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Extrinsic GFR Regulation: Sympathetic Nervous System
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Extrinsic GFR Regulation: Sympathetic Nervous System

Extrinsic GFR Regulation: Sympathetic Nervous System
The sympathetic division of the nervous system is an extrinsic mechanism of GFR regulation.
It is activated when mean arterial blood pressure drops below 80 mmHg.
Sympathetic activation rapidly induces vasoconstriction of the arterioles to the glomerulus to reduce GFR and to divert blood away from the kidneys to support other body tissues: the kidneys typically receive 20-25 % of total cardiac output, when this extrinsic regulator is activated, the percentage is much less.
This is particularly important in response to hemorrhage, in which loss of blood volume lowers blood pressure, so blood is shunted away from the kidneys to avoid body tissue necrosis.
Sympathetic Regulation Steps:
Low blood pressure decreases carotid sinus activity.
Cardiovascular centers of medulla in brainstem respond by releasing norepinephrine via sympathetic nerves.
Norepinephrine activates alpha 1 receptors on arterioles, initiates vasoconstriction. – Because afferent arteriole has more alpha 1 receptors, it constricts to a greater degree. – This reduces renal blood flow, hydrostatic capillary pressure, and GFR.
Norepinephrine also activates beta 1 receptors of juxtaglomerular cells of afferent arteriole, which induces renin release.
In the bloodstream, renin catalyzes hormonal conversion that eventually leads to production of angiotensin II.
Angiotensin II induces vasoconstriction, especially of the efferent arteriole.
Ultimately, both RBF and GFR are reduced in response to sympathetic stimulation.
See Renin-Angiotensin System
See Intrinsic Mechanisms of GFR regulation

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