Kidney International, Vol. 15 (1979), pp. 276 -282
Angiotensins I and II in renal vein blood PETER F. SEMPLE, ALISON M. M. CUMMING, and JOHN A. MILLAR Medical Research Council Blood Pressure Unit, Western Infirmary, Glasgow, Scotland
Al et All étaient supérieures, dans le plasma veineux du rein
Angiotensins I and II in renal vein blood. The concentrations of
lésé, a celles du rein intact alors que les concentrations
active renin (PRC), angiotensin I (Al) and angiotensin II (All) were measured by radioimmunoassay in blood drawn simultane-
moyennes de rénine, de Al et All Ctaient de 4
ously and in triplicate from both renal veins and an artery in each of 17 patients with hypertension, 10 of whom had evidence of renal arterial or parenchymal disease. Plasma concentrations of
+32)% et 35
4%, 7 (—36 a
5%, respectivement, inférieures dans le plasma vei-
neux du rein intact par comparaison au plasma artériel. Le rap-
port de Ia concentration plasmatique de All 5. celle de refine était inferieur dans le plasma veineux au méme rapport dans le
all three substances were found to be remarkably constant in each of the three samples drawn within 5 mm from each site in each patient. In the 6 patients who did not have unilateral renal or renovascular disease, concentrations of renin and Al were (± 3% and 25 (—14 to +144)% higher, sEM), respectively, 11 whereas All was 16 6% lower, in renal venous plasma than it was in arterial plasma. In the 8 patients with predominantly unilateral renin secretion, concentrations of Al and All were consistently higher in venous plasma from the affected kidney than they were from the unaffected kidney, whereas the respective
plasma artériet. Les concentrations plasmatiques de Al et de rénine active Ctaient étroitement liees dans le méme sens, quelle que soit l'origine de l'échantillon. 11 existe des correlations positives
mean concentrations of renin, Al, and All were 4
tion renale.
trés significatives entre PRC et Al, PRC et All, et Al et All, aussi bien dans le plasma veineux renal que dans le plasma arté-
0,79 a 0,86, P < 0.001). Les résultats obtenus confirment ainsi, par des mesures directes in vivo, Ia capacité du rein normal a soustraire All de Ia circulation et mettent en ëvidence le caractCre limité de Ia formation de All dans Ia circula-
riel (r =
4%, 7%
(—36 to +32)%, and 35 5% lower in venous plasma from the unaffected kidney than they were in arterial plasma. The ratios of
the plasma concentrations of All to renin were lower in renal
Concurrent assessment of the plasma concentrations of renin, angiotensin I (Al), and angiotensin II (All) in renal venous and arterial blood are of considerable potential interest for three principal reasons. All, perhaps largely generated within the kid-
venous than they were in arterial plasma. Plasma concentrations of Al were closely and similarly related to PRC at all sites. There were highly significant positive correlations between PRC and
Al, PRC and All, and Al and All, both in arterial and renal venous plasma (r = 0.79 to 0.86. P 0
50
0 = 0 E E
———
100 -
Right renal vein
50 -
I
0
8
I
I
I
16
— All
24
I
32
I
40
— —All [des—(Asp1, Arg2)] All! [des—Asp1] [des—(Asp1, Arg2, Vs13)1 All
Fig. 1. Angiotensin II (Al!) immunoreactive material recovered from paper chromatograms of extracts of arterial blood (upper panel), left renal vein blood (middle panel), and right renal vein blood (lower panel) from patient 14. The positions of reference standards are shown.
279
Angiotensin and the kidney Table 1. Renin, Al, and All in arterial and renal venous plasma from patients without unilateral renal disease
Left renal vein
Right renal vein
Artery
Renal
Patient Age arteriography PRC PlasmaAI PlasmaAll PRC PlasmaAI PlasmaAll PRC PlasmaAl PlasmaAll no. yr finding UI,nl pmole/liter pmolelliter pAl/mi pmoie/liter pmoielliter 1zUImi pmoielliter pmole/liter 1
18
2 3 4 5
50 40 35 32
6
18
Normal Normal Normal Normal
32 52 37
Normal Normal
Table 2. Renin,
no. yr
10
20
60 35
4 22
16
44
—
23 12
15
38 56 39 46
9 5 19 —
44 15
7
15
16
7
15
15
6
13
102
13
33
117
12
20
139
13
19
Al, and All in arterial and renal venous plasma from
Renal arteriography finding
15 14 14
18 14 12 14
patients with renal or renovascular disease Unaffected renal vein
Affected renal vein
Artery
Pa—
tient Age
39
10 4 9 —
PRC Plasma Al Plasma All PRC Plasma Al Plasma All PRC Plasma Al Plasma All /.LU/ml pmolelliter prnolelliter pAl/mi pmole/liier pmolelliter p.U/ml pmole/liter pmole/liter
With evidence of unilateral renal secretion
7 57 R. renal artery occlusions 8 50 L. renal artery occlusion 9 46 R. renal artery occlusion 10 47 R. renal artery stenosis 11 56 L. renal artery stenosis 12 23 Small L. kidney
13 36 L.hydronephrosis 14 26 Normalc
50 295
10
20
138"
58"
31"
49 22
102
195"
188" 94b 17'
11
28 21
28 23 95
—
9
2
16
746" 484" 59" 47') 28"
18
20
108
39
43
31
6
64
16
15 23
6
3
7
99 48
99" 20b
49 276 101
47 30
8
14
52
46 17
15 10
12
—
I 1" 14"
III"
10" 27b
15b
17 83
12
11
146"
81"
36b
108
61
25
30 67
7
16 21
30 80
5
16
17
18
19
6
10
— 2
9 10
No evidence of unilateral r,'nin secretion
15 60 R.renalarterystenosis 16 38 SmallR.kidney
Affected renal vein
Affected renal vein
17 62 Bilateralrenalartery
10
7
10
7
stenosis"
Bethanidine was given until 24 hours before sampling. those in the other renal vein in all three pairs of samples. Patient had previous malignant phase hypertension.
