Theoretical modeling suggests that high juxtaglomerular contractility can only be attributed to a myogenic mechanism if extravascular pressure in the juxtaglomerular segment is subatmospheric.
Preclinical resistance localization warrants no clinical translation; leaves open myogenic attribution without subatmospheric pressures.
To examine whether local myogenic mechanisms account for autoregulation of renal blood flow, a theoretical analysis was undertaken on a model of the pre-glomerular vascular tree consisting of a main and a short, narrow juxtaglomerular segment. At atmospheric extravascular pressure in vitro data are consistent with a relationship r=r0(1 + k - pk) between radius (r) and transmural pressure (p) at p > 60 mmHg, where k can be estimated from in vitro data and r=r0 at complete autoregulatory vasodilation. After introducing r=r(0)(1 + k - pk), Poiseuille's formula was integrated along the main segment, Deltax long, between arterial pressure P(1) and P(2) at the end of the main segment. At the lowest autoregulatory pressure P(1)=65 mmHg pre-glomerular blood flow is F=5Kr(0)(4)/Deltax. At P(1)=140 mmHg a pressure drop of only 17 mmHg to P2=123 mmHg is sufficient to fulfil the criterion for complete autoregulation: F=5Kr(0)(4)/Deltax. Thus, 80% of the total pre-glomerular vascular resistance is localized to the juxtaglomerular segment. Loop diuretics may abolish juxtaglomerular contractility. Calculated flow/pressure relationships after eliminating juxtaglomerular contractility are similar to those obtained after administering ethacrynic acid. If a constant tension hypothesis (r=60r(0)/p) rather than the transmural pressure hypothesis [r=r(0)(1 + k - pk)] applies, complete autoregulation is maintained to P(2)=89 mmHg, but the effect of loop diuretics is not mimicked. In conclusion, high juxtaglomerular contractility may be attributed to a myogenic mechanism only if extravascular pressure in the juxtaglomerular segment is subatmospheric.
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Fredrik Kiil (2002) studied this question.
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