Page 220 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

"
NaCl intake. In these patients, aldosterone re- tors; see below) or angiotensin receptor an-
lease is so strongly inhibited even at “normal” tagonists.
+
Na intake (> 100 mmol/d) that it cannot be The various forms of secondary hyperten-
lowered any further. A diet with low NaCl in- sion make up only 5–10% of all hypertensive
take would in this case bring NaCl balance cases (→ B2,3,4), but contrary to primary H.
into the aldosterone regulatory range. their cause can usually be treated. Because of
The actual connection between NaCl sensi- the late consequences of H. (→ E), such treat-
tivity and primary H. has not been fully eluci- ment must be initiated as early as possible. Re-
dated, but the possibility is being considered nal hypertension, the most common form of
that responsiveness to catecholamines is secondary H., can have the following, often
raised in people sensitive to NaCl. This results, partly overlapping, causes (→ B2, see also
for example, on psychological stress, in a p.114): Every renal ischemia, for example, re-
greater than normal rise in blood pressure, on sulting from aortic coarctation or renal artery
stenosis, but also from narrowing of the renal
the one hand, due directly to the effect of in-
Heart and Circulation and, on the other hand, indirectly as a result of hypertension-induced atherosclerosis), leads
arterioles and capillaries (glomerulonephritis,
creased cardiac stimulation (→ B, upper right)
to the release of renin in the kidneys. It splits
increased renal absorption and thus retention
+
the dekapeptide angiotensin I from angioten-
of Na (rise in extracellular volume leads to
sinogen in plasma. A peptidase (angiotensin–
hyperdynamic H.). The increased blood pres-
sure leads to pressure diuresis with increased
converting enzyme, ACE), highly concentrated
+
+
This mechanism also exists in healthy people,
acids to form angiotensin II. This octapeptide
but the pressure increase required for excre-
has a strong vasoconstrictor action (TPR rises)
7 Na excretion, restoring Na balance (Guyton). especially in the lungs, removes two amino
tion of large amounts of NaCl is much lower and also releases aldosterone from the adrenal
+
(→ C, a ! b). In primary H. (as in disorders of cortex (Na retention and increase in cardiac
renal function) the NaCl-dependent increase output), both these actions raising the blood
in blood pressure is greater than normal (→ C, pressure (→ B2). In kidney disease with a sig-
+
c ! d). A diet that is low in Na can thus lower nificant reduction of the functioning renal
+
(not yet fixed) H. in these cases (C, c ! e). A si- mass, Na retention can therefore occur even
+
+
multaneously elevated K supply accentuates during normal Na supply. The renal function
+
this effect for unknown reasons. The cellular curve is steeper than normal, so that Na bal-
mechanism of salt sensitivity still awaits clari- ance is restored only at hypertensive blood
fication. It is possible that changes in cellular pressure levels (→ C, c ! d). Glomerulonephri-
+
Na transport are important. In fact cellular tis, renal failure, and nephropathy of pregnan-
Na + concentration is raised in primary H., cy are some of the causes of the primarily hy-
which decreases the driving force for the 3 pervolemic form of renal H. Renal H. can also
+
Na /Ca 2+ exchange carrier in the cell mem- be caused by a renin-producing tumor or (for
brane, as a result of which the intracellular unknown reasons) by a polycystic kidney. The
Ca 2+ concentration rises, which in turn in- kidney is also central to other forms of hyper-
creases the tone of the vasoconstrictor mus- tension that do not primarily originate from it
cles (Blaustein). It is possible that digitalis- (primary H., hyperaldosteronism, adrenogen-
+
+
like inhibitors of Na -K -ATPase are involved ital syndrome, Cushing’s syndrome). Further-
(ouabain?). They may be present in larger more, in every case of chronic H. secondary
amounts, or there may be a special sensitivity changes will occur sooner or later (vascular
to them in primary H. Atriopeptin (= atrial na- wall hypertrophy, atherosclerosis): they fix
triuretic peptide [ANP]), which has vasodilator the H. even with effective treatment of the pri-
and natriuretic effects, is probably not in- mary cause. If unilateral renal artery stenosis is
volved in the development of primary H. Al- repaired surgically rather late, for example, the
though the concentration of renin is not other kidney, damaged in the meantime by the
elevated in primary H., blood pressure can be hypertension, will maintain the H.
210 reduced even in primary H. by inhibiting the Hormonal hypertension can have several
angiotensin-converting enzyme (ACE inhibi- causes (→ B3):
"
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.