There are other renal mechanisms which can have major effects on water excretion and which act independently of the thirst-ADH effector system discussed above. These are additional effector mechanisms which are important and which all act to alter renal water or sodium excretion.
The major additional mechanisms which act at the local renal level are:
- Glomerulotubular Balance
- Intrinsic Pressure-Volume Control System
Glomerulotubular balance is a strictly local renal mechanism. It refers to the finding that the proximal tubule tends to reabsorb a constant proportion of the glomerular filtrate rather than a constant amount. The effect of this is to minimise the effect of changes in GFR on sodium and water excretion.
How does this mechanism work? This is not completely understood but there are probably several factors involved. Changes in oncotic pressure are undoubtably important and the mechanism can be understood from a consideration of this factor alone. Changes in hydrostatic pressure & in delivery of certain solutes to the proximal tubule are probably also involved.
When GFR increases, the protein concentration (& oncotic pressure) in the efferent arteriole is immediately increased resulting in increased oncotic pressure in the peritubular capillaries. This results in an increased gradient favouring reabsorption and counteracts (balances) the effect of an increased GFR on volume of fluid leaving the proximal tubule. This is a self-regulating mechanism acting locally. It has effects on water excretion if the oncotic pressure of plasma is lowered.
Autoregulation of Renal Blood Flow
Autoregulation of renal blood flow is another local renal mechanism which has effects on water excretion. If the renal perfusion pressure increases, the afferent arterioles vasoconstrict so that renal plasma flow (RPF) and GFR are maintained constant. The mechanism of this pressure autoregulation is not understood but may be due to a local myogenic response (ie. the vascular smooth muscle of the afferent arteriole may respond to the increased stretch by contracting and increasing afferent arteriolar resistance). Most likely however, other renal mechanisms such as tubulo-glomerular feedback are important.
RPF and GFR are autoregulated and kept fairly constant and this greatly minimises the effect of changes in BP on urine output. However urine flow is not autoregulated! An increase in blood pressure will cause an increase in urine flow even though GFR is minimally affected. How can this be so? The increase in GFR is small but may still result in a significant increase in urine flow even though most of the effect of the increased GFR is buffered by the glomerulotubular balance mechanism. This is a local renal mechanism which is of major importance in maintenance of a constant intravascular volume. The altered blood pressure will also have effects on ADH secretion via carotid baroreceptor input and this will affect water excretion in the same direction as the local renal mechanism.
Intrinsic Pressure-Volume Control System
The pressure-volume control system mentioned above is the intrinsic control system for maintaining a constant blood volume.
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