Efferent sympathetic nerve activity (ESNA) to the
kidney is a major signaling pathway by which the kidney is apprised of
vascular volume changes (Fig. 8-9). Volume receptors in the atria
(Fig. 8-2) alter ESNA in response to changes in venous volume.
Baroreceptors in the carotid sinus and aortic arch alter ESNA in response
to changes in arterial pressure. The atrial stretch receptors have a
greater effect on ESNA directed to the kidney than do the arterial
baroreceptors. ESNA will have the following effects:
1. Acting through
receptors, ESNA causes vasoconstriction of the arterioles.
This tends to reduce RBF and GFR. Because of the buffering by the
autoregulatory mechanisms, the fractional change in GFR is usually much
smaller than the change in RBF. This results in an increase in the
filtration fraction. The fall in pressure in peritubular capillaries
coupled with the effect of the change in filtration fraction on
peritubular b
tends to increase salt and water reabsorption in the proximal tubule
(See Fig. 8-7).
2. Acting through
receptors on the granular cells, ESNA will increase the rate of renin
releasewhich leads to increased
formation of AII.
3. Sympathetic nerve fibers also innervate the
proximal and distal tubules and the thick ascending limb of Henle's
loop. ESNA directly stimulates tubular reabsorption of salt and
water (
receptors).
4. Circulating catecholamines have the same effect as
ESNA.
5. Low levels of ESNA probably increase salt and
water reabsorption without affecting GFR. Denervation increases salt
and water excretion.
QUESTIONS:
14.
Describe how efferent sympathetic nervous
activity is increased in response to a loss of blood?
15. How does activation of
receptors in the kidney affect salt and water excretion? Activation of
receptors?
16. How does ESNA affect salt and water
reabsorption in the proximal tubule? In the collecting tubule?