Sympathetic nerve fibers have an innervation in the glomerulus, as well as the cells of the nephron, specifically the afferent and efferent arterioles. When the extracellular fluid volume (ECFV) contracts, the activation of low and high-pressure vascular baroreceptors results in the stimulation of sympathetic nerve activity, including those fibers that innervate the kidneys. This stimulation has several effects: 

1. Constriction of the afferent and efferent arterioles occurs, with a greater impact on the afferent arteriole. This vasoconstriction, mediated by α-adrenergic receptors, reduces the hydrostatic pressure within the glomerular capillary lumen, resulting in a decrease in glomerular filtration rate (GFR) and a reduction in filtered Na+.

2. Renin secretion is stimulated by the cells of the afferent arterioles, mediated by β-adrenergic receptors. This ultimately leads to increased circulating levels of angiotensin II and aldosterone, which in turn stimulate Na+ reabsorption by the nephron.

3. NaCl reabsorption along the nephron is directly stimulated by α-adrenergic receptors on the cells of the nephron. The proximal tubule experiences the largest effect due to the substantial amount of Na+ reabsorption taking place in this segment. Consequently, increased renal sympathetic nerve activity decreases NaCl excretion, helping to restore ECFV to normal levels. Conversely, when ECFV expands, renal sympathetic nerve activity is reduced, reversing the previously described effects.

The juxtaglomerular cells, also known as granular cells, located in the afferent arterioles, play a vital role in the synthesis, storage, and release of the proteolytic enzyme renin. Three factors influence the stimulation of renin secretion:

1. Perfusion pressure: When perfusion pressure to the kidneys decreases, renin secretion is stimulated. Conversely, an increase in perfusion pressure inhibits renin release.

2. Sympathetic nerve activity: Activation of sympathetic nerve fibers innervating the afferent arterioles increases renin secretion, mediated by β-adrenergic receptors.

Renin secretion decreases as renal sympathetic nerve activity decreases.
, sympathetic nerve fibers innervate the afferent and efferent arterioles of the glomerulus as well as the cells of the nephron. With ECFV contraction, activation of the lowand high-pressure vascular baroreceptors results in stimulation of sympathetic nerve activity, including those fibers innervating the kidneys. This stimulation has the following effects: 1.
The afferent and efferent arterioles are constricted (mediated by α-adrenergic receptors). This vasoconstriction (the effect is greater on the afferent arteriole) decreases the hydrostatic pressure within the glomerular capillary lumen, which results in a decrease in GFR. With this decrease in GFR, the filtered amount of Na+ is reduced.
2.
Renin secretion is stimulated by the cells of the afferent arterioles (mediated by β-adrenergic receptors). As • BOX 35.1 Signals Involved in Control of Renal NaCl and Water Excretion
Renal Sympathetic Nerves (↑Activity: reabsorption along the nephron
Renin-Angiotensin-Aldosterone (↑Secretion:
II stimulates Na+ reabsorption along the nephron stimulates Na+ reabsorption in the distal tubule and collecting duct and to a lesser degree in the thick ascending limb of Henle’s loop
Natriuretic Peptides: ANP, BNP & Urodilatin (↑Secretion: ↑NaCl Excretion) and water reabsorption by the collecting duct secretion and inhibition of AVP action on the distal tubule and collecting duct
AVP (↑Secretion: ↓H2O Excretion) ↑H2O reabsorption by the distal tubule and collecting duct described later, renin ultimately increases the circulating levels of angiotensin II and aldosterone, both of which stimulate Na+ reabsorption by the nephron.
3. NaCl reabsorption along the nephron is directly stimulated (mediated by α-adrenergic receptors on the cells of the nephron). Because of the large amount of Na+ reabsorbed by the proximal tubule, the effect of increased sympathetic nerve activity is quantitatively most important for this segment. As a result of these actions, increased renal sympathetic nerve activity decreases NaCl excretion, an adaptive response that works to restore ECFV to normal. With ECFV expansion, renal sympathetic nerve activity is reduced. This generally reverses the effects just described.
Cells in the afferent arterioles (juxtaglomerular cells, also known as granular cells) are the site of synthesis, storage, and release of the proteolytic enzyme renin. Three factors are important in stimulating renin secretion: 1.
Perfusion pressure. The afferent arteriole behaves as a high-pressure baroreceptor. When perfusion pressure to the kidneys is reduced, renin secretion is stimulated. Conversely, an increase in perfusion pressure inhibits renin release.
2.
Sympathetic nerve activity. Activation of the sympathetic nerve fibers that innervate the afferent arterioles increases renin secretion (mediated by β-adrenergic receptors).
CHAPTER 35 Control of Body Fluid Osmolality and Volume
Renin secretion is decreased as renal sympathetic nerve activity is decreased.