[The effects of vitamin D in bone health have been known since the 1920s. Recently, it has been proven that its role in the body is much more complex. Activated vitamin D is a steroid hormone that regulates transcription of more than 200 human genes through its receptor that is detectable in almost all types of cells. In contrast to the former conceptions, it can be activated not only in the kidneys; moreover, local 1-α-hydroxylation plays a greater role in its extraskeletal effects. Vitamin D deficiency, currently defined as serum levels of <30 ng/ml, is caused by the lack of ‘effective’ sunlight exposition. Thus, vitamin D deficiency is one of the most frequent deficiencies in the developed world that plays a role not only in the development of skeletal conditions but many other diseases, as well. A low vitamin D level causes a reduced calcium absorption, a higher bone remodelling rate and increased bone loss. It also reduces muscle strength and increases the risk of falling. Normal vitamin D status is required for the effectiveness of drugs for osteoporosis treatment; however vitamin D treatment in itself is not effective in osteoporosis. An increasing number of studies show the benefits of vitamin D supplementation and treatment in extraskeletal conditions. Vitamin D plays an important role in the prevention of several auto-immune diseases, infections, cardiovascular diseases, and cancers. Therefore, all UV-B radiation-deprived adults require an intake of vitamin D to maintain a level of >30 ng/ml. Vitamin D3 treatment is safe. The necessary dose can be reliably approximated by the calculation that an incremental consumption of 100 IU/day raises serum vitamin levels by 1,0 ng/ml. Clinical trials suggest that for the vast majority of individuals, a prolonged intake of 10,000 IU/day does not pose any risk.]

[The effects of vitamin D in bone health have been known since the 1920s. Recently, it has been proven that its role in the body is much more complex. Activated vitamin D is a steroid hormone that regulates transcription of more than 200 human genes through its receptor that is detectable in almost all types of cells. In contrast to the former conceptions, it can be activated not only in the kidneys; moreover, local 1-α-hydroxylation plays a greater role in its extraskeletal effects. Vitamin D deficiency, currently defined as serum levels of <30 ng/ml, is caused by the lack of ‘effective’ sunlight exposition. Thus, vitamin D deficiency is one of the most frequent deficiencies in the developed world that plays a role not only in the development of skeletal conditions but many other diseases, as well. A low vitamin D level causes a reduced calcium absorption, a higher bone remodelling rate and increased bone loss. It also reduces muscle strength and increases the risk of falling. Normal vitamin D status is required for the effectiveness of drugs for osteoporosis treatment; however vitamin D treatment in itself is not effective in osteoporosis. An increasing number of studies show the benefits of vitamin D supplementation and treatment in extraskeletal conditions. Vitamin D plays an important role in the prevention of several auto-immune diseases, infections, cardiovascular diseases, and cancers. Therefore, all UV-B radiation-deprived adults require an intake of vitamin D to maintain a level of >30 ng/ml. Vitamin D3 treatment is safe. The necessary dose can be reliably approximated by the calculation that an incremental consumption of 100 IU/day raises serum vitamin levels by 1,0 ng/ml. Clinical trials suggest that for the vast majority of individuals, a prolonged intake of 10,000 IU/day does not pose any risk.]

[It is known that hypertension shows several gender specific elements both in pathogenesis and in therapy. Understanding this phenomenon may bring us closer to individualized therapy. That was the reason why we examined process of hypertensive adaptation on the level of small intramural coronary arteries. 10-10 male and female Sprague-Dawley rats were used in this study. Animals received osmotic pumps in anaesthesia, which emitted 100 ng/bwkg/min angiotensin II acetate for four weeks. After four weeks treatment, animals were sacrified and heart weights were measured. We isolated intramural, small branches of the left anterior descendant coronary artery, placed them into vessel chamber and tested biomechanical properties and pharmacological reactivity. Heart weight and wall thickness were higher in females comparing to males. However, basal vascular tone and thromboxane-mediated vasoconstriction were elevated in males. Bradykinin relaxation was bigger in females. In female animals inward eutrophic remodeling was found, while in males increased wall stress and elastic moduli dominated the adaptation process. In conclusion, initial steps of angiotensin II mediated hypertension induced markedly gender dependent alterations.]

[Resistant hypertension developed in a 60-year-old male patient with chronic renal insufficiency due to untreated high blood pressure for decades despite of the coadministration of furosemide, β-blocker, calcium channel blocker, angiotensin converting enzyme inhibitor and angiotensin receptor blocker. Breakthrough could be achieved by the combination of a tiazide compound and a loop diuretic (furosemide). It seemed to be worthwile publishing the case because the tiazide drug could be successfully administered below 30 ml/min GFR, where it is generally thought to be ineffective, and because both elements of the combination was given in very low doses relative to the kidney disease. The literature of the most important combinations of the tiazide preparations and the loop diuretics are reviewed and some historical aspects are given as well.]