Enhanced myogenic responsiveness of renal interlobular arteries in spontaneously hypertensive rats

We recently demonstrated that the interlobular artery (ILA) constricts in response to elevating renal arterial pressure (RAP), suggesting that the ILA contributes to renal autoregulation. In the present study, we examined the segmental myogenic responsiveness of the ILA in kidneys from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The tapered nature of the ILA allowed us to characterize the regional responsiveness, using the basal diameter to define segments as either proximal (greater than 60 μm), intermediate (40-60 μm), or distal (less than 40 μm). At 80 mm Hg, segmental diameters were similar in WKY and SHR arteries (proximal, 76.0±3.1 versus 71.6±3.5 μm; intermediate, 48.2±1.4 versus 48.1±1.7 μm; distal, 30.7±0.9 versus 27.9±1.3 μm for WKY and SHR, respectively). In both strains, intermediate and distal segments exhibited graded reductions in diameter as RAP was elevated, whereas proximal segments did not. Pressure-induced decrements in the diameters of distal ILA segments were similar in WKY (-24±2%) and SHR (-20±2%;p>0.1). The intermediate ILA of SHR exhibited an augmented myogenic responsiveness, constricting at lower RAP levels and exhibiting greater maximal decrements in diameter at 180 mm Hg (i.e., -19±2% and -12±2% for SHR and WKY, respectively; p<0.05). Nifedipine (1.0 μm) reduced pressure-induced vasoconstriction of intermediate and distal ILA segments by 56±11% and 79±7%, respectively, in WKY. In contrast, nifedipine completely abolished pressure responses of both segments in SHR kidneys, suggesting a greater involvement of calcium channels in mediating myogenic vasoconstriction of the ILA in SHR. In concert, these observations indicate an augmented myogenic reactivity of the intermediate ILA segment in SHR and suggest that this adaptation reflects an enhanced activity of calcium channels.