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—Experimental evidence  suggests that the acute hypertensive response induced in anephric  animals by infusion of a hypertonic saline solution is mediated by  disinhibition of the presynaptic sympathoinhibitory  α2 -adrenergic receptors (α2 -AR) of the  central nervous system. The purpose of the present  experiments was to dissect the role of the 3 distinct  α2 -AR subtypes (α2A -, α2B , -  and α2C -AR) in this response. Groups of genetically  engineered mice deficient in each one of these α2 -AR  subtype genes were submitted to bilateral nephrectomy followed by a  0.4-mL infusion of 4% saline over a 2-hour period, with constant  direct blood pressure (BP) monitoring. The  α2A -AR–deficient and α2C -AR–deficient  mice responded with significant BP elevations (by 11.8±2.5 and  16.7±1.7 mm Hg, respectively), and so did their wild-type  counterparts (17.8±2.5 and 11.8±2.0 mm Hg, respectively) and  the wild-type α2B +/+ (13.1±2.4 mm Hg). However,  the α2B -AR–deficient mice were unable to raise their BP  and had a slightly lowered BP (by −3.0±4.0 mm Hg) at the end of  the infusion period. All 6 groups exhibited elevated plasma  norepinephrine levels ranging between 0.8 and 1.8 ng/mL at  the end of the infusion. In all cases, the  α2 -AR–deficient groups tended to have higher  norepinephrine levels than their wild-type counterparts.  Surprisingly, this difference was significant only in the  α2B -AR–deficient mice, which, despite the elevated  norepinephrine, were unable to raise their BP. The data  suggest that a full complement of the α2B -AR is needed to  mediate the hypertensive response to acute saline load, even though its  absence does not prevent the release of norepinephrine  under these conditions.

Role of α 2 -Adrenergic Receptor Subtypes in the Acute Hypertensive Response to Hypertonic Saline Infusion in Anephric Mice

Role of α ₂ -Adrenergic Receptor Subtypes in the Acute Hypertensive Response to Hypertonic Saline Infusion in Anephric Mice