title: Functional subtypes of renal alpha1-adrenoceptor in diabetic and non-diabetic 2K1C Goldblatt renovascular hypertension.
abstract: OBJECTIVE
  This study investigates the subtypes of the alpha1-adrenoceptor mediating the adrenergically-induced renal vasoconstrictor responses in streptozotocin-induced diabetic and non-diabetic 2-kidney one clip (2K1C) Goldblatt hypertensive rats.
  
  
  METHODS
  The renal blood flow responses to renal nerve stimulation, noradrenaline, phenylephrine, and methoxamine were measured in the absence and presence of nitrendipine, 5-methylurapidil, chloroethylclonidine and BMY 7378.
  
  
  RESULTS
  The renal vasoconstrictor responses were markedly attenuated by nitrendipine and 5- methylurapidil in the diabetic rats (all P< 0.05). In the non-diabetic rats, these responses were markedly attenuated by nitrendipine, 5-methylurapidil, and BMY 7378 (all P< 0.05). In both experimental groups, chloroethylclonidine markedly accentuated the renal vasoconstrictions caused by all the adrenergic stimuli (all P< 0.05).
  
  
  CONCLUSIONS
  These observations indicate that alpha 1A-adrenoceptor subtypes play a major role in mediating adrenergically-induced renal vasoconstriction in the diabetic 2K1C Goldblatt hypertensive rats. In the non-diabetic 2K1C Goldblatt hypertensive rats, contributions of alpha 1A and alpha 1D-adrenoceptor subtypes were proposed. Apart from post-synaptic alpha 1-adrenoceptors, both in the diabetic and non-diabetic 2K1C Goldblatt hypertensive rats, the potential involvement of presynaptic alpha 1- adrenoceptors is also suggested.
authors.affiliation: School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang 11800, Malaysia.
authors.forename: A
authors.initials: A
authors.lastname: Armenia
authors.forename: Munavvar Abdul
authors.initials: MA
authors.lastname: Sattar
authors.forename: Nor Azizan
authors.initials: NA
authors.lastname: Abdullah
authors.forename: Md Abdul Hye
authors.initials: MA
authors.lastname: Khan
authors.forename: Edward James
authors.initials: EJ
authors.lastname: Johns
mesh_terms: D058646:Adrenergic alpha-1 Receptor Agonists; D058668:Adrenergic alpha-1 Receptor Antagonists; D000818:Animals; D003000:Clonidine / Q000031:analogs & derivatives / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply* / Q000294:innervation / Q000503:physiopathology; D008297:Male; D008729:Methoxamine / Q000494:pharmacology; D009568:Nitrendipine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D058646:Adrenergic alpha-1 Receptor Agonists; D058668:Adrenergic alpha-1 Receptor Antagonists; D010879:Piperazines; C057446:5-methylurapidil; D010656:Phenylephrine; C051731:chlorethylclonidine; D009568:Nitrendipine; D008729:Methoxamine; C053428:BMY 7378; D003000:Clonidine; D009638:Norepinephrine