Abnormal Pressure Natriuresis in the Dog Model of Obesity-Induced Hypertension.
Granger, Joey P.; West, David; Scott, Janet
Proceedings of the Tenth Scientific Meeting of the Inter-American Society of Hypertension. 23(1) Supplement I:I-8-I-11, January 1994.
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Obesity is considered to be a major factor in the pathogenesis of hypertension in industrialized countries. Recent studies have suggested that the kidneys may play an important role in the development of obesity-induced hypertension. The purpose of this study was to determine whether obesity-induced hypertension is associated with abnormalities in the pressure-natriuresis relation. Renal function studies were performed in anesthetized control dogs (body weight, 20.2 /-0.8 kg) and obese dogs (body weight, 26.4 /-0.7 kg) that were maintained on a high-fat diet for 5 to 6 weeks. Mean arterial pressure averaged 122 /-5 mm Hg in the control group (n=6) and 148 /-7 mm Hg in the obese group (n=8). The effects of renal perfusion pressure on renal hemodynamics as well as sodium and water excretions were examined at five levels of renal perfusion pressure ranging from 75 to 165 mm Hg. Pressure-natriuretic and diuretic responses were reduced in the obese dogs by 40% to 50%. The renal blood flow and glomerular filtration rate autoregulatory responses and fractional lithium excretion responses to changes in renal perfusion pressure were similar in the control and obese dog groups. Associated with the attenuated natriuretic response to renal perfusion pressure in the obese dogs were significant elevations in plasma renin activity (4.3 /-1.6 versus 1.6 /-0.5 ng angiotensin I/mL per hour), plasma aldosterone concentration (34.4 /-6.4 versus 15.3 /-3.2 ng/dL), and plasma insulin concentration (30.5 /-6.8 versus 20.9 /-2.9 IU/mL). The results of this study establish that obesity-induced hypertension in the dog is associated with a shift in the pressurenatriuresis relation. The underlying mechanism responsible for the abnormal pressure-natriuresis relation in this model of obesity may be due to activation of various sodiumretaining systems such as the renin-angiotensin-aldosterone system.
(C) 1994 American Heart Association, Inc.