PLASMA RENIN ACTIVITY IN WILMS' TUMOUR

1971 ◽  
Vol 67 (1) ◽  
pp. 197-202 ◽  
Author(s):  
P. A. Voûte ◽  
J. van der Meer ◽  
W. Staugaard-Kloosterziel
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Renal Vein ◽  
Plasma Renin ◽  
Renin Activity ◽  
Wilms Tumour ◽  
Angiotensin I ◽  
Normal Children ◽  
Significant Fall ◽  
Before And After

ABSTRACT Plasma renin activity (PRA) was measured by means of a radioimmunoassay for angiotensin I in 8 children with Wilms' tumour and in 12 normal children. Blood pressure in the patients was in the upper range of normal or just above. Before nephrectomy PRA levels were significantly higher than in normal children and adults. Five patients were studied before and after operation. A significant fall in PRA was observed. In one case blood was taken from the renal vein of the affected kidney; a high PRA level was detected. The results are in accordance with recent findings that Wilms' tumour may secrete increased amounts of renin.

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.

Plasma Renin in Long-Term Diuretic Treatment of Hypertension: Effect of Discontinuation and Restarting Therapy

1982 ◽  
Vol 63 (2) ◽  
pp. 121-125 ◽  
Author(s):  
S. Swart ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Significant Rise ◽  
Renin Activity ◽  
Hypertensive Patients ◽  
Diuretic Treatment ◽  
Low Renin Hypertension ◽  
Before And After

1. Plasma renin activity, body weight and blood pressure were measured before and after 7 days' treatment with bendrofluazide in ten hypertensive subjects. They were then treated with bendrofluazide alone (5 mg daily) for a minimum of 3 years. The diuretic was then discontinued and the measurements were repeated before and again after 7 days with bendrofluazide. The results were compared with those obtained before chronic treatment with the diuretic. 2. Chronic diuretic treatment was associated with a persistent and progressive rise in plasma renin activity, that fell promptly to pretreatment levels when diuretics were discontinued. This was associated with significant weight gain but no immediate significant rise in blood pressure. 3. When acutely challenged with bendrofluazide the patients showed a greater increase in plasma renin activity on the second occasion than on the first. Three out of five patients with an initially subnormal response had normal responses after chronic diuretic treatment. 4. Chronic diuretic treatment increased the responsiveness of the juxtaglomerular apparatus in some hypertensive patients. 5. Classification of hypertensive patients into renin subgroups may be influenced by previous therapy, even when that therapy has been discontinued for 4 weeks. In particular ‘low renin hypertension’ may be masked by recent use of diuretics, as shown by three of the five patients in this subgroup in the present study.

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.

Oestradiol-induced hypotension in spontaneously hypertensive rats: putative role for intracellular cations, sodium-potassium flux and prostanoids

1992 ◽  
Vol 82 (4) ◽  
pp. 389-395 ◽  
Author(s):  
C. Stonier ◽  
J. Bennett ◽  
E. A. Messenger ◽  
G. M. Aber
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive

