Abnormalities of Calcium Metabolism in Essential Hypertension

Strazzullo, Pasquale; Nunziata, V.; Cirillo, Massimo; Giannattasio, R.; Ferrara, Liberato; Mattioli, Pier Luigi; Mancini, Mario

doi:10.1042/cs0650137

Cited by 207 publications

(87 citation statements)

References 21 publications

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“…[1][2][3][4][5][6][7] Consistently, studies in hypertensive rats have shown that hypercalciuria and ensuing hyperparathyroidism lead to reduced growth and detectable decrease in total bonemineral content later in life. 8,9) Recently, it was also shown that higher blood pressure in elderly white women is statistically associated with increased bone loss at the femoral neck, which may contribute to bone fracture.…”

mentioning

confidence: 86%

Effects of Various Antihypertensive Drugs on the Function of Osteoblast.

Nishiya

Sugimoto

2001

Biological & Pharmaceutical Bulletin

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Several studies have suggested that high blood pressure is associated with abnormalities in calcium metabolism, leading to increased calcium loss, secondary activation of the parathyroid gland, and increased removal of calcium from bone. [1][2][3][4][5][6][7] Consistently, studies in hypertensive rats have shown that hypercalciuria and ensuing hyperparathyroidism lead to reduced growth and detectable decrease in total bonemineral content later in life. 8,9) Recently, it was also shown that higher blood pressure in elderly white women is statistically associated with increased bone loss at the femoral neck, which may contribute to bone fracture. 10) Drugs used as primary choice for the treatment of hypertension include calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor type1 (AT1) antagonists, diuretics, b-blockers, and a-blockers. 11) The first three drugs are especially widely used in Japan. The mechanism by which each drug lowers blood pressure differs. Calcium channel blockers primarily inhibit calcium influx through the L-type voltage-dependent calcium channel at the level of vascular smooth muscle, thereby disrupting the excitation contraction process. 12,13) Both ACE inhibitors and AT1 antagonists interfere with the renin-angiotensin system (RAS). The former inactivates the conversion of angiotensin I into angiotensin II (Ang II), which is a vasoconstrictive peptide, while the latter blocks the binding of Ang II to its receptor. 14,15) Osteoblasts are derived from mesenchymal stem cells and play a pivotal role in bone formation. During differentiation, they first express type I collagen, then alkaline phosphatase (ALP), and other bone matrix proteins and finally form mineralized bone. Osteoblasts express voltage-dependent calcium channels. 16) Various bone regulatory factors such as vitamin D 3 , [17][18][19] parathyroid hormone, 17,20,21) and prostaglandin E 2 17,22) cause a rise in intracellular calcium concentration ([Ca 2ϩ ] i ), at least part of which is decreased by dihydropyridine-type calcium channel blockers. These factors also promote or inhibit osteoblast differentiation. [23][24][25][26] Thus, it is suggested that signaling through the L-type calcium channel may be important for osteoblast functions. However, the fact that these factors give rise to multiple signals independent of calcium influx (i.e., transcription of specific genes, 27) cAMP production, 20,28) release of calcium ion from intracellular store 17) ) obscures the role of L-type calcium channel. Recently, Kosaka and Uchii found that a calcium channel blocker benidipine, but not amlodipine or nifedipine, increased ALP activity of osteoblastic cells isolated from neonatal mouse calvaria. 29) We further investigated the effects of benidipine on osteoblastic functions using osteoblastic cell line MC3T3-E1, 30) which is widely used in studies on various aspects of osteoblast differentiation since it expresses osteoblast markers and forms a mineralized extracellular matrix. 31,32) There we ...

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confidence: 86%

Effects of Various Antihypertensive Drugs on the Function of Osteoblast.

Nishiya

Sugimoto

2001

Biological & Pharmaceutical Bulletin

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“…Apparently, the kidney in the offspring of hypertensive parents is less sensitive to PTH. Alternatively, the higher level of plasma intact PTH in the offspring of hypertensive parents may be viewed as secondary to a relative calcium deficiency, which could arise from a renal calcium leak as proposed by McCarron et al 13 and Strazullo et al 18 In the context of a decreased renal sensitivity to intact PTH , the level of 1,25-dihydroxyvitamin D 3 , activated by PTH in the kidney, can be regarded as inappropriately low in the offspring of hypertensive parents. More research on calcium metabolism in these groups of offspring is needed.…”

Section: Discussionmentioning

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

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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

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“…1, the BMD was significantly lower in WHT compared with WNT (0.595 ±0.019 g/cm 2 vs. 0.666±0.024 g/ cm 2 , p< 0.05). The T-score and Z-score were both significantly lower in WHT compared with WNT (p< 0.05, each).…”

Section: Bmdmentioning

confidence: 99%