Consequences of structural renovascular changes for renal barostat function.

During maximal vasodilatation the renal vascular beds of normotensive control rats (NCR), uninephrectomized NCR (U-NCR), spontaneously hypertensive rats (SHR), and two-kidney, one clip renal hypertensive rats (RHR) have been compared concerning glomerular filtration capacity, total renovascular resistance, and the relationship between perfusion pressure and glomerular filtration rate (GFR). The GFR reflects the important ratio between the preglomerular and postglomerular resistances that is a major determinant of GFR, and during maximal vasodilatation it shows whether, and how, this ratio is altered by differentiated renovascular structural adaptation. In SHR hypertension this ratio soon becomes increased to match the pressure rise as a result of structural changes, which implies a most efficient upward resetting of the renal barostat function. Later the postglomerular resistance is also raised in SHR as a result of structural changes. This adaptation presumably occurs to offset the gradual deterioration in glomerular filtration capacity. In the clipped, "low-pressure" RHR kidney, only the preglomerular resistance is reduced, a local adaptation tending to offset the effect of the artificial inflow hindrance on GFR as a result of structural changes. In the "pressure-exposed" RHR kidney the preglomerular and postglomerular resistances are both equally increased, again as a result of structural changes. In this situation, therefore, resetting of the renal barostat function occurs less efficiently than in SHR. This may explain the observation that arterial pressure readily normalizes in RHR on declipping. The hypertrophic U-NCR kidney shows a proportional and uniform outgrowth of the renovascular bed, thus without altering the pre-postglomerular resistance ratio.(ABSTRACT TRUNCATED AT 250 WORDS)