The hydronephrotic kidney of Inactin-anesthetized female Wistar rats was exteriorized in a controlled bath to directly observe preglomerular and postglomerular vessels via television microscopy. Nitrendipine, added to the bath in a concentration that did not alter blood pressure, induced a concentration-dependent dilation of preglomerular vessels. The arcuate artery maximally dilated by 29 +/- 4%, the interlobular artery by 24 +/- 5%, the afferent arteriole near the interlobular artery by 60 +/- 9%, and near the glomerulus by 28 +/- 13%. In contrast the efferent arteriole near the glomerulus dilated by only 11 +/- 6% and near the welling point by 7 +/- 9%. Similarly, diltiazem significantly dilated preglomerular vessels but not efferent arterioles. Acetylcholine significantly dilated all preglomerular vessels and dilated the afferent arterioles near the glomerulus (by 51 +/- 8%) to a greater extent than the calcium blockers. Acetylcholine also significantly dilated the efferent arterioles (near the glomerulus by 26 +/- 5% and near the welling point by 12 +/- 3%). These data suggest that the tone of the preglomerular vessels of the hydronephrotic kidney is more dependent on the entry of extracellular calcium through calcium antagonist-sensitive channels (i.e., potential dependent) than is the tone of the afferent arterioles near the glomerulus and the efferent arterioles.
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Fleming et al. (1987) studied this question.