title: Nitric oxide opposes glucose-induced hypertension by suppressing sympathetic activity.
abstract: We have reported that glucose infusion in L-NAME-treated rats increased arterial pressure more than the additive responses to glucose and L-NAME alone. This suggested that nitric oxide synthesis inhibition potentiated the hypertensive response to chronic glucose infusion, and the heart rate data suggested an important role for the sympathetic nervous system. This study tested the role of the sympathetic nervous system by infusing glucose for 7 days in 4 groups of rats: L-NAME (L), L-NAME plus alpha- and beta-adrenergic receptor blockade (LB), vehicle, or vehicle plus adrenergic receptor blockade (blockers). Mean arterial pressure (MAP, 24 hours per day) increased significantly in both the vehicle and blockers groups, confirming our previous reports. Likewise, MAP increased significantly more during glucose infusion in the L rats, from 120+/-3 mm Hg to 158+/-4 mm Hg by day 7, which was >3 times the increase in the vehicle rats. Heart rate also increased significantly in the L rats, from 391+/-4 to 426+/-8 bpm, and that increase was prevented completely in the LB rats. However, although the increase in MAP in the LB rats was significantly less than in the L rats, the hypertension was not prevented completely. The explanation for that partial inhibition is not clear, but the overall effectiveness of adrenergic receptor blockade to attenuate the potentiated hypertensive and tachycardic responses to glucose infusion in the L-NAME-treated rats versus the normal rats suggests that nitric oxide may help protect against hypertension during glucose infusion through suppression of sympathetic activity.
authors.affiliation: Department of Physiology, University of Mississippi Medical Center, Jackson, USA.
authors.forename: Christie R
authors.initials: CR
authors.lastname: Claxton
authors.forename: Michael W
authors.initials: MW
authors.lastname: Brands
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000097:blood / Q000503:physiopathology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D011224:Prazosin / Q000031:analogs & derivatives* / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000097:blood; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000503:physiopathology
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D004791:Enzyme Inhibitors; D009569:Nitric Oxide; C041226:Terazosin; D011433:Propranolol; D019001:Nitric Oxide Synthase; D012083:Renin; D005947:Glucose; D019331:NG-Nitroarginine Methyl Ester; D011224:Prazosin