Glomerular hemodynamics and alpha 2-adrenoreceptor stimulation: the role of renal nerves

We evaluated the effects of alpha 2-adrenoceptor stimulation on the determinants of nephron filtration rate (SNGFR) using micropuncture in Munich-Wistar rats. Micropuncture was performed in animals 5-7 days after sham surgery (group 1) or renal denervation (DNX) (groups 2, 3, and 4). Glomerular hemodynamic measurements were made before and during a systemic infusion of the alpha 2-agonist, B-HT 933 (1.0 mg.kg-1.h-1) (groups 1, 2, and 3). Group 3 rats were pretreated with the alpha 2-antagonist, yohimbine (3 mg.kg-1.h-1). In group 4, hydralazine was substituted for B-HT 933 to dissociate specific alpha 2-effects from nonspecific effects on blood pressure. Arterial pressure declined by similar amounts between experimental periods in groups 1, 2, and 4. In group 1, B-HT 933 caused SNGFR to increase due to an increment in nephron plasma flow. In group 2, B-HT 933 caused SNGFR to decrease due to a decrement in glomerular ultrafiltration coefficient (LpA). In groups 3 and 4, SNGFR was unaffected by B-HT 933 or hydralazine. Ligand-binding studies in glomerular membranes documented the presence of alpha 2-adrenoreceptors (275 +/- 22 fmol/mg protein). Receptor density was not altered by DNX. These observations could be explained by an alpha 2-mediated inhibition of renal nerve activity combined with intrinsic sympathomimetic effects not dependent on renal nerves, with the latter effects unmasked by DNX and manifested by a decrease in LpA.