Renal effects of sympathetic activation
Increased sympathetic activity constricts the renal arterioles and increases sodium reabsorption, so the kidney holds on to salt and water and blood pressure rises.
Remember
Increased sympathetic activity to the kidney squeezes the renal arterioles, increases sodium reabsorption and stimulates renin release (renin is an enzyme that begins the renin-angiotensin-aldosterone system, or RAAS). The kidney therefore conserves salt and water.
The sympathetic nervous system is stimulated when blood pressure falls. Its nerve fibres supply the kidney, and when they fire more often, noradrenaline is released. Increased sympathetic activity at the kidney then has three linked effects, and each of them pushes blood pressure up.
The nerves constrict the renal arterioles, including the afferent arteriole (the small artery that delivers blood to the glomerulus, the kidney's filter). Less blood reaches the filter, so renal blood flow falls and so does the glomerular filtration rate (GFR, the volume of plasma filtered per minute). With less sodium filtered, less is lost in the urine.
They also act directly in the kidney to increase sodium reabsorption. Retained sodium brings water with it, the circulating volume expands, and blood pressure rises.
The nerves also stimulate the release of renin from the juxtaglomerular cells (granular cells next to the glomerulus that store renin). Renin begins the renin-angiotensin-aldosterone system (RAAS), which adds further sodium retention and vasoconstriction.
Together these effects make the kidney hold on to salt and water. While the sympathetic drive stays high, the pressure stays up, and overactivity of the renal nerves is therefore linked to hypertension.
Key facts
- Trigger
- The sympathetic nervous system is stimulated by a decrease in blood pressure.
- Arterioles
- Increased sympathetic activity constricts the renal arterioles, including the afferent arteriole, which lowers renal blood flow and GFR.
- Sodium
- The nerves act directly to increase sodium reabsorption, so sodium and water are retained.
- Renin
- Sympathetic stimulation of the juxtaglomerular cells, through beta-1 receptors (the receptors on these cells that noradrenaline acts on), increases renin release.
- Result
- Retained sodium brings water with it, the circulating volume expands and blood pressure rises.
Exam traps
- Sympathetic activity does not dilate the efferent arteriole (the vessel that drains the glomerulus) to increase renal plasma flow: it constricts renal vessels, and efferent dilation would also lower the pressure in the glomerulus.
- A rise in water excretion from reduced antidiuretic hormone (ADH, the hormone that makes the kidney conserve water) activity points the wrong way: reduced ADH activity would cause water loss and lower pressure, whereas sympathetic activity favours water retention.
- Renin is not released by the macula densa (cells that sense sodium chloride delivery) under alpha-1 control: it is stored in and secreted by the juxtaglomerular granular cells, and beta-1 receptors trigger that release.
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