Effect of Age on the Renin-Angiotensin-Aldosterone System in Normal Subjects: Simultaneous Measurement of Active and Inactive Renin, Renin Substrate, and Aldosterone in Plasma

1986 ◽  
Vol 62 (2) ◽  
pp. 384-389 ◽  
Author(s):  
KAZUO TZUNODA ◽  
KEISHI ABE ◽  
TOSHIKAZU GOTO ◽  
MINORU YASUJIMA ◽  
MAKITO SATO ◽  
...  
Keyword(s):  
Simultaneous Measurement ◽  
Normal Subjects ◽  
Renin Substrate ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Inactive Renin ◽  
Effect Of Age

Studies of the renin-angiotensin-aldosterone system in patients with hypertension and in normal subjects

1969 ◽  
Vol 46 (6) ◽  
pp. 844-861 ◽  
Author(s):  
David H.P. Streeten ◽  
Felix E. Schletter ◽  
George V. Clift ◽  
Carlos T. Stevenson ◽  
Theodore G. Dalakos
Keyword(s):  
Normal Subjects ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

Factors affecting Potassium Balance During Frusemide Administration

1984 ◽  
Vol 67 (2) ◽  
pp. 195-203 ◽  
Author(s):  
Christopher S. Wilcox ◽  
William E. Mitch ◽  
Ralph A. Kelly ◽  
Paul A. Friedman ◽  
Paul F. Souney ◽  
...  
Keyword(s):  
Salt Intake ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
High Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Water Load ◽  
Renin Angiotensin ◽  
High Salt Intake ◽  
Low Salt

1. We investigated the effects of Na+ intake, the renin-angiotensin-aldosterone system and antidiuretic hormone (ADH) on K+ balance during 3 days of frusemide administration to six normal subjects. Subjects received 40 mg of frusemide for 3 days during three different protocols: Na+ intake 270 mmol/day (high salt); Na+ intake 20 mmol/day to stimulate the renin-angiotensin-aldosterone system (low salt); Na+ intake 270 mmol/day plus captopril (25 mg/6 h) to prevent activation of the renin-angiotensin-aldosterone system. In a fourth protocol, a water load was given during high salt intake to prevent ADH release and then frusemide was given. 2. During high salt intake, frusemide increased K+ excretion (UKV) over 3 h, but the loss was counterbalanced by subsequent renal K+ retention so that daily K+ balance was neutral. 3. During low salt intake, the magnitude of the acute kaliuresis following the first dose of frusemide and the slope of the linear relationship between UKV and the log of frusemide excretion were increased compared with that found during the high salt intake. In addition, low salt intake abolished the compensatory renal retention of K+ after frusemide and cumulative K+ balance over 3 days of diuretic administration was uniformly negative (−86 ± 7 mmol/3 days; P < 0.001). 4. Captopril abolished the rise in plasma aldosterone concentration induced by frusemide. The acute kaliuresis after frusemide was unchanged compared with that observed during high salt intake. The compensatory reduction in UKV occurring after the diuretic was slightly potentiated. In fact, captopril given without the diuretic induced a small positive K+ balance. 5. When a water load was given concurrently with frusemide, the acute kaliuresis was >30% lower compared with that seen with frusemide alone, even though the natriuretic response was unchanged. 6. We conclude that: (a) K+ balance is maintained when frusemide is given during liberal Na+ intake because acute K+ losses are offset by subsequent renal K+ retention; (b) this compensatory K+ retention can be inhibited by aldosterone release which could account for the negative K+ balance seen during salt restriction; (c) the short-term kaliuretic response to frusemide is augmented by release of both ADH and aldosterone whereas changes in K+ balance over 3 days of frusemide are dependent on plasma aldosterone concentration.

Inhibition of the Renin-Angiotensin-Aldosterone System by l-Dopa with and without Inhibition of Extracerebral Dopa Decarboxylase in Man

1981 ◽  
Vol 61 (2) ◽  
pp. 187-190 ◽  
Author(s):  
C. Barbieri ◽  
R. Caldara ◽  
C. Ferrari ◽  
Rosa Maria Crossignani ◽  
M. Recchia
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Drugs Analysis ◽  
Catecholamine Levels

1. The present study was undertaken to investigate the possibility that central nervous system mono-aminergic pathways may play a role in the control of the renin-angiotensin-aldosterone system in man. 2. Eight normal subjects received in a randomized order placebo, l-dopa (500 mg, orally) and l-dopa (100 mg, orally) plus carbidopa (35 mg, orally) after pretreatment with carbidopa (50 mg every 6 h for four doses). 3. l-Dopa administration elicited a significant fall in plasma renin activity (PRA) (P < 0.01 at 120, 150 and 180 min) and in plasma aldosterone levels (P < 0.05 at 90, 120, 150 and 180 min); L-dopa plus carbidopa induced a decrease in PRA (P < 0.05 at 120 and 150 min, P < 0.01 at 180 min) and in plasma aldosterone concentration (P < 0.05 at 30 and 60 min, P < 0.01 at 90 and 120 min), in comparison with placebo administration; between-drugs analysis revealed no difference in the decreases in PRA and plasma aldosterone levels induced by the two regimens. 4. Since l-dopa, as well as l-dopa plus carbidopa, has been shown to augment catecholamine levels in the brain of various animal species, the present data suggest that in man PRA and plasma aldosterone concentration might be inhibited by increased central nervous system catecholamine levels.

