Renal vasodilation and uncoupling of blood flow and filtration rate autoregulation.

Renal vasodilation and uncoupling of blood flow and filtration rate autoregulation. Renal vasodilation experiments were conducted in dogs to examine the mechanism by which the kidney continues to autoregulate glomerular filtration rate during decreased blood flow autoregulatory efficiency. Following intraarterial infusions of acetylcholine, dopamine, papaverine or prostaglandin E 2 (PGE 2 ), renal blood flow increased by 40 to 100%, intrarenal venous pressure increased by 45 to 120%, and urine flow increased up to fivefold. GFR was not altered significantly except for a decrease observed during papaverine infusion. The magnitude of the diuretic responses was not directly related to either the increase in renal blood flow or the increase in intrarenal venous pressure. Blood flow autoregulatory efficiency during reductions in arterial pressure was decreased to a variable extent and most markedly with acetylcholine. Efficiency of GFR autoregulation was well maintained during vasodilation with acetylcholine, dopamine and PGE 2 . Intrarenal venous pressure and glomerular pressure (computed on the basis of minimal pre-glomerular resistance measurements) were elevated during vasodilation and became more responsive to changes in arterial pressure. The results indicate that while renal vasodilation decreases both pre- and post-glomerular resistances, a net increase in glomerular pressure occurs. The increase in intrarenal venous pressure suggests that proximal tubular pressure increases to offset the increased glomerular pressure. The concomitant changes in intrarenal venous pressure and glomerular pressure during reductions in arterial pressure suggest further that maintenance of effective filtration pressure and thus GFR during vasodilation may be effected by changes in proximal tubular pressure associated with the changes in glomerular pressure. Vasodilatation renale et dissociation de l'autoregulation du debit sanguin renal et du debit de filtration. Des experiences de vasodilatation renale ont ete realisees chez des chiens afin d'etudier le mecanisme par lequel le rein continue a reguler le debit de filtration glomerulaire alors que l'efficacite de la regulation du debit sanguin est diminuee. Apres la perfusion intra-arterielle d'acetylcholine, de dopamine, de papaverine ou de prostaglandine E 2 (PGE 2 ), le debit sanguin renal a augmente de 45 a 120% et le debit urinaire augmente jusqu'a 5 fois. Le debit de filtration glomerulaire n'a pas ete significativement modifie a l'exception d'une diminution observee au cours de la perfusion de papaverine. Aucune correlation n'a pu etre etablie entre l'importance de la reponse diuretique et l'augmentation du debit sanguin renal d'une part et l'augmentation de la pression veineuse intra-renale d'autre part. L'efficacite de l'autoregulation du debit sanguin renal en presence de diminutions de la pression arterielle a ete diminuee de facon variable, la diminution la plus importante a ete observee avec l'acetylcholine. L'efficacite de l'autoregulation du debit de filtration glomerulaire a ete bien maintenue au cours de la vasodilatation par l'acetylcholine, la dopamine et le PGE 2 . La pression veineuse intra-renale et la pression glomerulaire (calculees a partir de mesures de la resistance pre-glomerulaire minimale) ont ete plus influencees par les variations de la pression arterielle dans les situations de vasodilatation. Le resultat de ces experiences indique qu'alors que la vasodilatation renale diminue a la fois les resistances pre et post glomerulaires la pression glomerulaire augmente. L'augmentation de la pression veineuse intra-renale suggere que la pression tubulaire proximale augmente pour compenser l'augmentation de la pression glomerulaire. Les modifications concomitantes de la pression veineuse intra-renale et de la pression glomerulaire au cours des reductions de la pression arterielle indiquent que le maintien d'une pression effective de filtration, et donc du debit de filtration glomerulaire, au cours de la vasodilatation est effectue par une modification de la pression tubulaire proximale associee aux changements de la pression glomerulaire.