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Am J Physiol Renal Physiol 258: F21-F27, 1990;
0363-6127/90 $5.00
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AJP - Renal Physiology, Vol 258, Issue 1 21-F27, Copyright © 1990 by American Physiological Society


ARTICLES

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

S. C. Thomson, B. J. Tucker, F. B. Gabbai and R. C. Blantz
Department of Medicine, University of California, San Diego, School of Medicine, La Jolla.

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.


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