[Show abstract][Hide abstract] ABSTRACT: Diabetes mellitus (DM) is an emerging health problem for industrialized societies with substantial morbidity and mortality
and an established risk factor for osteoporosis and fragility fractures.1 The skeletal alterations in patients with DM are due to insulin deficiency or resistance and hyperglycemia, alterations of
the bone marrow microenvironment and bone matrix quality, and impaired neuromuscular–skeletal interactions.2,3
[Show abstract][Hide abstract] ABSTRACT: The financial and social cost of hypertension and osteoporosis, clinically silent diseases, are determined by the consequences, such as a vascular disease and fractures. The relationship between these illnesses has not been clearly established, although many alterations in extracellular metabolism of calcium, which could determine the level of bone mineral density (BMD) in these patients, have been associated to hypertension. Despite these alterations, the lack of studies relating these two important diseases is surprising, and hypertension is not identified as a risk factor for osteoporosis. Interestingly, there is a lack of information of the long-term effects of antihypertensive treatment on bone mineral density, although 50 % of the hypertensive population is made up of postmenopausal women. Most studies analyzed the effects of thiazides and, to a lesser degree, the effects of calcium antagonist. The purpose of this review is evaluate the effect of the antihypertensive therapeutic group (diuretics, -blockers, calcium antagonists, angiotensin converting enzyme) on the bone mineral density (BMD) and osteoporotic fracture.
[Show abstract][Hide abstract] ABSTRACT: SLC12A3 encodes the thiazide-sensitive sodium chloride cotransporter (NCC), which is primarily expressed in the kidney, but also in intestine and bone. In the kidney, NCC is located in the apical plasma membrane of epithelial cells in the distal convoluted tubule. Although NCC reabsorbs only 5 to 10 % of filtered sodium, it is important for the fine-tuning of renal sodium excretion in response to various hormonal and non-hormonal stimuli. Several new roles for NCC in the regulation of sodium, potassium, and blood pressure have been unraveled recently. For example, the recent discoveries that NCC is activated by angiotensin II but inhibited by dietary potassium shed light on how the kidney handles sodium during hypovolemia (high angiotensin II) and hyperkalemia. The additive effect of angiotensin II and aldosterone maximizes sodium reabsorption during hypovolemia, whereas the inhibitory effect of potassium on NCC increases delivery of sodium to the potassium-secreting portion of the nephron. In addition, great steps have been made in unraveling the molecular machinery that controls NCC. This complex network consists of kinases and ubiquitinases, including WNKs, SGK1, SPAK, Nedd4-2, Cullin-3, and Kelch-like 3. The pathophysiological significance of this network is illustrated by the fact that modification of each individual protein in the network changes NCC activity and results in salt-dependent hypotension or hypertension. This review aims to summarize these new insights in an integrated manner while identifying unanswered questions.
Pflügers Archiv - European Journal of Physiology 12/2013; · 4.87 Impact Factor
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