Distention of the lateral intercellular spaces (LIS) in the proximal tubule cells of the non-stenosed kidney of the 2K-1C Goldblatt model of hypertension as evidence of pressure diuresis

This study shows the development of two major deformities in the non-stenosed kidney of the 2K-1C Goldblatt model; namely the widening of the LIS and the enlargement of the basilar interdigitations of the proximal tubule cells. These deformities were much less in the 2K-1C animals treated with the angiotensin I converting enzyme inhibitor (AICEI) cilazapril. From these findings it is suggested that the non-stenosed kidney is operating under the diuretic effect of the elevated systemic blood pressure (SBP) via an increase in the renal interstitial hydrostatic pressure (RIHP). Therefore, the AII antidiuretic effect is masked by the diuretic effect of the elevated SBP. The suggested rise in urine output fits well with the idea that kidneys lose water and sodium when SBP increases enormously. Therefore, in this model of hypertension, the non-stenosed kidney tries to lower SBP by losing water and sodium, an excretion behavior which is opposite to that of the stenosed kidney. Thus, the rise in SBP in this model is probably due to an increase in the vascular peripheral resistance rather than fluid accumulation.