title: Facets of the metabolic syndrome in Dahl hypertensive rats.
abstract: We recently established that the Dahl salt-sensitive rat, a model for genetic salt-sensitive hypertension, was insulin resistant. This study was undertaken to evaluate whether other features of the metabolic syndrome developed in this animal model. Two groups of 16 Dahl salt-sensitive (DSS) rats and their controls, Dahl salt-resistant (DSR) rats were used. For eight weeks, half of each group was fed a standard diet with low sodium content (85 mmol Na/kg diet) while the remainder was fed a high-sodium diet (340 mmol Na/kg diet). Weekly systolic and diastolic blood pressures were measured for all animals. At the end of eight weeks, the urinary Na(+)/K(+) ratio, fasting blood glucose, plasma uric acid and blood lipids were determined for all animals. The same parameters were measured in two additional matched weanling DSS and DSR groups of eight animals each. Adult DSS rats became hypertensive, with the DSS high-salt group exhibiting both genetic hypertension and the pressor effects of a high-salt diet. The DSS high-salt and weanling groups exhibited a lowered urinary Na(+)/K(+) ratio, indicative of greater sodium retention, when compared to their respective DSR groups (p < 0.05). No strain differences were observed in the uric acid levels. However a high-salt diet in both DSS and DSR groups elevated uric acid levels. Weanling and DSS high-salt groups showed increased total plasma cholesterol when compared to their corresponding DSR groups (p < 0.05). In addition, the DSS high-salt group also had both increased total plasma cholesterol and high-density lipoprotein (HDL) cholesterol when compared to the DSS low-salt group (p < 0.05). No significant differences in blood glucose and plasma insulin were observed in the adult groups. The weanling DSS group showed a marked hyperinsulinaemia, suggesting that DSS rats were possibly insulin resistant even before hypertension was fully established. This could indicate that insulin resistance and hypertension may be inherited as separate traits that develop in a parallel but independent manner.
authors.affiliation: School of Basic and Applied Medical Sciences, University of KwaZulu-Natal, Westville Campus, Private Bag X54001, Durban, South Africa.
authors.forename: M L
authors.initials: ML
authors.lastname: Channa
authors.forename: L
authors.initials: L
authors.lastname: Somova
authors.forename: A
authors.initials: A
authors.lastname: Nadar
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D005838:Genotype; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000235:genetics*; D024821:Metabolic Syndrome / Q000235:genetics* / Q000503:physiopathology; D008957:Models, Genetic; D011188:Potassium / Q000652:urine; D051381:Rats; D020303:Rats, Inbred Dahl; D012964:Sodium / Q000652:urine; D012982:Sodium, Dietary / Q000008:administration & dosage*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D012982:Sodium, Dietary; D002784:Cholesterol; D012964:Sodium; D011188:Potassium