Effect of nitrendipine on autoregulation of perfusion in the cortex and papilla of kidneys from Wistar and stroke prone spontaneously hypertensive rats.

1. This investigation examined the autoregulatory efficiency of different vascular regions of the normotensive and stroke prone-spontaneously hypertensive rat (SP-SHR) kidney and determined how these myogenic responses were dependent upon extracellular calcium. In acute studies, renal autoregulatory blood perfusion curves for cortex and papilla were generated, autoregulatory indices (AI's) calculated as a ratio of the perfusion change divided by the ratio of the pressure difference where zero represents perfect and 1 equates to no autoregulation. The influence of a calcium channel antagonist on this AI was measured at both cortex and papilla. 2. Rats were anaesthetized with sodium pentobarbitone, the kidney exposed and cortical and papillary perfusion measured by Laser-Doppler flowmetry. Groups of rats either received no drug or nitrendipine at either 0.125 or 0.25 micrograms kg-1 min-1. 3. In the Wistar normotensive rats there was efficient autoregulation in the cortex (AI = 0.21 +/- 0.17), from 127 to 90 mmHg, but not in the papilla (AI = 0.89 +/- 0.08), while below 90 mmHg perfusion in both regions decreased with renal perfusion pressure. Nitrendipine attenuated cortical autoregulation at the higher pressure range (AI = 0.62 +/- 0.13 and 0.92 +/- 0.10 at the low and high dose, respectively) while having no effect on the papillary pressure perfusion pattern. 4. In the SP-SHR, reduction in renal perfusion pressure, from 150 to 100 mmHg, gave a cortical AI of 0.49 +/- 0.10, indicating impaired autoregulation, whereas the papilla demonstrated little myogenic response. Over the high pressure range in the presence of both doses of nitrendipine there was neither cortical (AI of 0.75 +/- 0.11 and 0.94 +/- 0.12, respectively) nor papillary autoregulation. 5. Autoregulation in the renal cortex but not papilla of the young Wistar rats is well developed. The myogenic responses are attenuated by the calcium channel antagonists suggesting that they are dependent upon the availability of extracellular calcium. Cortical autoregulation in the SP-SHR is deficient compared to the normotensive rats and is further impaired by the calcium channel antagonists.