Impaired Zinc and Copper Status and Altered Fatty Acid Cell Membrane Composition in Essential Hypertension

The apparent antagonism between Zinc (Zn) and Copper (Cu) is a well-known phenomenon and has been documented in various chronic diseases. An impairment in Zn and Cu status has been shown in hypertensive animals (1), suggesting a possible relationship with the pathogenesis of hypertension. Zn and Cu are involved in lipid metabolism, and several studies indicated that a major aspect of Zn-Cu interaction may be related to the opposing effects on essential fatty acids (EFA) metabolism or by differential stimulation of the synthesis of prostaglandins (PGs), whose influence on blood pressure (BP) regulation has been widely documented (2). The conversion of C-18 polyunsaturated fatty acids (PUFA) into the longerchain metabolites proceeds through desaturation and elongation steps; desaturation processes are catalyzed by the Δ4-Δ5-Δ6 desaturases, which are the rate-limiting enzymes in the pathway, and whose activities specifically require Zn and Cu (2). Thus, Zn and Cu availability may modulate the balance of PGs precursors. Also, since C-20 and C-22 are the major PUFA found in phospholipids, most of the cellular functions (fluidity, permeability or the ion transport systems activity) are in some way related to their metabolism (3).