" Values exceeded
(c) Comparison of unaffected contralateral renal vein with artery. In contrast to the patients without unilateral renal disease, the mean concentration of renin in renal venous plasma from the contralateral kidneys was slightly (4 4%) but not significantly lower than it was in arterial plasma. Levels of Al in renal venous plasma from the contralateral kidneys were not significantly different from levels in arterial plasma (mean change, —7%; range, —32% to +36%). Plasma concentrations of All across these kidneys showed a greater percentage fall (35 5) than did concentrations across those kidneys of the group with lateralizing features (t, P < 0.05). Correlations between PRC, plasma Al, and All (all patients). There were positive correlations in arterial plasma between the concentrations of renin and AT (r = 0.82), renin and All (r = 0.86), and AT and All (r = 0.84). Similar correlations were seen in
< 0.001). Figure 2 shows these relationships. It is apparent that the relationship between the plasma concentrations of Al and renin was similar in arterial and renal venous blood. Plasma concentrations of All were, however, generally lower in relation to
renal venous plasma between renin and AT (r = 0.79), renin and All (r = 0.88), and Al and All (r =
Considerable variations in peripheral plasma renm activity have been reported in recumbent subjects sampled at intervals of 20 mm [23]. Judging
0.84). All the correlations were highly significant (P
renin in renal venous than they were in arterial blood. An analysis ol variance showed that the intercepts of the lines relating the plasma concentra-
tions of renin and All in both arterial and renal venous blood were not significantly different from zero. In comparison with arterial plasma, the ratios of the concentrations of All to renin were lower in venous plasma from the kidneys of patients without unilateral renal disease (paired t = —3.6, P
Angiotensins I and II in renal vein blood PETER F. SEMPLE, ALISON M. M. CUMMING, and JOHN A. MILLAR Medical Research Council Blood Pressure Unit, Western Infirmary, Glasgow, Scotland
Al et All étaient supérieures, dans le plasma veineux du rein
Angiotensins I and II in renal vein blood. The concentrations of
lésé, a celles du rein intact alors que les concentrations
active renin (PRC), angiotensin I (Al) and angiotensin II (All) were measured by radioimmunoassay in blood drawn simultane-
moyennes de rénine, de Al et All Ctaient de 4
ously and in triplicate from both renal veins and an artery in each of 17 patients with hypertension, 10 of whom had evidence of renal arterial or parenchymal disease. Plasma concentrations of
+32)% et 35
4%, 7 (—36 a
5%, respectivement, inférieures dans le plasma vei-
neux du rein intact par comparaison au plasma artériel. Le rap-
port de Ia concentration plasmatique de All 5. celle de refine était inferieur dans le plasma veineux au méme rapport dans le
all three substances were found to be remarkably constant in each of the three samples drawn within 5 mm from each site in each patient. In the 6 patients who did not have unilateral renal or renovascular disease, concentrations of renin and Al were (± 3% and 25 (—14 to +144)% higher, sEM), respectively, 11 whereas All was 16 6% lower, in renal venous plasma than it was in arterial plasma. In the 8 patients with predominantly unilateral renin secretion, concentrations of Al and All were consistently higher in venous plasma from the affected kidney than they were from the unaffected kidney, whereas the respective
plasma artériet. Les concentrations plasmatiques de Al et de rénine active Ctaient étroitement liees dans le méme sens, quelle que soit l'origine de l'échantillon. 11 existe des correlations positives
mean concentrations of renin, Al, and All were 4
tion renale.
