Impaired catecholamine inactivation. A prohypertensive stimulus after dietary linoleate deficiency in salt-loaded rats?
Experiments were carried out on salt-loaded rats (1.5% NaCl as drinking fluid) to further explore the mechanisms by which blood pressure increases after a linoleic acid-deficient (LAd) diet. In 4-week-old LAd rats (0.5 cal% LA, hydrogenated palm kernel fat) compared to linoleic acid-rich rats (LAr, 13.3 cal% LA, sunflower oil), we observed, from the base of a reduced content of omega-6-polyunsaturated fatty acids in the tissues, an increase in blood pressure by 12 mm Hg (p less than 0.001), a diminished formation of prostaglandin E (PGE), and an unchanged formation of PGF in the aorta as well as a reduction in the in vitro uptake of 14C-norepinephrine into cardiac, aortic, and renal tissues, and a reduced degradation rate of 14C-norepinephrine in cardiac tissue. These differences in LAr vs LAd rats were not exaggerated. With respect to aortic PGE formation, 14C-norepinephrine uptake into aortic and renal tissues and 14C-norepinephrine degradation even lessened when the diet was begun prenatally, although the reduction of omega 6-polyunsaturated fatty acids in the tissues was aggravated. Our conclusion is that a fault in catecholamine inactivation may be involved in the pathogenesis of increased sympathetic activity and blood pressure elevation in LAd-fed, salt-loaded rats, possibly via alterations of endogenous prostanoid formation.