Page 124 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Renal Hypertension
+
Most renal diseases can cause hypertension; sensitive”—an excessive supply of Na . It is
about 7% of all forms of hypertension can be possible that hypervolemia promotes the re-
traced back to renal disease. In addition, the lease of ouabain, which increases vascular
kidneys play a significant role in the genesis smooth muscle tone through the inhibition of
+
+
and course of hypertensive disease, even Na /K -ATPase and the subsequent increase in
+
when there is no primary renal disease intracellular Na concentration, reversal of the
+
(→ p. 208ff.). 3Na /Ca 2+ exchanger, and a rise in cytosolic
Renal ischemia is an important cause of hy- Ca 2+ concentration (→ p.112). This hypothesis
Kidney, Salt and Water Balance blatt kidney). This happens regardless of the tension without the above-mentioned primary
pertension brought about by renal disease. Re-
has not, however, been definitively proved.
Nevertheless, hypervolemia regularly results
duction of renal perfusion pressure also leads
in hypertension (→ p. 208ff.).
to hypertension in animal experiments (Gold-
Other diseases can also bring about hyper-
site where renal blood flow is decreased,
whether intrarenally in the course of renal
causes being involved. Thus, for example, a re-
nin-producing renal tumor or a polycystic kid-
disease (e.g., glomerulonephritis [→ p.102].
ney can (in an unknown manner) lead to hy-
pyelonephritis [→ p.106]), in the renal artery
(renal artery stenosis), or in the aorta above
perreninism and thus hypertension without
tion) (→ A1).
Lack of renal production of vasodilating
prostaglandins (→ p. 296) probably plays a
Reduced perfusion of the kidney results in
subordinate role in the development of renal
hypertension via stimulation of the renin–an-
5 the origin of the renal arteries (aortic coarcta- ischemia.
giotensin mechanism (→ A2), in which renin hypertension.
is released in the juxtaglomerular apparatus, The effects of hypertension are, primarily,
for example, by renal ischemia, and splits off damage to heart and vessels (→ A, bottom). Ev-
angiotensin I from angiotensinogen, a plasma ery form of hypertension leads to damage to
protein originating in the liver. Angiotensin I the kidney. Longer lasting hypertension dam-
is then changed into angiotensin II through ages the renal arterioles (→ p. 208ff.) and the
the mediation of a converting enzyme that is glomeruli (nephrosclerosis) and in due course
present in many tissues. Angiotensin II has a leads to renal ischemia. Thus, primary extrare-
strong vasoconstrictor action which causes a nal hypertension can develop into renal hyper-
rise in blood pressure. At the same time angio- tension through the development of nephro-
tensin II stimulates the release of aldosterone sclerosis. All this results in a vicious circle in
and ADH, which bring about the retention of which the renal ischemia and hypertension
NaCl and of water through the activation of mutually reinforce one another. A kidney with
+
Na channels and water channels, respectively renal arterial stenosis or both kidneys in aortic
(→ A3). coarctation are unaffected by this vicious cir-
The plasma concentration of the angioten- cle, because there is a normal or even reduced
sinogen formed in the liver does not saturate blood pressure distal to the stenosis, prevent-
renin, i.e., an increase in angiotensinogen con- ing arteriolar damage. A special case arises
centration can raise the blood pressure further. when the development of hypertension due to
Thus, overexpression of angiotensinogen fa- renal artery stenosis damages the contralater-
vors the development of hypertension as does al, originally healthy, kidney. After removal of
overexpression of renin. the stenosis, the hypertension due to en-
Hypertension is caused by the retention of hanced renin production of the contralateral
sodium and water even without the renin–an- kidney may persist.
giotensin mechanism. A primary increase in
aldosterone release (hyperaldosteronism;
→ p. 266) leads to hypertension just as an
114 overactive Na + channel does (Liddle’s syn-
drome; → p. 98) and—in those who are “salt-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.