Abstract
Background. Elevated dietary sodium intake exacerbates the elevation of blood pressure in spontaneously hypertensive rats (SHR) which is associated with increased renal vascular resistance and fluid reabsorption. The renal sympathetic nerves exert their action via alpha(1)-adrenoceptors (alpha(1)-AR) with alpha(1A) as the major subtype in regulating renal hemodynamics and excretory function.
Objectives. This study investigated whether the contribution of alpha(1A)-AR in regulating renal vasoconstriction and excretory function was enhanced in SHR receiving high sodium intake.
Material and Methods. SHR received either water (SHRNNa) or normal saline (SHRHNa) for six weeks. Metabolic cage studies followed by acute experiments were carried out on these SHR to examine renal vasoconstrictor and excretory responses to catecholamine viz. noradrenaline (NA), phenylephrine (PE) and methoxamine (ME) in the presence and absence of a alpha 1A-AR blocker, 5-methylurapidil (5-MeU).
Results. Daily water intake and urine output were increased in SHRHNa (P < 0.05 vs. SHRNNa). Renal cortical vascular responses to NA, PE and ME were enhanced in SHRHNa (P < 0.05 vs. SHRNNa) and the greatest effect was seen with ME. Intra-renal infusion of PE caused antidiuresis and antinatriuresis. Irrespective of the sodium intake, 5-MeU markedly blunted adrenergically induced renal cortical vasoconstrictions in SHR, while the antinatriuretic and antidiuretic responses to PE were inhibited by 5-MeU in SHRHNA only (P < 0.05).
Conclusions. The data suggest that, irrespective of the level of dietary sodium intake, alpha(1A)-ARs are the functional subtypes in SHR. However, there also appears to be a role for alpha(1A)-AR in mediating enhanced renal cortical vascular resistance, augmented tubular Na+ and water reabsorption in SHRHNa rats (Adv Clin Exp Med 2011, 20, 1, 47-55).