Sustained suppression of sympathetic activity and arterial pressure during chronic activation of the carotid baroreflex.
Following sinoaortic denervation, which eliminates arterial baroreceptor input into the brain, there are slowly developing adaptations that abolish initial sympathetic activation and hypertension. In comparison, electrical stimulation of the carotid sinus for 1 wk produces sustained reductions in sympathetic activity and arterial pressure. However, whether compensations occur subsequently to diminish these responses is unclear. Therefore, we determined whether there are important central and/or peripheral adaptations that diminish the sympathoinhibitory and blood pressure-lowering effects of more sustained carotid sinus stimulation. To this end, we measured whole body plasma norepinephrine spillover and alpha(1)-adrenergic vascular reactivity in six dogs over a 3-wk period of baroreflex activation. During the first week of baroreflex activation, there was an approximately 45% decrease in plasma norepinephrine spillover, along with reductions in mean arterial pressure and heart rate of approximately 20 mmHg and 15 beats/min, respectively; additionally, plasma renin activity did not increase. Most importantly, these responses during week 1 were largely sustained throughout the 3 wk of baroreflex activation. Acute pressor responses to alpha-adrenergic stimulation during ganglionic blockade were similar throughout the study, indicating no compensatory increases in adrenergic vascular reactivity. These findings indicate that the sympathoinhibition and lowering of blood pressure and heart rate induced by chronic activation of the carotid baroreflex are not diminished by adaptations in the brain and peripheral circulation. Furthermore, by providing evidence that baroreflexes have long-term effects on sympathetic activity and arterial pressure, they present a perspective that is opposite from studies of sinoaortic denervation.
Dept. of Physiology, Univ. of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505, USA. tlohmeier@umc.edu
Thomas E
TE
Lohmeier
Radu
R
Iliescu
Terry M
TM
Dwyer
Eric D
ED
Irwin
Adam W
AW
Cates
Martin A
MA
Rossing
D000222:Adaptation, Physiological; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000294:innervation*; D017704:Baroreflex / Q000187:drug effects; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001794:Blood Pressure / Q000187:drug effects; D002346:Carotid Sinus / Q000294:innervation*; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D005730:Ganglionic Blockers / Q000494:pharmacology; D006339:Heart Rate; D006400:Hematocrit; D009433:Neural Inhibition / Q000187:drug effects; D009638:Norepinephrine / Q000097:blood; D011188:Potassium / Q000097:blood / Q000652:urine; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism; D012083:Renin / Q000097:blood; D012964:Sodium / Q000652:urine; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D013997:Time Factors
D000316:Adrenergic alpha-Agonists; D015415:Biomarkers; D005730:Ganglionic Blockers; D018340:Receptors, Adrenergic, alpha-1; D012964:Sodium; D012083:Renin; D011188:Potassium; D009638:Norepinephrine