Aviv A
Hypertension Research Center, University of Medicine and Dentistry of New Jersey-N.J. Medical School, Newark 07103-2714.
J Am Soc Nephrol. 1992 Nov;3(5):1049-63. doi: 10.1681/ASN.V351049.
There is evidence that the cytosolic free Ca2+, protein kinase C, and the Na(+)-H+ antiport cross-communicate with one another through positive and negative feedback mechanisms, thereby maintaining cellular Ca2+ and pH homeostasis. This triumvirate may play a role in the development of insulin resistance--a common characteristic of both essential hypertension and non-insulin-dependent diabetes mellitus. Circulating cells from patients with essential hypertension and non-insulin-dependent diabetes mellitus demonstrate elevated cytosolic free Ca2+, increased protein kinase C activity, or both, and these perturbations are associated with augmented activity of the Na(+)-H+ antiport. If present in other cells (e.g., striated muscle cells and adipocytes), these alterations could underlie insulin resistance in essential hypertension and non-insulin-dependent diabetes mellitus.
有证据表明，胞质游离钙离子、蛋白激酶C和钠氢反向转运体通过正负反馈机制相互交叉作用，从而维持细胞内钙离子和pH值的稳态。这个三联体可能在胰岛素抵抗的发生发展中起作用，而胰岛素抵抗是原发性高血压和非胰岛素依赖型糖尿病的共同特征。原发性高血压和非胰岛素依赖型糖尿病患者的循环细胞显示胞质游离钙离子升高、蛋白激酶C活性增加，或两者兼有，并且这些紊乱与钠氢反向转运体活性增强有关。如果这些改变存在于其他细胞（如横纹肌细胞和脂肪细胞）中，那么它们可能是原发性高血压和非胰岛素依赖型糖尿病中胰岛素抵抗的基础。
