Prolonged Activation of the Baroreflex Abolishes Obesity-Induced Hypertension
Thomas E. Lohmeier; Terry M. Dwyer; Eric D. Irwin; Martin A. Rossing; Robert S. Kieval
From the Department of Physiology (T.E.L., T.M.D.), University of Mississippi Medical Center, Jackson; Trauma Services (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; and CVRx, Inc. (M.A.R., R.S.K.), Maple Grove, Minn.
Prolonged electrical activation of the carotid baroreflex produces sustained reductions in sympathetic activity and arterial pressure in normotensive dogs.
The main goal of this study was to assess the influence of prolonged baroreflex activation on arterial pressure and neurohormonal responses in 6 dogs with obesity-induced hypertension.
After control measurements, the diet was supplemented with cooked beef fat for 6 weeks, whereas sodium intake was held constant. After 4 weeks of the high-fat diet, there were increments in body weight from 25.8±0.7 to 38.6±1.0 kg, mean arterial pressure from 97±2 to 110±3 mm Hg, heart rate from 67±3 to 91±4 bpm, and plasma norepinephrine concentration from 141±35 to 280±52 pg/mL. Plasma glucose and insulin concentrations were elevated, but increases in plasma renin activity during the initial weeks of the high-fat diet were not sustained. During week 5, baroreflex activation resulted in sustained reductions in mean arterial pressure, heart rate, and plasma norepinephrine concentration; at the end of week 5, these values were 87±2 mm Hg, 77±4 bpm, and 166±45 pg/mL, respectively. These suppressed values returned to week 4 levels during a 7-day recovery period after baroreflex activation. There were no changes in plasma glucose or insulin concentrations, or plasma renin activity during prolonged baroreflex activation.
These findings indicate that baroreflex activation can chronically suppress the sympathoexcitation associated with obesity and abolish the attendant hypertension while having no effect on hyperinsulinemia or hyperglycemia.
Key Words: baroreflex • hypertension • heart rate • obesity • sympathetic nervous system • norepinephrine • renin–angiotensin system
Hypertension, June, 2007,Vol.49, №6; p.1307.
© 2007 American Heart Association, Inc.
From the Department of Physiology (T.E.L., T.M.D.), University of Mississippi Medical Center, Jackson; Trauma Services (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; and CVRx, Inc. (M.A.R., R.S.K.), Maple Grove, Minn.
Prolonged electrical activation of the carotid baroreflex produces sustained reductions in sympathetic activity and arterial pressure in normotensive dogs.
The main goal of this study was to assess the influence of prolonged baroreflex activation on arterial pressure and neurohormonal responses in 6 dogs with obesity-induced hypertension.
After control measurements, the diet was supplemented with cooked beef fat for 6 weeks, whereas sodium intake was held constant. After 4 weeks of the high-fat diet, there were increments in body weight from 25.8±0.7 to 38.6±1.0 kg, mean arterial pressure from 97±2 to 110±3 mm Hg, heart rate from 67±3 to 91±4 bpm, and plasma norepinephrine concentration from 141±35 to 280±52 pg/mL. Plasma glucose and insulin concentrations were elevated, but increases in plasma renin activity during the initial weeks of the high-fat diet were not sustained. During week 5, baroreflex activation resulted in sustained reductions in mean arterial pressure, heart rate, and plasma norepinephrine concentration; at the end of week 5, these values were 87±2 mm Hg, 77±4 bpm, and 166±45 pg/mL, respectively. These suppressed values returned to week 4 levels during a 7-day recovery period after baroreflex activation. There were no changes in plasma glucose or insulin concentrations, or plasma renin activity during prolonged baroreflex activation.
These findings indicate that baroreflex activation can chronically suppress the sympathoexcitation associated with obesity and abolish the attendant hypertension while having no effect on hyperinsulinemia or hyperglycemia.
Key Words: baroreflex • hypertension • heart rate • obesity • sympathetic nervous system • norepinephrine • renin–angiotensin system
Hypertension, June, 2007,Vol.49, №6; p.1307.
© 2007 American Heart Association, Inc.
1 comment:
Hypertension,When to Treat?
The blood pressure treatment guideline is based on the famous Framingham Study which showed the health benefits of blood pressure reduction. The 18 year Framingham Blood Pressure study found increased risk of heart disease and death in people with increased blood pressure 140 to 160, and even more risk above 160.
If you examine the original data from the Framingham study you will find computer smoothing of the data as published in the medical journals. This gives a smooth gradual line of increasing mortality as blood pressure goes up between 140 and 160. This is called the Linear Model. However, if you examine the raw data, as S. Port did as published in Lancet 1/15/2000, you will find a non-linear threshold of increased risk above 160 systolic, and no increased mortality below 160.
For a more complete review of this controversy in Blood Pressure guidelines, see my newsletter
Blood Pressure Pills for Hypertension, When to Treat? by Jeffrey Dach MD
Jeffrey Dach MD
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