Rhesus monkeys were fed corn or coconut oil-based diets for 3-6 mo to determine effects on the composition of all lipoprotein classes and on the metabolism of high density lipoproteins (HDL). Major findings included the following. (a) Coconut oil feeding increased concentrations of all classes of plasma lipoproteins without altering lipoprotein size, suggesting an increase in particle number. (b) The percentage of saturated fatty acids in the cholesteryl esters (CE) of low density lipoproteins (LDL) and HDL reached 40% with coconut oil feeding. This value probably constitutes a minimum estimate of the CE which were of intracellular rather than intraplasmic origin. (c) The CE in LDL and HDL were nearly identical suggesting virtually complete equilibration by the core lipid transfer reaction. The CE in very low density lipoproteins, in contrast, were significantly more saturated than those in LDL and HDL irrespective of diet. (d) Lower HDL levels on the corn oil diet were associated with higher fractional catabolic rates for both apolipoprotein A-I (OA2 vs. 031 d-l) and apolipoprotein A-Il (OA5 vs. 0.30 d-').
SUMMARY The present study assessed the contribution of the renin-angiotensln system (RAS), dietary sodium, and cardiac output (CO) to the genesis of primate hypertension in a one-kidney model which was developed to test species-specific renin inhibitors. Reduction of renal perfusion pressure increased mean arterial pressure (MAP) from 105 ± 4 to 127 ± 3 mm Hg (p < 0.0005), associated with increased plasma renin activity (PRA) from 4.9 ± 0.7 to 13.8 db 1.1 ng'ml of hypertension in the nonhuman primate is limited. This reflects in part the difficulty of producing a model that may be studied in both acute and chronic stages of the disease. A better understanding of such mechanisms is necessitated by primate studies, which have demonstrated a correlation of hypertension with cardiac and cerebrovascular atherosclerosis, analogous to human pathologic conditions.
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