Intrarenal ‘vascular reflexes’
Physiology and pharmacology
The ‘starting pressure’ is determined by the blood flow to the kidneys and most importantly to the afferent glomerular arteriole, as discussed in the previous section. Glomerular autoregulation then comes in to play to ensure that the pressure within the glomerular tuft is in the optimal range for filtration to occur.
The flow into the glomerular ‘tuft’ (and therefore pressure within the tuft) can be maintained in the face of falling renal blood flow by dilatation of the afferent glomerular arteriole. Increase in the outgoing resistance will also maintain perfusion pressure within the glomerular tuft, in the face of reduced flow. This efferent arteriolar constriction is mediated by local angiotensin II production. This can be thought of as the ‘hose-pipe effect’: Pressure in the hose can be increased by turning the tap up, or partially blocking the end of the hose.
Overall, these reflexes act to maintain the perfusion pressure within the glomerulus at an optimal level, compensating for changes in renal blood flow. Thus, in the normal kidney, changes in intravascular volume status may affect renal blood flow, but have no effect on glomerular perfusion pressure because of these reflexes. Autoregulation happens also in the cerebral and coronary circulations; other tissues particularly dependent on maintaining perfusion.
This can be summarised as follows:
- Glomerular Filtration Rate is determined by the pressure in the glomerular capillaries (Glomerular Perfusion Pressure)
- Glomerular Perfusion Pressure is determined by the blood flow into the glomerulus and the outgoing resistance to flow (Efferent Arteriolar Resistance)
- The blood flow into the glomerulus is determined by overall renal blood flow and the tone in the afferent arteriole supplying the glomerulus
- The outgoing resistance is determined by the tone in the efferent arteriole draining the glomerulus
- Afferent arteriolar dilatation (increasing flow) is mediated by prostaglandin E2
- Efferent arteriolar constriction (increasing pressure) is mediated by angiotensin II