trés significatives entre PRC et Al, PRC et All, et Al et All, aussi bien dans le plasma veineux renal que dans le plasma arté-
0,79 a 0,86, P < 0.001). Les résultats obtenus confirment ainsi, par des mesures directes in vivo, Ia capacité du rein normal a soustraire All de Ia circulation et mettent en ëvidence le caractCre limité de Ia formation de All dans Ia circula-
riel (r =
4%, 7%
(—36 to +32)%, and 35 5% lower in venous plasma from the unaffected kidney than they were in arterial plasma. The ratios of
the plasma concentrations of All to renin were lower in renal
Concurrent assessment of the plasma concentrations of renin, angiotensin I (Al), and angiotensin II (All) in renal venous and arterial blood are of considerable potential interest for three principal reasons. All, perhaps largely generated within the kid-
venous than they were in arterial plasma. Plasma concentrations of Al were closely and similarly related to PRC at all sites. There were highly significant positive correlations between PRC and
Al, PRC and All, and Al and All, both in arterial and renal venous plasma (r = 0.79 to 0.86. P 0
50
0 = 0 E E
———
100 -
Right renal vein
50 -
I
0
8
I
I
I
16
— All
24
I
32
I
40
— —All [des—(Asp1, Arg2)] All! [des—Asp1] [des—(Asp1, Arg2, Vs13)1 All
Fig. 1. Angiotensin II (Al!) immunoreactive material recovered from paper chromatograms of extracts of arterial blood (upper panel), left renal vein blood (middle panel), and right renal vein blood (lower panel) from patient 14. The positions of reference standards are shown.
279
Angiotensin and the kidney Table 1. Renin, Al, and All in arterial and renal venous plasma from patients without unilateral renal disease
Left renal vein
Right renal vein
Artery
Renal
Patient Age arteriography PRC PlasmaAI PlasmaAll PRC PlasmaAI PlasmaAll PRC PlasmaAl PlasmaAll no. yr finding UI,nl pmole/liter pmolelliter pAl/mi pmoie/liter pmoielliter 1zUImi pmoielliter pmole/liter 1
18
2 3 4 5
50 40 35 32
6
18
Normal Normal Normal Normal
32 52 37
Normal Normal
Table 2. Renin,
no. yr
10
20
60 35
4 22
16
44
—
23 12
15
38 56 39 46
9 5 19 —
44 15
7
15
16
7
15
15
6
13
102
13
33
117
12
20
139
13
19
Al, and All in arterial and renal venous plasma from
Renal arteriography finding
15 14 14
18 14 12 14
patients with renal or renovascular disease Unaffected renal vein
Affected renal vein
Artery
Pa—
tient Age
39
10 4 9 —
PRC Plasma Al Plasma All PRC Plasma Al Plasma All PRC Plasma Al Plasma All /.LU/ml pmolelliter prnolelliter pAl/mi pmole/liier pmolelliter p.U/ml pmole/liter pmole/liter
With evidence of unilateral renal secretion
7 57 R. renal artery occlusions 8 50 L. renal artery occlusion 9 46 R. renal artery occlusion 10 47 R. renal artery stenosis 11 56 L. renal artery stenosis 12 23 Small L. kidney
13 36 L.hydronephrosis 14 26 Normalc
50 295
10
20
138"
58"
31"
49 22
102
195"
188" 94b 17'
11
28 21
28 23 95
—
9
2
16
746" 484" 59" 47') 28"
18
20
108
39
43
31
6
64
16
15 23
6
3
7
99 48
99" 20b
49 276 101
47 30
8
14
52
46 17
15 10
12
—
I 1" 14"
III"
10" 27b
15b
17 83
12
11
146"
81"
36b
108
61
25
30 67
7
16 21
30 80
5
16
17
18
19
6
10
— 2
9 10
No evidence of unilateral r,'nin secretion
15 60 R.renalarterystenosis 16 38 SmallR.kidney
Affected renal vein
Affected renal vein
17 62 Bilateralrenalartery
10
7
10
7
stenosis"
Bethanidine was given until 24 hours before sampling. those in the other renal vein in all three pairs of samples. Patient had previous malignant phase hypertension.
" Values exceeded
(c) Comparison of unaffected contralateral renal vein with artery. In contrast to the patients without unilateral renal disease, the mean concentration of renin in renal venous plasma from the contralateral kidneys was slightly (4 4%) but not significantly lower than it was in arterial plasma. Levels of Al in renal venous plasma from the contralateral kidneys were not significantly different from levels in arterial plasma (mean change, —7%; range, —32% to +36%). Plasma concentrations of All across these kidneys showed a greater percentage fall (35 5) than did concentrations across those kidneys of the group with lateralizing features (t, P < 0.05). Correlations between PRC, plasma Al, and All (all patients). There were positive correlations in arterial plasma between the concentrations of renin and AT (r = 0.82), renin and All (r = 0.86), and AT and All (r = 0.84). Similar correlations were seen in
< 0.001). Figure 2 shows these relationships. It is apparent that the relationship between the plasma concentrations of Al and renin was similar in arterial and renal venous blood. Plasma concentrations of All were, however, generally lower in relation to
renal venous plasma between renin and AT (r = 0.79), renin and All (r = 0.88), and Al and All (r =
Considerable variations in peripheral plasma renm activity have been reported in recumbent subjects sampled at intervals of 20 mm [23]. Judging
0.84). All the correlations were highly significant (P
renin in renal venous than they were in arterial blood. An analysis ol variance showed that the intercepts of the lines relating the plasma concentra-
tions of renin and All in both arterial and renal venous blood were not significantly different from zero. In comparison with arterial plasma, the ratios of the concentrations of All to renin were lower in venous plasma from the kidneys of patients without unilateral renal disease (paired t = —3.6, P
