Renin, Blood Volume and Response to Saralasin in Patients on Chronic Haemodialysis: Evidence against Volume- and Renin-‘Dependent’ Hypertension

1978 ◽  
Vol 54 (3) ◽  
pp. 305-312
Author(s):  
B. P. McGrath ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Dietary Sodium ◽  
Chronic Haemodialysis ◽  
Plasma Angiotensin

1. No significant relationship was found between blood pressure and blood volume, sulphate space or plasma angiotensin II concentration in 59 non-nephrectomized haemodialysis patients, of whom 42 were hypertensive. Supine mean blood pressure was only weakly correlated with plasma renin activity and the correlation was not improved when blood pressure was related to expressions combining renin and volume. 2. Changes in supine mean blood pressure during saralasin infusion were related to pre-infusion plasma renin activity (P < 0·001) or plasma angiotensin II (P < 0·02) but also to blood volume (P < 0·001) or sulphate space (P < 0·001). A fall of more than 10% in mean blood pressure during saralasin infusion was observed in only 12 patients (one normotensive), in five of whom there was evidence of volume depletion. 3. Thirteen patients (nine hypertensive) were studied at two levels of dietary sodium: 100 mmol/day and < 20 mmol/day. Supine mean blood pressure in hypertensive patients was lower during the period of higher salt intake despite increased volumes. 4. Hypertension in haemodialysis patients cannot be adequately explained by abnormalities either in volume homeostasis and/or in the renin—angiotensin system.

Hypertension in Dahl salt-sensitive rats: biochemical and immunohistochemical studies

1992 ◽  
Vol 83 (1) ◽  
pp. 13-22 ◽  
Author(s):  
J. Bouhnik ◽  
J. P. Richoux ◽  
H. Huang ◽  
F. Savoie ◽  
T. Baussant ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
High Salt ◽  
Renin Activity ◽  
Deficient Diet ◽  
High Salt Diet ◽  
Salt Diet ◽  
Plasma Angiotensin

1. The renin-angiotensin and kinin-kallikrein systems of Dahl salt-sensitive and salt-resistant rats fed diets with different salt contents were analysed using biochemical and immunocytochemical techniques. 2. Blood pressure increased by 45% in salt-sensitive rats only, after 4 weeks on a high-salt diet. The plasma renin activity and plasma angiotensin II concentration remained at the same levels in salt-sensitive rats on the high-salt diet as on the normal salt diet, whereas the plasma renin activity and plasma angiotensin II concentration of salt-resistant rats fed the high-salt diet were lower. The plasma renin activity and the plasma angiotensin II concentration were elevated in both salt-resistant and salt-sensitive rats fed the salt-deficient diet but were much more elevated in salt-resistant than in salt-sensitive rats. 3. The kidney immunocytochemical data paralleled the data on plasma parameters. Salt-sensitive rats had fewer renin positive juxtaglomerular apparatuses than salt-resistant rats on the normal diet, and the increase on the sodium-deficient diet was also smaller in salt-sensitive rats. Salt-sensitive rats fed the high-salt diet and the standard diet had almost no angiotensin II immunoreactivity compared with the salt-resistant rats on the same diets. 4. The total renal kallikrein content of salt-sensitive rats was lower than that of salt-resistant rats on all three diets, as was the amount of kallikrein excreted in the urine on the standard and the high-salt diets. The differences resulted from a reduction in active kallikrein. The increase in kallikrein in salt-sensitive and salt-resistant rats on the salt-deficient diet was not significantly different. 5. There were similar changes in immunopositive kallikrein in the kidneys of salt-sensitive and salt-resistant rats with diet, with a large increase in kallikrein biosynthesis on the low-salt diet. The plasma concentration of high-molecular-mass kininogen was not significantly different in salt-sensitive and salt-resistant rats, but there was a significant increase in T-kininogen in salt-sensitive rats fed the high-salt diet. 6. In conclusion, the absence of decreases in the plasma renin activity and the plasma angiotensin II concentration in salt-sensitive rats fed the high-salt diet might partially explain the increase in blood pressure.

