title: Analysis of responses to valerian root extract in the feline pulmonary vascular bed.
abstract: OBJECTIVE
  This study was undertaken to investigate pulmonary vascular response to valerian (Valeriana officinalis) in the feline pulmonary vasculature under constant flow conditions.
  
  
  METHODS
  In separate experiments, the effects of NG-L-nitro-L-arginine methyl ester (L-NIO), a nitric oxide synthase inhibitor, glibenclamide, an adenosine triphosphate (ATP)-sensitive potassium (K+) channel blocker, meclofenamate, a nonselective cyclooxygenase (COX) inhibitor, bicuculline, a GABA(A) receptor antagonist, and saclofen, a GABA(B) antagonist, were investigated on pulmonary arterial responses to various agonists in the feline pulmonary vascular bed. These agonists included valerian, muscimol, a GABA(A) agonist, SKF-97541 a GABA(B) agonist, acetylcholine (ACh), and bradykinin, both inducers of nitric oxide synthase, arachidonic acid, a COX substrate, and pinacidil, an ATP-sensitive K+ channel activator, during increased tone conditions induced by the thromboxane A2 mimic, U46619.
  
  
  METHODS
  Laboratory investigation.
  
  
  METHODS
  Mongrel cats of either gender.
  
  
  METHODS
  Injections of the abovementioned agonists and antagonists were given.
  
  
  METHODS
  Baseline pulmonary tone, responses to the agonists, and responses to the agonists after injections of antagonists were all measured via a pulmonary catheter transducer and recorded.
  
  
  RESULTS
  Valerian root extract is a potent smooth muscle dilator in the feline pulmonary vascular bed. The vasodilatory effects of valerian root extract were unchanged after the administration of L-NIO, glibenclamide, and meclofenamate. These effects were ablated, however, by both saclofen and bicuculline. The ability of saclofen and bicuculline to modulate the dilatory effects of valerian root extract was not statistically different.
  
  
  CONCLUSIONS
  The vasodilatory effects of valerian root extract are mediated by a nonselective GABA mechanism.
authors.affiliation: Flushing Hospital Medical Center, Flushing, NY, USA.
authors.forename: Aaron M
authors.initials: AM
authors.lastname: Fields
authors.forename: Todd A
authors.initials: TA
authors.lastname: Richards
authors.forename: Jason A
authors.initials: JA
authors.lastname: Felton
authors.forename: Shaili K
authors.initials: SK
authors.lastname: Felton
authors.forename: Erin Z
authors.initials: EZ
authors.lastname: Bayer
authors.forename: Ikhlass N
authors.initials: IN
authors.lastname: Ibrahim
authors.forename: Alan David
authors.initials: AD
authors.lastname: Kaye
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology; D001920:Bradykinin / Q000494:pharmacology; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002415:Cats; D004195:Disease Models, Animal; D005260:Female; D006973:Hypertension / Q000139:chemically induced; D008297:Male; D009118:Muscimol / Q000494:pharmacology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D005996:Nitroglycerin / Q000494:pharmacology; D009943:Organophosphorus Compounds / Q000494:pharmacology; D008517:Phytotherapy; D020110:Pinacidil / Q000494:pharmacology; D010936:Plant Extracts / Q000494:pharmacology; D018517:Plant Roots; D011651:Pulmonary Artery / Q000187:drug effects*; D011652:Pulmonary Circulation / Q000187:drug effects*; D051381:Rats; D013997:Time Factors; D014632:Valerian; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D002120:Calcium Channel Agonists; D020030:Nitric Oxide Donors; D009943:Organophosphorus Compounds; D010936:Plant Extracts; C068457:3-aminopropyl(methyl)phosphinic acid; D009118:Muscimol; D016718:Arachidonic Acid; D020110:Pinacidil; D005996:Nitroglycerin; D000109:Acetylcholine; D001920:Bradykinin