We have previously proposed that renal microvessels exhibit a unique regional heterogeneity. Studies with calcium channel agonists and antagonists suggest that potential-dependent calcium channels may play a more prominent role in the activation of the afferent arteriole than the efferent arteriole. Because KCl-induced depolarization elicits vasoconstriction exclusively by the activation of potential-dependent calcium channels, we tested this postulate directly by ascertaining the vasoconstrictor effects of KCl and countervailing effects of a calcium channel blocker on the afferent and efferent arteriole of isolated perfused hydronephrotic kidneys. Increasing media potassium concentration from 5 to 30 mM resulted in a marked renal vasoconstriction decreasing renal perfusate flow by 61 ± 4%. An examination of the microvascular response to KCl revealed a predominant response of the afferent arteriole. Thus afferent arteriolar diameter decreased by 38 ± 6% (i.e., from 20.7 ± 1.5 to 13.0 ± 1.8 μm, P < 0.005), whereas efferent arteriolar diameter decreased by only 12 ± 4% (i.e., from 15.8 ± 1.6 to 13.8 ± 1.4 μm, P = 0.05). Nifedipine completely returned afferent arteriolar diameter to control levels with a mean effective dose of 41 ± 2 nM. These findings indicate that the afferent arteriole is more responsive to depolarization-induced vasoconstrictor stimuli than is the efferent arteriole and suggest a greater prevalence of potential-dependent calcium channels in this vessel.
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Publication status||Published - 1989 Jan 1|
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