Enzymatic Activity of Renin in Plasma of Normal and Uraemic Subjects

1984 ◽  
Vol 67 (3) ◽  
pp. 365-368 ◽  
Author(s):  
Theodore A. Kotchen ◽  
Tam T. Guyenne ◽  
Pierre Corvol ◽  
Joel Menard
Keyword(s):  
Renal Failure ◽  
Enzymatic Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Inactive Renin ◽  
Substrate Concentrations

1. Plasma renin reactivity (PRR) is the rate of angiotensin I production after addition of renin to plasma, minus endogenous renin activity. PRR is increased in plasma of patients with renal failure compared with that of normal subjects. The present study was carried out to determine if increased PRR in uraemic plasma is related to differences of endogenous active or inactive renin, endogenous renin substrate, or pH of the incubation in vitro. 2. PRR in plasma of ten uraemic patients was greater (P<0.02) than that in plasma of ten normal subjects in incubations carried out at pH 7.4 and 5.7. 3. Increased PRR was not accounted for by differences of endogenous active and inactive renin activity. 4. After addition of renin, renin concentration (measured by direct radioimmunoassay) did not differ in normal and uraemic plasma. 5. Renin substrate concentration, measured both indirectly and by direct radioimmunoassay, also did not differ in normal and uraemic plasma. 6. Increased PRR in uraemic plasma is not related to alterations of renin or renin substrate concentrations. These observations are consistent with our earlier hypothesis that there is a deficiency of a renin inhibitor in uraemic plasma.

Evidence for two independent effects of oestradiol benzoate on the renin-angiotensin-aldosterone system

1982 ◽  
Vol 100 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Helmut Kaulhausen ◽  
Cornelia Weyand
Keyword(s):  
Time Course ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Renin Substrate ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Oestradiol Benzoate ◽  
Independent Effects

Abstract. Plasma renin concentrations (PRC), plasma renin substrate concentration (PRS), plasma aldosterone and cortisol concentrations as well as plama renin activity (PRA) were measured in ovariectomized subjects after im administration of 10 mg oestradiol benzoate (EB). The esterified oestrogen exerts two independent effects on the renin-angiotensin-aldosterone system. 1) 48 h after EB administration, PRS was significantly increased. Similar results were obtained for total plasma cortisol, reflecting transcortin concentration. In both cases, the increase was quantitatively related to the basal concentrations. These observations are consistent with the well known oestrogen-induced protein synthesis in the liver. 2) The elevation of PRC preceded that of PRS and was already significant 11 h after EB injection. The early rise in plasma renin activity was essentially caused by the increase in PRC, whereas an influence of the activated substrate synthesis was found later, between the 2nd and the 4th day post injection. The time course of plasma aldosterone concentration correlated well with the increased PRA. The results provide evidence that EB has two different effects on the renin-aldosterone axis: an early one by elevating renin release and a delayed one by increasing renin substrate synthesis. Whereas the second mechanism can clearly be localized in the liver, extrarenal as well as direct renal effects of EB may be responsible for the renin stimulation.

Does the Renin—Angiotensin System Maintain Blood Pressure in Both Hypertensive and Normotensive Subjects? a Comparison of Propranolol, Saralasin and Captopril

1979 ◽  
Vol 57 (s5) ◽  
pp. 145s-148s ◽  
Author(s):  
G. A. MacGregor ◽  
N. D. Markandu ◽  
J. E. Roulston
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Normotensive Subjects

1. Propranolol, saralasin and captopril changed blood pressure in normotensive as well as hypertensive subjects. 2. The percentage change in blood pressure with these three drugs for a given plasma renin activity was similar in normotensive and hypertensive subjects. 3. This suggests that when the renin-angiotensin system is maintaining blood pressure, it maintains the blood pressure to the same extent in percentage terms in normotensive and hypertensive subjects for a given plasma renin activity. 4. Saralasin has marked agonist activity, and probably underestimates the participation of the renin—angiotensin—aldosterone system in the maintenance of blood pressure. The fall in blood pressure that occurred with captopril in normal subjects on their normal sodium intake suggests that the renin—angiotensin—aldosterone system may have an important role in the control of blood pressure in normal subjects on their normal sodium intake. If it does, our results suggest that the renin—angiotensin—aldosterone system plays no greater role in maintaining blood pressure in patients with essential hypertension than normotensive subjects for a given plasma renin activity.

The Renin-Angiotensin-Aldosterone System in the Maintenance of Blood Pressure, Aldosterone Secretion and Sodium Balance in Normotensive Subjects

1980 ◽  
Vol 59 (s6) ◽  
pp. 95s-99s ◽  
Author(s):  
G. A. MacGregor ◽  
N. D. Markandu ◽  
J. E. Roulston ◽  
J. C. Jones ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Normal Subjects ◽  
Sodium Balance ◽  
Aldosterone Secretion ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
High Sodium ◽  
Sodium Diet ◽  
Normotensive Subjects ◽  
High Sodium Diet

1. Captopril given for 5 days caused a fall in blood pressure in normotensive subjects. The percentage fall in mean supine pressure was greatest on a low sodium diet (10 mmol/day), 19.6%, least on a high sodium diet (350 mmol/day), 11%, and in between on a normal sodium diet (120 mmol/day), 16.5%. 2. Captopril caused a marked fall in plasma aldosterone in normal subjects on all three sodium intakes. 3. Captopril caused an increase in sodium excretion on the normal (120 mmol/day) and low (10 mmol/day) sodium diet but not the high sodium diet. 4. These results suggest that the renin-angiotensin-aldosterone system is a normal mechanism for maintaining blood pressure and aldosterone secretion in normotensive man. The system may also be involved in the maintenance of sodium balance. 5. These results may lead to a better understanding of the role of the renin-angiotensin-aldosterone system in the maintenance or causation of high blood pressure in essential hypertension.

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