Calcium ion dependence of myogenic renal plasma flow autoregulation: evidence from the isolated perfused rat kidney.

1. The independent roles of Ca2+ and glomerular filtration in the control of renal plasma flow autoregulation were examined in the isolated perfused rat kidney. Control kidneys autoregulated plasma flow between perfusion pressures of 120 and 160 mmHg. 2. Complete ischaemia, induced by clamping of the renal artery cannula for 1 h induced relative vasoconstriction and a loss of autoregulatory capacity. 3. The addition of either nifedipine (10(-7) M) or verapamil (10(-4) M) to the perfusion medium produced vasodilation and a loss of autoregulation. 4. Kidneys that were rendered non-filtering by raising the perfusate albumin concentration from 65 to 100 g/l appeared to shift autoregulatory capacity to a higher pressure range, whereas raising it to 150 g/l reduced autoregulation at all pressures studied. 5. The addition of ouabain (10(-3) M) restored autoregulation to the lower pressure range in non-filtering kidneys perfused with an albumin concentration of 100 g/l. Ouabain-treated non-filtering kidneys displayed a loss of autoregulation when perfused either with nifedipine or with reduced perfusate Ca2+. 6. Plasma flow was reduced in isolated kidneys perfused at pressures of 100 or 150 mmHg when ionized Ca2+ in the medium was raised from 0 to 1.8 mM. However, no decrement in flow was observed in kidneys perfused at 50 mmHg when ionized Ca2+ in the perfusate was raised to the same level. Thus the vasoconstrictive effect of raised ionized Ca2+ was pressure-dependent. 7. We conclude that renal plasma flow autoregulation occurs in the isolated kidney in the absence of glomerular filtration and is at least in part a myogenic phenomenon. Myogenic control of renal plasma flow autoregulation is regulated by smooth muscle permeability to Ca2+. Changes in smooth muscle Ca2+ permeability appear to be pressure-regulated.