Obesity-induced hypertension in the dog.

Abstract

To study the relationship between body weight and blood pressure, we have developed an animal model of obestiy-induced hypertension. Nine adult mongrel dogs were chronically instrumented with aortic and vena caval catheters. After a 2-week control period, all dogs were made to gain weight by adding 2 Ib/day of beef fat to their diet for 5 weeks. Blood pressure, heart rate, and body weight were measured daily before the addition of dietary fat, during the 5 weeks of the high fat diet, and for 6 weeks after the fat supplement was stopped. Plasma volume and cardiac output were measured prior to and after 5 weeks of the fat diet. During the 5-week high fat diet, the dogs' body weight increased from 22.2 ± 2.1 to 27.4 ± 3 kg (p<0.001); mean blood pressure increased from 90 ± 5 to 112 ± 6 mm Hg (p<0.01); and heart rate increased from 70 ± 7 to 85 ± 5 beats/min (p<0.05). Blood pressure, heart rate, and body weight returned to near control values after the fat diet was stopped. Over the 5-week fat diet, the dogs' plasma volume increased from 920 ± 130 to 1059 ± 195 ml (p<0.05); cardiac output increased from 2.5 ± 0.4 to 3.1 ± 0.3 L/min (p<0.05); and systemic vascular resistance increased from 35.3 ± 8 to 38.9 ± 9 mm Hg/L/min (p<0.1). Weight gain in the dogs was also associated with hyperinsulinemia and insulin resistance. Our findings have demonstrated that weight gain in the dog is associated with an increase in heart rate, blood pressure, cardiac output, plasma volume, and fasting insulin concentration, and we think that our animal model should be ideal for studying the pathogenesis of obesity-induced hypertension. (Hypertension 9 [Suppl III]: III-64-III-68, 1987) KEY WORDS • obesity • hypertension • hyperinsulinemia

Effects of weight loss on the cardiac parameters of obese dogs

“…As in this work, Brown et al (2007) observed that overweight dogs possessed higher reference range arterial pressures in relation to those of ideal body weight. As such, food restriction is considered an important non-pharmacological treatment for controlling arterial pressure, especially in dogs of excessive weight (Rocchini et al 1987, Rocchini et al 1989.…”

“…At the end of the weight loss program it was observed that the analyzed variables gradually returned to their basal values (Rocchini et al 1987).…”

Insulin downregulates M2-muscarinic receptors in adult rat atrial cardiomyocytes: a link between obesity and cardiovascular complications

“…[9][10][11] This could, like sympathetic overactivation, explain the tachycardia and the increased risk of cardiovascular mortality through hypertension and sudden cardiac death 9,12 in obese patients. Using a canine model of dietary-induced obesity (dogs fed a high-fat diet), which mimics many of the characteristics of human obesity, [13][14][15] we observed atrial muscarinic receptor downregulation 16 and a decreased high frequency power (HF) of heart rate variability (HRV), which reflects cardiac parasympathetic activity. Both of these modifications led to tachycardia, and demonstrate a defective cardiac parasympathetic system.…”

ACE, angiotensinogen and obesity: a potential pathway leading to hypertension

“…9 Elevated PRA has likewise The renin-angiotensin system (RAS) is a powerful been found in dogs after 5 weeks on a high-fat diet, humoral regulator of fluid volume and blood pressdespite marked sodium retention and increased ure (BP). 1,2 Despite the effectiveness of pharmacolextracellular fluid volume.…”

“…Although obesity is the weight, BP and the RAS have been infrequent. [9][10][11][12][13] most important single modifiable risk factor for Rochini et al 9 reported increased aldosterone hypertension, little is known about the mechanism linking the two conditions. We initiated a com- approximately balanced between persons above and *P Ͻ 0.000; **P Ͻ 0.05; ***P Ͻ 0.01 between obese and nonbelow the 140/90 hypertension cut-point were obese groups.…”