1. The effect of oestradiol alone and in combination with indomethacin on blood pressure, erythrocyte cation concentration and Na+−K+ flux has been studied in adult female normotensive and spontaneously hypertensive rats. 2. Oestradiol alone resulted in a significant decrease in blood pressure in spontaneously hypertensive rats (from 165.3 ± 3.9 to 146.4 ± 2.7 mmHg, P < 0.001), whereas it induced a significant increase in normotensive rats (from 111.8 ± 1.8 to 124.1 ± 3.6 mmHg, P < 0.001). When indomethacin and oestradiol were administered simultaneously or when indomethacin was given alone, no change in blood pressure occurred in spontaneously hypertensive rats (158.6 ± 6.9 and 159.8 ± 6.2 mmHg, respectively). 3. The fall in blood pressure induced by oestradiol in spontaneously hypertensive rats was associated with significant reductions in erythrocyte K+ concentration (from 127.4 ± 1.2 to 116.9 ± 1.7 mmol/l of cells, P < 0.001), in erythrocyte Na+ concentration (from 14.3 ± 0.8 to 13.0 ± 0.6 mmol/l of cells, P < 0.02), in ouabain-sensitive erythrocyte Na+ flux (from 17.8 ± 0.3 to 16.0 ± 0.4 mmol h−1 (1 of cells)−1, P < 0.01) and in ouabain-sensitive erythrocyte K+ flux (from 11.4 ± 0.2 to 10.4 ± 0.2 mmol h−1 (1 of cells)−1, P < 0.01). No change in blood pressure, erythrocyte cation concentration or Na+−K+ flux occurred when oestradiol and indomethacin were given together or when indomethacin was administered alone. 4. The hypertensive influence of oestradiol in normotensive rats was unaccompanied by any changes in erythrocyte K+ concentration, erythrocyte Na+ concentration and total, ouabain-sensitive and ouabain-resistant Na+−K+ flux. 5. The divergent changes in blood pressure noted in the two strains occurred despite comparable changes in plasma renin activity after oestradiol, with significant increases in plasma renin activity in normotensive rats (from 16.4 ± 4.2 to 28.4 ± 6.6 ng of angiotensin I h−1 ml−1, P < 0.05) and in spontaneously hypertensive rats (from 28.3 ± 2.7 to 39.5 ± 5.7 ng of angiotensin I h−1 ml−1, P < 0.01). The plasma renin activity in spontaneously hypertensive rats receiving oestradiol or indomethacin and oestradiol were similar with values of 39.5 ± 5.7 and 40.6 ± 5.7 ng of angiotensin I h−1 ml−1, respectively, but were significantly higher than that seen in control animals (28.3 ± 2.7 ng of angiotensin I h−1 ml−1, P < 0.01). Similarly, indomethacin alone induced a significant increase in plasma renin activity in spontaneously hypertensive rats to 35.8 ± 7.6 ng of angiotensin I h−1 ml−1 (P < 0.05). 6. The contrasting effects of oestradiol on blood pressure in the two rat strains occurred without any change in packed cell volume. Likewise, the changes in blood pressure in spontaneously hypertensive rats with either oestradiol alone or in combination with indomethacin occurred without any change in packed cell volume, although indomethacin alone resulted in a significant reduction in packed cell volume (from 30.9 ± 1.6 to 26.8 ± 2.0, P < 0.01). 7. The results suggest that the hypotensive action of oestradiol in spontaneously hypertensive rats might be mediated through its influence on erythrocyte cation concentration and/or the modulation of Na+−K+ flux either directly or via the action of prostanoids.

Abnormal responses for blood pressure in children and adults with surgically corrected aortic coarctation

2000 ◽  
Vol 10 (4) ◽  
pp. 353-357 ◽  
Author(s):  
Michael Hauser ◽  
Andreas Kuehn ◽  
Neil Wilson
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Aortic Coarctation ◽  
Surgical Repair ◽  
Plasma Renin ◽  
Left Ventricular ◽  
Renin Activity ◽  
White Coat Hypertension ◽  
Before And After ◽  
Blood Pressures

AbstractBackgroundDespite successful surgical repair of aortic coarctation, life expectancy is reduced, and up to one-third of patients remain or become hypertensive. So as to characterize the responses for blood pressure, we have studied 55 patients with surgically repaired coarctation. Their mean age was 11.3 ± 5.97 years. We documented maximal uptake of oxygen, anaerobic threshold, plasma renin activity and blood pressures during a Bruce protocol treadmill test. The velocity across the site of repair as imaged by crosssectional echocardiography was measured before and after exercise. We measured the changes in heart rate and blood pressure subsequent to an infusion of 1 ug per kg of isoprenalin, monitoring blood pressure over 24 hours in all patients.ResultsWhen compared with 40 healthy age-matched controls, the patients with coarctation had a normal exercise capacity. Resting systolic blood pressures above the 95th percentile were present in 45% of the patients. Exercise-induced hypertension, and an elevation in the average systolic 24 hour blood pressures, were observed, but less frequently than elevated baseline values, suggesting that socalled white-coat” hypertension may be present in this population. Abnormal reactions and elevation of plasma renin activity were related to a history of paradoxical hypertension at the time of surgery. Attenuation of the circadian rhythm for blood pressure was a frequent finding, and may have implications in the development of long-term damage to end-organs. A high correlation was found between mean systolic blood pressure measured by 24 hour monitoring and left ventricular hypertrophy (r=0.65, p<0.05).ConclusionsAbnormalities in blood pressure occurred independently of significant mechanical obstruction. Despite successful surgical repair, abnormalities in the shape of the aortic arch, reduced sensitivity of baroreceptor reflexes, and neurohumoral factors may all contribute to the development of hypertension.

