Page 197 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Tubuloglomerular Feedback, Renin–angiotensin system (RAS). If the mean
Renin–Angiotensin System renal blood pressure acutely drops below
90 mmHg or so, renal baroreceptors will trig-
The juxtaglomerular apparatus (JGA) consists ger the release of renin, thereby increasing the
of (a) juxtaglomerular cells of the afferent arte- systemic plasma renin conc. Renin is a pep-
riole (including renin-containing and sympa- tidase that catalyzes the cleavage of angioten-
thetically innervated granulated cells) and sin I from the renin substrate angiotensinogen
efferent arteriole, (b) macula densa cells of the (released from the liver). Angiotensin-convert-
thick ascending limb of the loop of Henle and ing enzyme (ACE) produced in the lung, etc.
Kidneys, Salt, and Water Balance nephron via angiotensin II (ATII) and (2) sys- threshold for renin release is raised by α 1-
cleaves two amino acids from angiotensin I to
(c) juxtaglomerular mesangial cells (polkissen,
produce angiotensin II approx. 30–60 minutes
! A) of a given nephron (! A).
after the drop in blood pressure (! B).
JGA functions: (1) local transmission of
Control of the RAS (! B). The blood pressure
tubuloglomerular feedback (TGF) at its own
adrenoceptors, and basal renin secretion is in-
temic production of angiotensin II as part of
creased by " 1-adrenoceptors. Angiotensin II
the renin–angiotensin system (RAS).
and aldosterone are the most important effec-
Tubuloglomerular feedback (TGF). Since the daily
tors of the RAS. Angiotensin II stimulates the
GFR is 10 times larger than the total ECF volume
release of aldosterone by adrenal cortex (see
precisely adjusted according to uptake. Acute
indirectly (delayed action) lead to a renewed
changes in the GFR of the individual nephron (iGFR)
increase in arterial blood pressure (! B), and
and the amount of NaCl filtered per unit time can
7 (! p. 168), the excretion of salt and water must be below). Both hormones directly (fast action) or
occur for several reasons. An excessive iGFR is as-
renin release therefore decreases to normal
sociated with the risk that the distal mechanisms for levels. Moreover, both hormones inhibit renin
NaCl reabsorption will be overloaded and that too release (negative feedback).
much NaCl and H 2O will be lost in the urine. A too low
iGFR means that too much NaCl and H 2O will be re- If the mean blood pressure is decreased in only one
tained. The extent of NaCl and H 2O reabsorption in kidney (e.g., due to stenosis of the affected renal
the proximal tubule determines how quickly the artery), the affected kidney will also start to release
tubular urine will flow through the loop of Henle. more renin which, in this case, will lead to renal
When less is absorbed upstream, the urine flows hypertension in the rest of the circulation.
more quickly through the thick ascending limb of the
loop, resulting in a lower extent of urine dilution Angiotensin II effects: Beside altering the
(! p. 162) and a higher NaCl concentration at the structure of the myocardium and blood vessels
macula densa, [NaCl] MD. If the [NaCl] MD becomes too (mainly via AT 2 receptors), angiotensin II has
high, the afferent arteriole will constrict to curb the the following fast or delayed effects mediated
GFR of the affected nephron within 10 s or vice versa by AT 1 receptors (! A).
(negative feedback). It is unclear how the [NaCl] MD re- ! Vessels: Angiotensin II has potent vasoconstrictive
sults in the signal to constrict, but type 1 A angioten- and hypertensive action, which (via endothelin)
sin II (AT 1A) receptors play a key role. takes effect in the arterioles (fast action).
If, however, the [NaCl] MD changes due to chronic
shifts in total body NaCl and an associated change ! CNS: Angiotensin II takes effect in the hypo-
in ECF volume, rigid coupling of the iGFR with the thalamus, resulting in vasoconstriction through the
circulatory “center” (rapid action). It also increases
[NaCl] MD through TGF would be fatal. Since long- ADH secretion in the hypothalamus, which stimu-
term increases in the ECF volume reduce proximal lates thirst and a craving for salt (delayed action).
NaCl reabsorption, the [NaCl] MD would increase, re- ! Kidney: Angiotensin II plays a major role in regulat-
sulting in a decrease in the GFR and a further increase ing renal circulation and GFR by constricting of the
in the ECF volume. The reverse occurs in ECF volume afferent and/or efferent arteriole (delayed action; cf.
deficit. To prevent these effects, the [NaCl] MD/iGFR re- autoregulation, ! p. 150). It directly stimulates Na +
sponse curve is shifted in the appropriate direction by
certain substances. Nitric oxide (NO) shifts the curve reabsorption in the proximal tubule (delayed action).
! Adrenal gland: Angiotensin II stimulates aldo-
when there is an ECF excess (increased iGFR at same sterone synthesis in the adrenal cortex (delayed ac-
[NaCl] MD), and (only locally effective) angiotensin II tion; ! p. 182) and leads to the release of epineph-
184 shifts it in the other direction when there is an ECF rine in the adrenal medulla (fast action).
deficit.
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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