Chromosome abnormalities in protein-energy malnutrition of salt-sensitive hypertensive rats

The experiment was carried out on Dahl salt-resistant (DSR) and Dahl salt-sensitive (DSS) rats on normal protein (NP; P23%), low-protein (LP; P4.6%) and high-carbohydrate/normal protein (HC/NP; sucrose 63% compared to 47% in the NP) diets for two months, after which they were switched to normal complete diet for one month recovery. The results, in summary, showed: 1) DSS on NP diet developed gradually, by the end of the 2nd month of diet, typical for this strain diastolic hypertension (BP 150/114 mmHg). By the end of the 3rd month the hypertensive state was further increased (BP 160/126 mmHg), 2) the same DSS group on LP failed to develop hypertension by the end of the second month, but when switched to NP diet for a further month, gradually became hypertensive (BP 153/92), 3) DSR remained normotensive for the duration of the three month experiment and HC/NP diet did not change the blood pressure status of both DSR and DSS groups, 4) consistent with LP diet were CAs in both DSR and DSS groups. The mean abberration rates were 9.66% and 12% respectively, compared to 1.66% and 2% in control NP diet rats. After rehabilitation the CAs almost completely recovered, indicating that Protein-energy malnutrition (PEM) per se was a causative factor for CAs in LP diet rats. The original finding in the present experiment was the delayed development of hypertension in DSS rats in PEM condition. Considering the specific nature of hypertension in this strain (salt-sensitive, insulin-resistant hypertension), it was hypothesized that an increased insulin efficiency of glucose utilization and a conversion of insulin-resistant into insulin-sensitive state was the cause of delayed hypertension. (C) 1999 Elsevier Science Inc.