Angiotensin II Blockade before and after Marked Sodium Depletion in Patients with Hypertension

1978 ◽  
Vol 54 (1) ◽  
pp. 75-83 ◽  
Author(s):  
P. Van Hoogdalem ◽  
A. J. M. Donker ◽  
F. H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Sodium Depletion ◽  
Before And After

1. Angiotensin II blockade before and after marked sodium depletion in patients with hypertension [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar1-Ala8-angiotensin II (saralasin). 2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respectively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity. 3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension subgroups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate decreased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion. 4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently independent of the aetiology of the hypertension. The decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

Solitary Kidney and Ageing as Causes of Low Renin and Aldosterone Concentrations: Relevance to ‘Low-Renin’ Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 177s-180s ◽  
Author(s):  
R. Gordon ◽  
Freda Doran ◽  
M. Thomas ◽  
Frances Thomas ◽  
P. Cheras
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Normotensive Subjects ◽  
The Mean

1. As experimental models of reduced nephron population in man, (a) twelve men aged 15–32 years who had one kidney removed 1–13 years previously and (b) fourteen normotensive men aged 70–90 years were studied. Results were compared with those in eighteen normotensive men aged 18–28 years and eleven men aged 19–33 years with essential hypertension. 2. While the subjects followed a routine of normal diet and daily activity, measurements were made, after overnight recumbency and in the fasting state, of plasma volume and renin activity on one occasion in hospital and of blood pressure on five to fourteen occasions in the home. Blood pressure was also measured after standing for 2 min and plasma renin activity after 1 h standing, sitting or walking. Twenty-four hour urinary aldosterone excretion was also measured. 3. The measurements were repeated in the normotensive subjects and subjects in (a) and (b) above after 10 days of sodium-restricted diet (40 mmol of sodium/day). 4. The mean plasma renin activity (recumbent) in essential hypertensive subjects was higher than in normotensive subjects. In subjects of (a) and (b) above, it was lower than normotensive subjects, and was not increased by dietary sodium restriction in subjects of (a). 5. The mean aldosterone excretion level was lower in old normotensive subjects than in the other groups, and increased in each group after dietary sodium restriction. 6. Mean plasma volume/surface area was not different between the four groups and in normotensive, essential hypertensive and nephrectomized subjects but not subjects aged 70–90 years was negatively correlated with standing diastolic blood pressure.

Measurement of Plasma Renin Activity as a Valid Estimation of Plasma Angiotensin Status

1978 ◽  
Vol 15 (1-6) ◽  
pp. 250-252 ◽  
Author(s):  
J. E. Roulston ◽  
G. A. Macgregor ◽  
Theresa Adam ◽  
Nirmala D. Markandu
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Activity Measurement ◽  
Plasma Samples ◽  
Angiotensin I ◽  
Plasma Angiotensin ◽  
Rate Limiting

Measurement of plasma renin activity is widely used as an indirect assessment of plasma angiotensin II concentration. There has been some controversy over the validity of this assay as an estimate of circulating angiotensin II levels because, during the in vitro generation of angiotensin I by renin, over a period of time, substrate concentration may diminish to such an extent that it becomes rate-limiting, giving an artificially low reflection of angiotensin II levels. In this paper the initial angiotensin I concentration, that is the concentration before in vitro angiotensin I generation, has been compared with the corresponding plasma renin activity for 2752 individual plasma samples. A linear relationship was found between the initial angiotensin I concentration and the plasma renin activity below 60 ng ml−1 h−1. This indicates that, under the conditions of this assay, substrate does not appear to become rate-limiting except at exceedingly high levels of plasma renin activity. These results appear to provide further validation for the use of plasma renin activity measurement as a reflection of the concentration of circulating angiotensin II levels.

Development of two-kidney Goldblatt hypertension in rats under dietary sodium restriction

1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Goldblatt Hypertension

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.

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