Urinary Electrolyte Excretion and Orthostatic Response of Blood Pressure and Plasma Renin Activity in Children with Postural Hypotension before and after Treatment with Dihydergot®

1985 ◽  
Vol 13 (1) ◽  
pp. 54-58 ◽  
Author(s):  
Makoto Uchiyama ◽  
Kaoru Sakai
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Postural Hypotension ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Point Of View ◽  
Renin Activity ◽  
Electrolyte Excretion ◽  
Venous Pooling ◽  
Before And After

Na and K metabolism, and orthostatic response of blood pressure and plasma renin activity (PRA) were studied in six children, aged 10 to 15 years, with postural hypotension before and after treatment with Dihydergot®(DHE). All abnormal findings which we had already observed in children with postural hypotension (i.e. low fractional excretion of filtered Na in spite of low PRA, extremely high PRA on fainting, great postural fall in blood pressure, and so on) improved on treatment with DHE. This suggests that these abnormal physiological findings found in children with postural hypotension may result from increased venous pooling which can be reduced by DHE. Consequently, DHE seems an excellent drug to treat postural hypotension from the physiological point of view.

Blood Pressure Control in End-Stage Renal Disease in Man: Indirect Evidence of a Complex Pathogenic Mechanism besides Renin or Blood Volume

1977 ◽  
Vol 52 (1) ◽  
pp. 19-21
Author(s):  
G. Cannella ◽  
A. Castellani ◽  
G. Mioni ◽  
M. Usberti ◽  
U. Guerra ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Indirect Evidence ◽  
Plasma Renin ◽  
Pressure Control ◽  
High Plasma ◽  
Renin Activity ◽  
Before And After ◽  
Stage Renal Disease

1. In twenty-three uraemic patients on regular dialysis, plasma renin activity and blood volume were measured before and after a single dialysis. Three groups were identified; the first had a low or normal plasma renin activity and a high or normal blood volume, the second had a high plasma renin activity and a low blood volume and the third had both variables above normal. 2. In spite of these differences, diastolic blood pressure before and after dialysis was the same in the three groups and multiple regression analyses failed to demonstrate any dependence of blood pressure on plasma renin activity, blood volume or body weight taken separately or together. 3. We conclude that other factors besides plasma renin activity and blood volume are important in maintaining arterial hypertension in terminal renal failure.

Effects of Clonidine on Biochemical Indices of Sympathetic Function and Plasma Renin Activity in Normotensive Man

1977 ◽  
Vol 53 (1) ◽  
pp. 45-53 ◽  
Author(s):  
L. M. H. Wing ◽  
J. L. Reid ◽  
C. A. Hamilton ◽  
P. Sever ◽  
D. S. Davies ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Nervous Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Angiotensin I ◽  
Sympathetic Function ◽  
Normotensive Subjects

1. A single oral dose of clonidine hydrochloride (300 μg) lowered systolic blood pressure by 20 ± 2 mmHg and diastolic blood pressure by 15 ± 2 mmHg in seven healthy normotensive subjects. 2. Resting supine plasma noradrenaline concentration fell from 2·42 ± 0·47 nmol/l before dosing to a minimum of 0·59 ± 0·18 nmol/l at 6 h. The value subsequently rose and was not significantly different from that before the dose at 12 h. There was a significant reduction in urinary free catecholamine excretion in the first 12 h after dosing. 3. Resting supine plasma renin activity before dosing was 0·95 ± 0·16 pmol of angiotensin I h−1 ml−1 of plasma and rose significantly after clonidine to 3·50 ± 0·39 pmol of angiotensin I h−1 ml−1 of plasma at 6 h. By 12 h plasma renin activity had returned to control values. 4. When the same subjects were studied on a control, drug-free, day under the same conditions, there was no significant change in blood pressure or plasma noradrenaline. Although plasma renin activity rose during this control day, it was significantly lower than after clonidine. 5. In normotensive subjects single doses of clonidine lower blood pressure and are associated with a reduction of sympathetic nervous activity. Delayed elevation of plasma renin activity may be secondary to the fall in blood pressure. There is no evidence for an overshoot of sympathetic activity after a single dose of clonidine.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

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