Why the study?
Does a high-fat overfeeding regimen alter autonomic control of blood pressure and heart rate in dogs?
Does a high-fat overfeeding regimen alter autonomic control of blood pressure and heart rate in dogs?
In a canine model, obesity-induced hypertension and tachycardia appear to be driven by decreased parasympathetic inhibition and altered sympathetic control of peripheral vascular resistance.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for autonomic mechanisms in canine obesity hypertension; leaves open translation to human pathophysiology.
Autonomic control of cardiovascular function was evaluated in nine dogs before and after a high-fat overfeeding regimen. Body weight increased significantly (from 19.8 +/- 0.9 to 29.5 +/- 2.1 kg; P < 0.01) with overfeeding. Mean arterial pressure (MAP) increased from 94.6 +/- 2.1 to 105.5 +/- 3.7 mmHg (P < 0.05), and heart rate (HR) increased from 94.8 +/- 3.5 to 112.3 +/- 5.6 beats/min (P < 0.01). After ganglionic blockade with chlorisondamine, dose response of MAP and HR to methoxamine (alpha-agonist) or isoproterenol (beta-agonist) was evaluated. Peak MAP response to methoxamine was blunted in obese dogs. HR response to isoproterenol was not different between lean and obese dogs. Atropine in the presence of propranolol increased HR from 80.8 +/- 7 to 202.8 +/- 8.9 beats/min in lean dogs and from 113.8 +/- 12.1 to 131.7 +/- 18.2 in obese dogs. These data suggest the increase in HR observed in obese dogs may be due to a decrease in parasympathetic inhibition rather than an increase in sympathetic stimulation. The blunted response to methoxamine in obese hypertensive dogs suggests that the sympathetic control of peripheral vascular resistance is altered in obesity.
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Truett et al. (1996) studied this question.
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