正常血圧者,本態性高血圧患者における高インスリン血症のカルシウム代謝に及ぼす加齢の影響
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Insulin resistance and accompanying hyperinsulinemia are often linked with essential hypertension. The proposed hypertensive mechanisms of insulin are as follows: the enhancement of renal tubular sodium reabsorption, the augmentation of renin-angiotensin aldosterone system, sympathetic nerve stimulation and intracellular calcium accumulation. On the other hand, it has also been reported that acute insulin administration has elicited renal calcium retention and might contribute to the development of hypertension. To clarify the effect of hyperinsulinemia on calcium metabolism, the euglycemic hyperinsulinemic glucose clamp technique (GC) was applied in 43 normotensives and 35 essential hypertensives. The subjects were divided into four groups, young (<40 years old) and elder (≧40 years old) normotensives and hypertensives. Insulin sensitivity was evaluated as M value (mg/m2/min), blood and urine samples were collected before and at the end of 2-hour hyperinsulinemia to measure the following parameters: plasma free calcium ion (pCa2+), serum inorganic phosphorus (Pi), plasma parathyroid hormone (PTH), urinary calcium, inorganic phosphorus and sodium excretion (UCaV, UPiV and UNaV), fractional excretion of calcium, inorganic phosphorus and sodium (FECa, FEPi and FENa). Elder normotensives and both young and elder hypertensives showed significantly lower M values than young normotensives. After GC, pCa2+ was elevated and Pi and PTH had decreased significantly in both normotensives and hypertensives. UCaV, FECa, UNaV and FENa increased significantly during GC only in young normotensives. In the other three groups, UNaV and FENa decreased significantly, and UCaV and FECa showed no change under hyperinsulinemia. On the other hand, diminished UPiV and FEPi were observed in all four groups through GC. Significant negative correlations were found between age and changes of UNaV, UCaV, FENa or FECa in normotensives, but not in hypertensives. There were significant positive correlations between the changes of UNaV and those of UCaV, and between the changes of FENa and those of FECa. In summary, 1) insulin sensitivity decreased with aging in normotensives, while hypertensives were insulin resistant regardless of age; 2) in young hypertensives, hyperinsulinemia augmented renal sodium excretion and concomitant renal calcium excretion, and 3) hyperinsulinemia caused sodium retention in elder normotensives and both young and elder hypertensives with suppressed calcium excretion. These results suggest that hyperinsulinemia associated with insulin resistance could contribute to blood pressure elevation due to sodium and calcium retention.
- 札幌医科大学の論文
- 1996-10-01
札幌医科大学 | 論文
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