Warnock D G
Departments of Medicine and Physiology and Biophysics, and Nephrology Research and Training Center, University of Alabama at Birmingham, 35294-0007, USA.
Curr Opin Nephrol Hypertens. 2001 Jul;10(4):493-9. doi: 10.1097/00041552-200107000-00003.
Our basic understanding of sodium mechanisms provides unique insights into epithelial transport processes, and unusual clinical syndromes can arise from mutations of these ion transporters. These genetic disorders affect sodium balance, with both sodium-retaining and sodium-wasting conditions being the consequence. A major focus of such studies has been the epithelial sodium channel, which can be activated by mutations in the channel subunits or mineralocorticoid receptor, and changes in the response to or production of mineralocorticoids. As a result, there are now clearly defined Mendelian syndromes in which epithelial sodium channel activity is 'dysregulated', with the subsequent development of systemic hypertension with suppressed plasma renin activity that can be attributed to a primary renal mechanism. Applying these insights to the far more common disorder of low renin hypertension may shed new light on the underlying pathophysiology of this common form of human hypertension, and more clearly define the interactions of dietary constituents such as sodium and potassium in the regulation of blood pressure.
我们对钠机制的基本理解为上皮运输过程提供了独特的见解，这些离子转运体的突变可引发异常的临床综合征。这些遗传性疾病会影响钠平衡，导致钠潴留和钠丢失情况的出现。此类研究的一个主要焦点是上皮钠通道，该通道可因通道亚基或盐皮质激素受体的突变以及对盐皮质激素反应或生成的改变而被激活。因此，现在已有明确界定的孟德尔综合征，其中上皮钠通道活性“失调”，随后会出现系统性高血压且血浆肾素活性受到抑制，这可归因于原发性肾脏机制。将这些见解应用于更为常见的低肾素性高血压疾病，可能会为这种常见人类高血压形式的潜在病理生理学带来新的认识，并更清晰地界定饮食成分（如钠和钾）在血压调节中的相互作用。
