title: Development of sugar-induced blood pressure elevation after uninephrectomy in a resistant rat strain.
abstract: Certain rat strains acutely increase blood pressure (BP) when given diets high in NaCl. Prior results showed that "salt-sensitive" rat strains, at least the ones studied, also increase BP in response to sugar loading. To examine this relationship further and learn more about the pathogenesis of sucrose-induced BP elevations, we examined the effects of unilateral nephrectomy (uninephrectomy) on sucrose-induced BP changes. The rationale is based upon the findings that renal mass removal sensitizes BP response to salt loading. Over 15 weeks, augmented sugar (sucrose) consumption by Long-Evans (LE) rats did not increase BP markedly compared to rats consuming a diet relatively low in sugar unless uninephrectomy was performed. The differences in BP caused by the high sugar diet in a uninephrectomized rat could not be explained adequately by alterations in catecholamine excretion, plasma renin activity, excesses in blood volume, or the other parameters examined. However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. Among the dietary groups, there was a significant correlation between the ability of plasma to depress PAH and TEA renal slice uptake and the difference in BP. This is consistent with the presence of a circulating factor affecting cell transport that has its greatest activity in the high sugar-uninephrectomy group of LE rats. We conclude that reducing renal mass potentiates sugar-induced BP elevation similar to salt-induced BP elevation in a normally resistant rat strain, and the rise of BP may be caused by a circulating factor.
authors.affiliation: Department of Medicine (Nephrology), Georgetown University Medical Center, Washington, D.C. 20007.
authors.forename: M
authors.initials: M
authors.lastname: el Zein
authors.forename: J L
authors.initials: JL
authors.lastname: Areas
authors.forename: J
authors.initials: J
authors.lastname: Knapka
authors.forename: D
authors.initials: D
authors.lastname: DiPette
authors.forename: B
authors.initials: B
authors.lastname: Holland
authors.forename: P
authors.initials: P
authors.lastname: al-Karadaghi
authors.forename: H G
authors.initials: HG
authors.lastname: Preuss
mesh_terms: D000375:Aging / Q000502:physiology; D000818:Animals; D001835:Body Weight; D002241:Carbohydrates / Q000494:pharmacology*; D002395:Catecholamines / Q000652:urine; D004040:Dietary Carbohydrates / Q000494:pharmacology; D006973:Hypertension / Q000097:blood / Q000209:etiology* / Q000652:urine; D009392:Nephrectomy; D009929:Organ Size; D010953:Plasma Volume; D051381:Rats; D012083:Renin / Q000097:blood; D012307:Risk Factors; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds; D010130:p-Aminohippuric Acid
chemical_list: D002241:Carbohydrates; D002395:Catecholamines; D004040:Dietary Carbohydrates; D013757:Tetraethylammonium Compounds; D019789:Tetraethylammonium; D012083:Renin; D010130:p-Aminohippuric Acid