The role of α1B-ARs in regulating renal hemodynamic and renal functions in hypertensive rats; impact of high dietary sodium intake

Abstract

Background: Renal α1B-adrenoreceptors (α1-ARs) contributes to the pathogenesis of hypertension in spontaneously hypertensive rats (SHR). The present study examined the role of α1B-ARs in renal hemodynamic and tubular functions in SHR subjected to high-salt diet (SHRHNa) for 6 weeks. Methods: Renal cortical vasoconstriction to noradrenaline (NA), phenylephrine (PE), and methoxamine (ME) in presence and absence of chloroethylclonidine (CEC) was measured in SHRHNa and SHR on normal sodium diet (SHRNNa). Renal tubular functional responses to PE and CEC were assessed as a measure of insulin clearance. Results: SHRHNa showed no significant change in the mean arterial pressure (MAP) as compared to SHRNNa. SHRHNa expressed enhanced renal cortical vascular sensitivity to NA, PE, and ME. Furthermore, renal vasoconstrictor response to NA, PE and ME was accentuated in the presence of CEC in SHRNNa. On the other hand in SHRHNa, renal cortical vasoconstriction to NA and ME was inhibited by CEC. However tubular response to PE was inhibited by CEC in SHRNNa and remains unaffected in SHRHNa. Conclusion: Thus it is concluded that, augmented α1-adrenergic response to adrenergic stimuli contribute to salt-related increase in renal vascular sensitivity in SHRHNa and these changes were independent of any further increase in MAP in SHRHNa. Irrespective of dietary sodium changes, α1-ARs are involved in mediation of tubular functions like antinatriuresis and antidiuresis of SHR. In addition, α1B-ARs are the functional subtypes that mediate renal cortical vasoconstriction in SHRHNa and tubular function in SHRNNa, while high sodium in SHR did not influence the functionality of α1B-ARs in mediating tubular functions.