[Clinical efficacy of calcium channel blockers slow the third generation of lercanidipine in the treatment of patients with arterial hypertension and metabolic disorders (review)].

Arterial hypertension is the most common risk factor in patients with metabolic disorders. In the selection of antihypertensive therapy it is necessary to consider not only the anti-hypertensive and organoprotective effects of drugs and their metabolic effects, which has prognostic value. Calcium antaginists, along. Lercanidipine related to the third generation dihydripyridine calcium antagonist, has been much more selective for the so-called slow calcium channels of vascular smooth muscle cells, which is associated with a good hypertensive, organo and metabolic action. Combination therapy with an ACE inhibitor and a calcium channel blocker is also a justified tactic for the management of patients with high-risk cardiovascular and metabolic disorders. Attention is paid new fixed combinations, including angiotensin converting enzyme inhibitors and calcium antagonists.

Changes in intra- and extracellular Ca2+ concentration and prostaglandin E2 synthesis in osteoblasts of the femoral bone in experimental hyper- and hypothyroidism.

Subclinical form of hypothyroidism was not associated with considerable changes in Ca(2+) content in osteoblasts and blood plasma and in the content of ATP and prostaglandin E2. Activation of prostaglandin E2 synthesis in response to binding of extracellular Ca(2+) in osteoblasts in the absence of ATP was less pronounced (by 11%) compared to the control. Progression of hypothyroidism and development of clinical signs of the disease were accompanied by a decrease in Ca(2+) content in osteoblasts and plasma by 45 and 12%, respectively, and ATP content in osteoblasts by 30%, and by activation of prostaglandin E2 synthesis by 117%. Moreover, the synthesis of prostaglandins in response to binding of extra- and intracellular Ca(2+) also considerably changed. Hyperthyroidism (2 months) was characterized by a moderate decrease in plasma content of Ca(2+) by 15% and ATP by 25%, together with an increase in prostaglandin E2 level by 55.5%. The release of prostaglandin E2 in response to chelation of extracellular Ca(2+) increased even more markedly, but somewhat decreased in response to addition of 5 mM ATP due to compensation of metabolic acidosis.