Suppression of the Renin—Aldosterone System in Mild Essential Hypertension

1976 ◽  
Vol 50 (4) ◽  
pp. 269-276
Author(s):  
A. M. Khokhar ◽  
J. D. H. Slater ◽  
T. P. Jowett ◽  
N. N. Payne

1. Suppression of the renin—aldosterone system by expansion of the extracellular fluid volume with extra sodium and mineralocorticoid for 6 days was studied in nine young men with very mild essential hypertension and in ten normotensive young men. 2. Plasma renin activity, measured both supine and after 45° head-up tilt, and the renal excretion of aldosterone 18-glucuronide were similar in both groups. However, after expansion of the extracellular fluid volume, hypertensive patients showed much less suppression of both variables. 3. This difference persisted despite matching for an equivalent degree of expansion of the extracellular fluid volume as indexed by the change in body weight. 4. Administration of extra sodium and mineralocorticoid produced a greater proportional fall of renal aldosterone excretion than of plasma renin activity in both groups and this dissociation was significantly more marked in the hypertensive group. 5. We suggest that (i) a relative autonomy of the renin—aldosterone system may be relevant to the pathogenesis and/or perpetuation of essential hypertension and (ii) that the syndrome of low-renin hypertension is unlikely to be associated with ‘mineralocorticoid’ excess.

1974 ◽  
Vol 48 (s2) ◽  
pp. 69s-71s
Author(s):  
G. G. Geyskes ◽  
P. Boer ◽  
F. H. H. Leenen ◽  
E. J. Dorhout Mees

1. In nineteen patients, five with unilateral renal artery stenosis and fourteen with essential hypertension (WHO grades I–II), blood pressure, plasma and extracellular fluid volumes and plasma renin activity were studied at the end of three sequential periods: (a) after at least 3 days on a 60 mmol Na+ diet; (b) after 3 days of salt depletion induced with a diuretic and sustained on a 20 mmol Na+ diet; (c) after 3 days during which the 20 mmol Na+ diet was continued and beta-receptor blockade was induced by increasing dosages of propranolol up to 320 mg daily. 2. After sodium depletion extracellular fluid volume and plasma volume decreased and plasma renin activity increased; blood pressure did not change significantly. 3. After adding propranolol, plasma volume and extracellular fluid volume remained low, and there was a significant decrease in plasma renin activity and blood pressure. 4. No correlation could be demonstrated between changes of blood pressure and plasma renin activity. 5. When the responses of the five patients with renal artery stenosis were compared with those of the fourteen patients with essential hypertension, no significant differences were found. 6. Propranolol has a strong anti-hypertensive effect after Na+ depletion, irrespective of the absolute activities of plasma renin.


1976 ◽  
Vol 51 (s3) ◽  
pp. 207s-210s ◽  
Author(s):  
S. Julius ◽  
M. Esler

1. Patients with mild low-renin hypertension characteristically have increased central blood volume. The total blood volume is normal; the larger central blood volume reflects a shift of the blood from peripheral to central (cardiopulmonary) segments of the capacity system. 2. A relationship between central blood volume and plasma renin activity is demonstrable during tilting in normal and hypertensive subjects. In thirteen individuals there was a strong correlation between the decrease of the central blood volume and the increase in plasma renin activity in response to 12 min of 35° head-up tilt. 3. We propose that the elevated central blood volume causes greater stretch of cardiopulmonary mechanoreceptors and this in turn depresses renin release in mild low-renin hypertension.


1970 ◽  
Vol 39 (5) ◽  
pp. 559-576 ◽  
Author(s):  
G. Bianchi ◽  
L. Campolo ◽  
A. Vegeto ◽  
V. Pietra ◽  
U. Piazza

