Visualization of renal autoregulation in the split hydronephrotic kidney of rats.
The autoregulatory ability of the renal vascular system in the split hydronephrotic kidney was quantitated with intravital microscopy. The luminal diameters of the arcuate and interlobular arteries as well as the afferent and efferent arterioles were measured. Glomerular blood flow was determined by the dual slit technique. In the first series of experiments, the renal perfusion pressure was reduced by graded clamping of the abdominal aorta. Pressure reduction from 118 mm Hg to 95 mm Hg induced dilation of all preglomerular vessels except for the distal afferent arteriole; there was no change in the efferent arteriole and the blood flow was maintained. Further pressure reductions to 71 and 43 mm Hg caused additional dilations of the preglomerular vessels, a marginal reduction in diameter of proximal efferent arterioles and flow reductions by 15% and 41%, respectively. In the second series, systemic blood pressure was increased by continuous i.v. infusions of norepinephrine (NE). NE constricted pre- and postglomerular vessels except for the distal afferent arteriole; glomerular flow was decreased. Reduction of renal perfusion pressure during NE infusion to the preinfusion value did not diminish glomerular blood flow, but reduced the constrictor response to NE in preglomerular vessels. In a third series of experiments we examined the effect of atrial natriuretic factor (ANF) on renal autoregulation. Addition of ANF (10(-9) to 10(-7) M) to the renal bath induced a dose-dependent dilation of all preglomerular vessels and a constriction of the efferent arteriole. Pressure reduction from 120 to 95 mm Hg resulted in a further preglomerular vasodilation. These experiments demonstrate that autoregulation is mediated primarily by diameter changes in all preglomerular vessels excluding the distal segment of the afferent arteriole. Further, these data suggest that ANF induced dilation of preglomerular vessels does not impair the myogenic response of these vessels.
I. Physiologisches, Institut, Universität Heidelberg, Federal Republic of Germany.
M
M
Steinhausen
M
M
Blum
J T
JT
Fleming
F G
FG
Holz
N
N
Parekh
D L
DL
Wiegman
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000502:physiology / Q000503:physiopathology; D005260:Female; D006706:Homeostasis; D006869:Hydronephrosis / Q000503:physiopathology*; D007668:Kidney / Q000502:physiology* / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000098:blood supply; D009638:Norepinephrine / Q000494:pharmacology; D010477:Perfusion; D011312:Pressure; D051381:Rats; D011919:Rats, Inbred Strains; D011920:Rats, Inbred WF; D012039:Regional Blood Flow / Q000187:drug effects; D012077:Renal Artery / Q000502:physiology* / Q000503:physiopathology; D012079:Renal Circulation / Q000187:drug effects
D000109:Acetylcholine; D009638:Norepinephrine