Premium
Prolonged activation of the baroreflex decreases arterial pressure in the presence of chronic adrenergic blockade
Author(s) -
Hildebrandt Drew,
Lohmeier Thomas E.,
Dwyer Terry M,
Irwin Eric D,
Rossing Martin A,
Kieval Robert S
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a516-c
Subject(s) - baroreflex , phenylephrine , prazosin , mean arterial pressure , propranolol , baroreceptor , heart rate , medicine , adrenergic antagonist , carotid sinus , adrenergic , blood pressure , sympathetic nervous system , antagonist , norepinephrine , endocrinology , anesthesia , receptor , dopamine
Prolonged baroreflex activation (PBA) by electrical stimulation of the carotid sinus baroreceptors produces sustained reductions in mean arterial pressure (MAP) and suppression of the sympathetic nervous system. The goal of this study was to determine whether PBA lowers MAP when α‐1 and β‐adrenoceptors are blocked by high doses of adrenergic antagonists (AB). This was studied in 6 dogs under control conditions, following administration of prazosin (α‐1 antagonist, 5mg/kg/d, tid) + propranolol (nonselective β‐blocker, 10mg/kg/d, IV infusion) for 7 days (AB), and then for an additional 7 days during AB+PBA. MAP and heart rate (HR) responses to bolus injections of phenylephrine (MAP=+44±3 mmHg; HR=−29±2 bpm) and isoproterenol (HR=+59±8 bpm) were completely blocked during AB. Chronic MAP, HR, and plasma norepinephrine (NE, pg/ml) responses to AB and AB+PBA were: MAP decreased substantially during AB despite increased central sympathetic outflow as evidenced by increased NE. Moreover, in the presence of AB, MAP decreased further during PBA. This further decline in MAP in response to central sympathoinhibition by PBA may reflect suppression of cotransmitter release from adrenergic neurons or altered hormonal secretion. (HL‐51971)