Despite autoregulation, renal haemodynamics vary considerably. Autoregulation means that changes in blood pressure per se in the autoregulatory range have little effect on blood flow, but it does not mean that blood flow is always constant. In many circumstances (e.g. physical or mental stress, haemorrhage), there are increases in the sympathetic nervous activity to the kidney (and to other parts of the body), causing vasoconstriction and, hence, a reduction in renal blood flow, even though the perfusion pressure is still in the autoregulatory range. This suggests that the kidneys play a part in maintaining systemic blood pressure, rather than reacting passively to it.
Figure RE.4 Autoregulation of renal blood flow
Other mechanisms include:
• Renal prostaglandin production—renal vasoconstriction in response to renal sympathetic nerve activity is attenuated to some extent by the intrarenal production of vasodilator prostaglandins
• Angiotensin II—when the renal blood flow is reduced, there is generally an increased filtration fraction, brought about by efferent arteriolar vasoconstriction (mediated by angiotensin II), so that GFR tends to be maintained
• Tubulo glomerular feedback mechanism—this mechanism may also contribute significantly to renal autoregulation
• Vaso-active agents—the regulation of GFR also involves other vaso-active agents, which are present within blood vessel walls throughout the body, but may be of particular importance in the kidney, including endothelin (vasoconstrictor) and the vasodilator nitric oxide
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