Neuroendocrine Regulation of GFR and RBF
| Overview |
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- A variety of neuroendocrine factors regulate Renal Blood Flow (RBF) and Glomerular Filtration Rate (GFR) by modulating the resistance of the renal afferent and efferent arterioles. The regulatory mechanisms of these neuroendocrine mediators are diverse and discussed in detail elsewhere. Here we only outline these factors and briefly mention their effect on the GFR and RBF.
| Neuroendocrine Factors |
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- Angiotensin II
- Angiotensin II, released as part of the Renin-Angiotensin-Aldosterone System (RAAS), directly induces vasoconstriction of the renal efferent arterioles and in doing so increases the GFR while decreasing the RBF (See: RAAS).
- Sympathetic Nervous System (SNS)
- The SNS and circulating catecholamines induce vasoconstriction of both renal afferent and efferent arterioles thus reducing both GFR and RBF (See: SNS - Renal Effects).
- Prostoglandins
- Prostaglandins PGE2 and PGI2 are locally released and prevent excessive vasoconstriction of the renal afferent and efferent arterioles. This is especially important in contexts where there is significant glomerular SNS tone and Angiotensin II concentrations as might be occur during contexts of considerable hypotension, such as volume depletion or major hemorrhages. In the absence of prostaglandins, excessive neuroendocrine-mediated vasoconstriction of the afferent and efferent arterioles can lead to disastrous drops in renal blood flow and trigger infarctions. This is why aspirin administration in context of low circulating volumes is a risk factor for renal infarctions.