title: Alpha1B-adrenoceptors mediate adrenergically-induced renal vasoconstrictions in rats with renal impairment.
abstract: OBJECTIVE
  This study examined whether alpha1B-adrenoceptors are involved in mediating adrenergically-induced renal vasoconstrictor responses in rats with pathophysiological and normal physiological states.
  
  
  METHODS
  Male Wistar Kyoto and spontaneously hypertensive rats were induced with acute renal failure or experimental early diabetic nephropathy by cisplatin or streptozotocin, respectively. Cisplatin-induced renal failure was confirmed by impaired renal function and pronounced tubular damage. Experimental early diabetic nephropathy was confirmed by hyperglycemia, changes in physiological parameters, and renal function. The hemodynamic study was conducted on anesthetized rats after 7 d of cisplatin (renal failure) and 4 weeks of streptozotocin (experimental early diabetic nephropathy).
  
  
  RESULTS
  In the rats with renal failure and experimental early diabetic nephropathy, there were marked reductions in their baseline renal blood flow (P<0.01). The baseline mean arterial blood pressure was either unaltered or lower (all P>0.05) in the renal failure and experimental early diabetic nephropathy rats, respectively, as compared to their non-renal failure and non-diabetic nephropathy controls. In the rats with renal impairment, chloroethylclonidine caused either accentuation or attenuation (all P<0.01) of the renal vasoconstrictor responses elicited by the adrenergic stimuli. However, in the non-renal failure and in the non-diabetic nephropathy rats, chloroethylclonidine did not cause any alteration in such responses (P>0.05).
  
  
  CONCLUSIONS
  This study demonstrated the presence of functional alpha1B-adrenoceptors that mediated the adrenergically-induced renal vasoconstrictions in rats with renal impairment, but not in rats with normal renal function.
authors.affiliation: School of Pharmaceutical Sciences, Universiti Sains Malaysia, 11800 Penang, Malaysia. abdul_hye_khan@yahoo.com
authors.forename: Md Abdul Hye
authors.initials: MA
authors.lastname: Khan
authors.forename: Munavvar-Abdul
authors.initials: MA
authors.lastname: Sattar
authors.forename: Nor Azizan
authors.initials: NA
authors.lastname: Abdullah
authors.forename: Edward James
authors.initials: EJ
authors.lastname: Johns
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D003000:Clonidine / Q000031:analogs & derivatives / Q000494:pharmacology; D003928:Diabetic Nephropathies / Q000503:physiopathology; D066298:In Vitro Techniques; D007674:Kidney Diseases / Q000503:physiopathology*; D008297:Male; D009129:Muscle Tonus / Q000187:drug effects; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D012079:Renal Circulation / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D018340:Receptors, Adrenergic, alpha-1; C051731:chlorethylclonidine; D003000:Clonidine