The contribution of α1B-adrenoceptor subtype in the renal vasculature of fructose-fed Sprague-Dawley rats.
OBJECTIVE
Fructose feeding induces a moderate increase in blood pressure, insulin resistance, and hyperinsulinemia. This study investigated the role of α(1B)-adrenoceptor subtype in the control of renal hemodynamic responses to exogenously administered angiotensin II (Ang II) and a set of adrenergic agonists in a model of high fructose-fed rats.


METHODS
Sprague-Dawley rats were fed for 8 weeks with 20% fructose in drinking water (FFR). The renal cortical vasoconstriction to noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II in the presence and absence of chloroethylclonidine (CEC) (α(1B)-adrenoceptor antagonist) was determined. Data, mean ± SEM or SD were subjected to ANOVA with significance at p < .05.


RESULTS
FFR showed significant increase in the systolic blood pressure, plasma glucose, and insulin levels when compared to control. FFR expressed reduced renal cortical vascular sensitivity to NA, PE, ME, and Ang II. Furthermore, renal cortical vasoconstriction response to NA, PE, ME, and Ang II was blunted in the presence of CEC in control. While in FFR, renal cortical vasoconstriction to NA, PE, and ME was enhanced by CEC. Renal cortical vasoconstriction to Ang II in FFR was reduced in the presence of CEC.


CONCLUSIONS
In the presence of a hyperinsulinemic state resulting from chronic and high fructose feeding, an attenuated AT(1) and α(1)-adrenoceptors response to Ang II and adrenergic stimuli respectively, is expected. In addition, α(1B)-adrenoceptor is the functional subtype that mediates renal cortical vasoconstriction in control rat, while high fructose feeding did influence the functionality of α(1B)-adrenoceptor in mediating the renal cortical hemodynamic changes.
Abdulla
Mohammed H
MH
School of Pharmaceutical Sciences, Universiti Sains Malaysia, Minden, 11800, Penang, Malaysia. mdapharm78@yahoo.co.uk
Sattar
Munavvar A
MA
Abdullah
Nor A
NA
Hye Khan
Md Abdul
MA
Anand Swarup
Kolla R L
KR
Johns
Edward J
EJ
D058646:Adrenergic alpha-1 Receptor Agonists / Q000008:administration & dosage / Q000494:pharmacology; D058668:Adrenergic alpha-1 Receptor Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D004040:Dietary Carbohydrates / Q000009:adverse effects*; D004305:Dose-Response Relationship, Drug; D005632:Fructose / Q000009:adverse effects*; D006439:Hemodynamics / Q000187:drug effects; D006943:Hyperglycemia / Q000209:etiology; D006946:Hyperinsulinism / Q000209:etiology / Q000503:physiopathology*; D006973:Hypertension / Q000209:etiology*; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects / Q000503:physiopathology; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D018340:Receptors, Adrenergic, alpha-1 / Q000737:chemistry / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology
C547718:Adra1b protein, rat; D058646:Adrenergic alpha-1 Receptor Agonists; D058668:Adrenergic alpha-1 Receptor Antagonists; D004040:Dietary Carbohydrates; D044140:Receptor, Angiotensin, Type 1; D018340:Receptors, Adrenergic, alpha-1; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D005632:Fructose