1. Plasma renin concentration (PRC) has been measured in 212 hypertensive patients. In fourteen patients with essential hypertension and in seventeen patients with renovascular hypertension, plasma volume (PV) and extracellular fluid volume (ECFV) were measured. 2. The results obtained have been discussed in three ways: (a) PRC in relation to the aetiology of hypertension; (b) PRC in relation to the effect on blood pressure of surgery for unilateral renal diseases; (c) PRC, PV and ECFV in ‘essential’ and renovascular hypertension. 3. Excluding patients with ophthalmoscopic signs of malignant hypertension, PRC is significantly higher in renovascular hypertension than in normal subjects and patients suffering from ‘essential’ hypertension and hypertension associated with bilateral renal disease; but the overlapping of the single values of the patients with these diseases is marked. Thus a normal PRC has no diagnostic value, while a high PRC without sodium deficiency or retinopathy might favour a diagnosis of renovascular disease. 4. In twenty-seven out of thirty-three patients submitted to surgery for unilateral renal disease and followed up for 12 months or longer, blood pressure has been significantly reduced. This group includes twelve patients with a normal preoperative PRC and fifteen patients with a high PRC. These results clearly demonstrate that unilateral renal disease may maintain a high blood pressure without increasing PRC and that PRC has no prognostic value. 5. Concurrent estimations of PRC, PV and ECFV in patients with renovascular or essential hypertension revealed the following differences. In cases of renovascular hypertension with normal PRC, PV and ECFV were significantly increased while in those with raised PRC, PV did not differ and ECFV was barely raised with respect to values obtained in patients with essential hypertension. PV of renovascular patients with normal renin was significantly higher than that of renovascular patients with high renin. The analysis of these results with quadratic discriminant functions demonstrated that an integrated evaluation of blood pressure, PV, ECFV and PRC allows a separation between the two types of hypertension. In other words these factors, taken together, in some way seem to reflect a difference between the two diseases. These results may indicate a new type of approach to the diagnosis and prognosis of renovascular hypertension.


1978 ◽  
Vol 55 (1) ◽  
pp. 51-55 ◽  
Author(s):  
A. Lechi ◽  
G. Covi ◽  
C. Lechi ◽  
A. Corgnati ◽  
E. Arosio ◽  
...  

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroups: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients β-adrenoreceptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.


1987 ◽  
Vol 65 (2) ◽  
pp. 257-259 ◽  
Author(s):  
Susan Kaufman

Rats were prepared with inflatable balloons at the superior vena cava – right atrium junction. After recovery 1 week later, when blood was taken from conscious, normovolaemic animals plasma renin activity was found not to be influenced by right atrial stretch. Plasma renin activity was then measured in rats in which an extracellular fluid deficit had been produced by peritoneal dialysis against a hyperoncotic, isotonic solution. Although basal plasma renin activity was elevated (6.8 ± 0.9 from 1.5 ± 0.2 ng∙mL∙h, n = 19), no depression was observed in the experimental group after 15 or 90 min of balloon inflation. In rats pretreated with isoprenaline (10 μg/kg body wt.) plasma renin activity was also increased over basal levels, but again balloon inflation caused no reduction in plasma renin activity. It would appear that right atrial stretch has little, if any, influence on renin release in the conscious rat.


1987 ◽  
Vol 16 (3) ◽  
pp. 171-177 ◽  
Author(s):  
ROSE ANNE KENNY ◽  
CALUM C. LYON ◽  
JOHN BAYLISS ◽  
STAFFORD L LIGHTMAN ◽  
RICHARD SUTTON

1978 ◽  
Vol 102 (1) ◽  
pp. 120-122 ◽  
Author(s):  
Pauli Yuitalo ◽  
Heikki Vapaatalo ◽  
Timo Metsä-Ketelä ◽  
Timo Pitkäjärvi

1975 ◽  
Vol 13 (26) ◽  
pp. 101-103

Thiazide diuretics such as bendrofluazide and chlorothiazide have been used for nearly 20 years in the treatment of hypertension. They have been regarded as rather weak antihypertensive agents which could be used alone only in mild hypertension and otherwise as adjuvants to more potent drugs in more serious cases.1 There are however some patients with ‘essential’ hypertension who are very sensitive to diuretics and in whom the pressure may be brought down to normal by a thiazide2 or spironolactone3 even when it is initially considerably raised. Furthermore a few patients who are responsive to thiazides are strikingly unresponsive to non-diuretic antihypertensive drugs. Patients particularly likely to respond to a thiazide diuretic4 or spironolactone3 commonly have low plasma renin activity and this occurs in about 25% of patients with essential hypertension.5 Since plasma renin activity is not routinely estimated it is simplest to identify these patients by observing the response to an adequate trial of a thiazide.


1976 ◽  
Vol 51 (s3) ◽  
pp. 177s-180s ◽  
Author(s):  
R. Gordon ◽  
Freda Doran ◽  
M. Thomas ◽  
Frances Thomas ◽  
P. Cheras

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.


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