Hydrochlorothiazide reduces loss of cortical bone in normal postmenopausal women: a randomized controlled trial

Reid, Ian R.; Ames, Ruth; Orr-Walker, Brandon; Clearwater, Judith; Horne, Anne; Evans, Margaret C.; Murray, M. A. F.; McNeil, Alan; Gamble, Greg

doi:10.1016/s0002-9343(00)00510-6

Cited by 166 publications

(122 citation statements)

References 45 publications

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“…This hypocalciuric effect provides therapeutic opportunities in for instance idiopathic hypercalciuria and nephrolithiasis. Furthermore, thiazides have been shown to increase bone mineral density and decrease fracture risk, spiking interest in the favorable long-term effects of these diuretics in counteracting osteoporosis (Reid et al 2000). The decreased Ca 2+ excretion during chronic thiazide administration has been explained by ECV contraction enhancing the paracellular Ca 2+ reabsorption in proximal tubules as well as a direct stimulation of active Ca 2+ reabsorption in the DCT (Costanzo et al 1978;Ellison 2000;Friedman 1998;Friedman and Bushinsky 1999;Loffing et al 2001;Nijenhuis et al 2003).…”

Section: Thiazide Diureticsmentioning

confidence: 99%

The epithelial calcium channels TRPV5 and TRPV6: regulation and implications for disease

Abel

Hoenderop

Bindels

2005

Naunyn-Schmiedeberg's Arch Pharmacol

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The epithelial Ca 2+ channels TRPV5 and TRPV6 represent a new family of Ca 2+ channels that belongs to the superfamily of transient receptor potential channels. TRPV5 and TRPV6 constitute the apical Ca 2+ entry mechanism in active Ca 2+ transport in kidney and intestine. The central role of TRPV5 and TRPV6 in active Ca 2+ (re)absorption makes it a prime target for regulation to maintain Ca 2+ balance. This review covers the hormonal regulation, interaction with accessory proteins and (patho)physiological implications of these epithelial Ca 2+ channels.

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Section: Thiazide Diureticsmentioning

confidence: 99%

The epithelial calcium channels TRPV5 and TRPV6: regulation and implications for disease

Abel

Hoenderop

Bindels

2005

Naunyn-Schmiedeberg's Arch Pharmacol

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“…[1][2][3][4][5] Several antihypertensive drugs, including thiazides, b-blockers and angiotensin-converting enzyme inhibitors, decreased the risk of bone fractures and increased bone mineral density (BMD) clinically. [6][7][8][9][10] However, meta-analysis of observational studies on the effects of antihypertensive drugs on fracture outcomes demonstrated no significant association between fractures and calcium channel blockers (CCBs). [11][12][13] CCBs are divided into several subtypes, and non-dihydropyridinetype CCBs, but not dihydropyridine-type CCBs, are reported to reduce the risk of bone fractures through the inhibition of hyperparathyroidism-induced calcium uptake into osteoblasts and an elevation of intracellular calcium in osteoclasts.…”

Section: Introductionmentioning

confidence: 99%

Cilnidipine, but not amlodipine, ameliorates osteoporosis in ovariectomized hypertensive rats through inhibition of the N-type calcium channel

et al. 2011

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Both osteoporosis and high blood pressure are major diseases in aging populations. Recent studies demonstrated that some antihypertensive drugs reduced the risk of bone fracture in elderly patients. Although calcium channel blockers (CCB) are widely used as first-line antihypertensive agents, there is no evidence that they prevent osteoporosis. In this study, we investigated the effects of two types of CCB on bone metabolism: cilnidipine (L-/N-type CCB), which suppresses norepinephrine release from the sympathetic nerve, and amlodipine (L-type CCB). In ovariectomized female spontaneous hypertensive rats, administration of cilnidipine, but not amlodipine, resulted in a significant increase in the ratio of alkaline phosphatase to tartrate-resistant acid phosphatase (TRAP) and a decrease in the number of osteoclasts, as assessed by TRAP staining in the proximal tibia. Bone mineral density, moreover, was significantly higher in the cilnidipine group as compared with the amlodipine group and was associated with a significant decrease in a urinary collagen degradation product (deoxypyridinoline). The degree of prevention of osteoporosis by cilnidipine was similar to that of carvedilol (a b-blocker) because b-blockers reduce fracture risks though the inhibition of osteoclast activation. Interestingly, these effects cannot be attributed to the reduction of blood pressure because all three drugs significantly decreased blood pressure. In contrast, both cilnidipine and carvedilol, but not amlodipine, significantly decreased heart rate, indicating that both cilnidipine and carvedilol suppressed sympathetic nervous activity. Overall, our present data showed that cilnidipine (L-/N-type CCB) ameliorated osteoporosis in ovariectomized hypertensive rats. These pleiotropic effects of antihypertensive drugs such as cilnidipine and carvedilol might provide additional benefits in the treatment of hypertensive postmenopausal women.

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“…7,9 Indeed, clinical studies have shown considerable evidence that antihypertensive drugs such as thiazides decreased the risk of hip fracture by reducing renal calcium excretion. 10,11 Interestingly, angiotensin-converting enzyme (ACE) inhibitors are also reported to reduce the risk of fractures. [12][13][14] spontaneous hypertensive rats (SHRs) (10-weeks old) were also purchased from SLC Japan), and bilateral OVX or sham operation was performed.…”

Section: Introductionmentioning

confidence: 99%

Prevention of osteoporosis by angiotensin-converting enzyme inhibitor in spontaneous hypertensive rats

et al. 2009

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A recent analysis of clinical studies suggests that angiotensin-converting enzyme (ACE) inhibitors might reduce bone fractures. In this study, we examined whether an ACE inhibitor might attenuate osteoporosis in a hypertensive rat model. In spontaneous hypertensive rats (SHRs), estrogen deficiency induced by ovariectomy (OVX) resulted in a significant increase in osteoclast activation as assessed by the tartrate-resistant acid phosphatase (TRAP) activity in the tibia, accompanied by a significant decrease in bone density evaluated by dual-energy X-ray absorptiometry and an increase in urinary deoxypyridinoline. Treatment with an ACE inhibitor, imidapril, attenuated OVX-induced decrease in bone density and increase in TRAP activity and urinary deoxypyridinoline. As ACE inhibitors possess the effects of blockade of the renin-angiotensin system (RAS) and activation of the bradykinin-nitric oxide pathway, we examined the contribution of both pathways in an OVX-induced osteoporosis model. Administration of nitro-L-arginine methylester (L-NAME) did not alter TRAP activity, urinary deoxypyridinoline or bone density, whereas the administration of a subpressor dose of angiotensin II accelerated the increase in TRAP activity in the tibia, accompanied by a significant decrease in bone density and an increase in urinary deoxypyridinoline. Thus, ACE inhibitors prevented osteoporosis, probably because of the inhibition of RAS, but not of nitric oxide. Overall, ACE inhibitors attenuated osteoporosis in a hypertensive rat model through the blockade of RAS.

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Hydrochlorothiazide reduces loss of cortical bone in normal postmenopausal women: a randomized controlled trial

Cited by 166 publications

References 45 publications

The epithelial calcium channels TRPV5 and TRPV6: regulation and implications for disease

The epithelial calcium channels TRPV5 and TRPV6: regulation and implications for disease

Cilnidipine, but not amlodipine, ameliorates osteoporosis in ovariectomized hypertensive rats through inhibition of the N-type calcium channel

Prevention of osteoporosis by angiotensin-converting enzyme inhibitor in spontaneous hypertensive rats

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