hypertension 11: 509-513, 1988 Yet hyperparathyroidism is often associated with increased BP in humans 6 " 8 and rats. 9 "" The cellular basis for chronic PTH action on BP regulation is unknown.12 " 14 PTH may influence the sympathetic nervous system and vasoactive hormones either directly or indirectly through changes in plasma ionic cal- cium. 15 ' l6 The accentuation of hypertension by hyperparathyroidism or long-term PTH administration, blunted vascular reactivity in the hypercalcemic state, 17 and hypocalcemia after parathyroidectomy are all consistent with the hypothesis that PTH exerts an ionophoretic and, therefore, a permissive effect on the vasoconstrictive and hypertensive action of extracellular fluid calcium.18 " 20 The purpose of the present study was to investigate the effect of long-term modifications of PTH status by surgical and dietary means in normotensive Sprague-Dawley rats on the hypotensive response to acute PTH administration. In addition, the plasma and bone calcemic parameters were measured to document the alterations in systemic calcium metabolism and PTH status.

show abstract

Section: Figure 2 Depressor Response To Parathyroid Hormone (Pth-[1 supporting

confidence: 83%

Hypotensive action of parathyroid hormone in hypoparathyroid and hyperparathyroid rats.

Baksi

1988

Hypertension

View full text Add to dashboard Cite

show abstract

“…The possibility exists that calcium-deficient diets elevate the arterial blood pressure through some mechanisms in which the increase in PTH that they cause may be involved. Indeed, parathyroidectomy has been shown to lower the blood pressure in animal models of hypertension [49, 50, 51]and also in experimental hypertension caused by dietary calcium deficiency [52, 53]. Moreover, the acute hypotensive effect of PTH(1–34) was not observed in the hypertension of calcium-deficient rats [54].…”

Section: Introductionmentioning

confidence: 99%

Parathyroid Hormone and Calcitriol in Hypertension Caused by Dietary Calcium Deficiency in Rats

López‐Miranda

Civantos²,

Blasco³

et al. 1998

J Vasc Res

View full text Add to dashboard Cite

Hypertension caused by calcium deficiency in the diet has been linked with an increase in parathyroid hormone (PTH) and calcitriol levels. We evaluated arterial blood pressure (ABP), PTH, and calcitriol in normotensive Sprague-Dawley rats (SDR) and in spontaneously hypertensive rats (SHR) fed from weaning on a control diet with a normal calcium content (1%) or a low-calcium diet (0.1%). The calcemia was also measured in the rats by colorimetric methods. The low-calcium diet decreased the calcemia in both strains and brought about an increase in the ABP which was significant in adult SDR and particularly noticeable during the early hypertensive phase in SHR. The rats fed on this diet had higher hormonal plasma levels when compared with the corresponding values in rats fed on the control diet. In particular, the SDR fed on the low-calcium diet showed much higher PTH (122.6 ± 31.0 pg/ml, p ≤ 0.05) and calcitriol (458.0 ± 13.1 pg/ml, p ≤ 0.01) values than the SDR fed on the control diet (PTH 31.7 ± 2.80 pg/ml; calcitriol 292.1 ± 17.5 pg/ml). These endocrine alterations could justify the increase in ABP caused by dietary calcium deficiency in normotensive rats. Nevertheless, the results of this study indicate that the modifications of the ABP caused by the low-calcium diet in SHR could not be correlated with significant increases in these hormones.

show abstract

“…22 In another study, however, genetically hypertensive rats fed a calcium-deficient diet did not show an increased blood pressure rise compared with rats fed a normal diet. 23 Parathyroidectomy in young genetically hypertensive rats, while keeping a normal serum calcium level, delayed the rise in systolic blood pressure for 42 weeks. 24 In humans, information on the part played by changes in calcium metabolism in the development of high blood pressure may be gained from comparison of parameters of calcium homeostasis between offspring of hypertensive parents and offspring of normotensive parents.…”

mentioning

confidence: 99%

Alterations in calcium metabolism in young people at risk for primary hypertension. The Dutch Hypertension and Offspring Study.

Hooft¹,

Grobbee²,

Frölich³

et al. 1993

Hypertension

View full text Add to dashboard Cite

Several disturbances in calcium metabolism have been reported in primary hypertensive subjects. It is, however, not clear whether these alterations predate the development of hypertension or occur as a consequence of high blood pressure. We studied indexes of calcium metabolism in three groups of normotensive children with different familial predispositions for hypertension, based on parental blood pressure levels, with two, one, or no hypertensive parents. Plasma intact parathyroid hormone pressure regulation. In some hypertensive subjects, urinary excretion of magnesium may be decreased and show an inverse relation with blood pressure.16 Serum phosphate concentration is reported to be lower in hypertension and negatively related to blood pressure. 17Besides changes in serum and urinary electrolytes, raised circulating parathyroid hormone (PTH) levels have been demonstrated in hypertensive individuals. 1318 We reported previously that plasma intact PTH is raised in young hypertensive subjects compared with normotensive subjects of similar age, suggesting that alterations in calcium metabolism may be important in the early phase of primary hypertension. 1920Discussion remains as to whether changes in calcium metabolism are causally related to the development of high blood pressure. 21 In genetically hypertensive rats, calcium supplementation during the developmental phase of hypertension diminished the blood pressure increase. 22 In another study, however, genetically hypertensive rats fed a calcium-deficient diet did not show an increased blood pressure rise compared with rats fed a normal diet. 23 Parathyroidectomy in young genetically hypertensive rats, while keeping a normal serum calcium level, delayed the rise in systolic blood pressure for 42 weeks. 24 In humans, information on the part played by changes in calcium metabolism in the development of high blood pressure may be gained from comparison of

show abstract

Evidence against the role of calcium deficiency in genetic hypertension.

Cited by 18 publications

References 22 publications

Hypotensive action of parathyroid hormone in hypoparathyroid and hyperparathyroid rats.

Hypotensive action of parathyroid hormone in hypoparathyroid and hyperparathyroid rats.

Parathyroid Hormone and Calcitriol in Hypertension Caused by Dietary Calcium Deficiency in Rats

Alterations in calcium metabolism in young people at risk for primary hypertension. The Dutch Hypertension and Offspring Study.

Contact Info

Product

Resources

About