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Comparative analysis of the vascular sympatho‐inhibition to moxonidine in control or streptozotocin‐induced diabetic rats
Author(s) -
Centurion David,
MorenoVázquez Eber,
VillamilHernández Ma. Trinidad,
AlcántaraVázquez Oscar,
AcostaCota Selene J.,
SánchezLópez Araceli
Publication year - 2013
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.27.1_supplement.1091.4
Subject(s) - moxonidine , endocrinology , medicine , streptozotocin , saline , stimulation , diabetes mellitus , bolus (digestion) , sympathetic nervous system , blood pressure , receptor , agonist
Moxonidine peripherally inhibits sympathetically‐induced vasopressor responses in pithed rats by α 2 ‐adrenoceptors and I 1 receptors. During diabetes, autonomic failure can occur and peripheral sympatho‐inhibition by moxonidine could be modified. This study has investigated in streptozotocin‐induced (STZ) diabetic rats the alterations of: (1) the vasopressor responses to sympathetic stimulation or exogenous noradrenaline; and (2) the inhibition to moxonidine on the vascular sympathetic outflow. Male Wistar rats were pre‐treated with STZ (60 mg/kg, i.p.) or vehicle. 14 days later, the rats were pithed and prepared for measurement of diastolic blood pressure and heart rate. Then, the vasopressor responses induced by either selective electrical stimulation (2 ms, 60 V, 0.03–3 Hz) of the vascular sympathetic outflow (T 7 ‐T 9 ) or i.v. bolus injections of exogenous noradrenaline (0.03–3 μg/kg) were determined before and during i.v. infusion of moxonidine (3 and 10 μg/kg min) or saline. In rats pretreated with STZ or vehicle, sympathetic stimulation or exogenous noradrenaline elicited frequency‐dependent or dose‐dependent vasopressor responses, respectively. The vasopressor responses were less marked in rats pretreated with STZ than in rats treated with vehicle. In rats pretreated with STZ or vehicle, i.v. continuous infusion of moxonidine (but not saline) significantly inhibited the vasopressor responses to sympathetic stimulation but not those induced by exogenous noradrenaline. The sympatho‐inhibition was less marked in rats pretreated with STZ. These results suggest that STZ‐induced diabetes produced a reduction of the vasopressor responses and the sympatho‐inhibition to moxonidine probably due to a decrease of density of receptors or decoupling of transductional mechanisms.