The Role of Intrarenal Vasoactive Substances in the Pathogenesis of Essential Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 363s-366s ◽  
Author(s):  
K. Abe ◽  
M. Yasujima ◽  
N. Irokawa ◽  
M. Seino ◽  
S. Chiba ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Urinary Excretion ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Prostaglandin E ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Vasoactive Substances ◽  
Angiotensin Ii Antagonist ◽  
Renal Kallikrein

To investigate the role of renal vasoactive substances in the pathogenesis of essential hypertension, urinary prostaglandin E excretion, urinary kallikrein excretion, plasma renin activity, plasma aldosterone concentration and urinary Na excretion were measured in normal subjects and patients with essential hypertension after stimulation of the renin—angiotensin—aldosterone system by the intravenous injection of frusemide or a low Na diet; after the inhibition of renin—angiotensin—aldosterone by an angiotensin II antagonist and after the inhibition of renal prostaglandin E synthesis by indomethacin. The urinary excretions of prostaglandin E and kallikrein, plasma renin activity and plasma aldosterone concentration increased after frusemide administration. The urinary excretion of kallikrein increased after frusemide or a low Na diet but decreased after the angiotensin II antagonist and indomethacin during Na depletion. Changes in urinary kallikrein excretion paralleled those in the renin—angiotensin—aldosterone system after various stimuli. The urinary excretion of prostaglandin E increased after frusemide. However, a dissociation between the urinary excretions of prostaglandin E and kallikrein was found during the low Na diet: the former decreased and the latter increased. The urinary excretion of prostaglandin E was closely related to urinary Na output after various stimuli. Basal levels of urinary prostaglandin E and kallikrein excretion were lower in essential hypertension than in normal subjects. The release of renal prostaglandin E and kallikrein after frusemide was also suppressed in essential hypertension compared with that in normal subjects. The data indicate that renal kallikrein—kinin and renin—angiotensin—aldosterone may interact in a dynamic fashion to maintain blood pressure, that renal prostaglandin E may be involved in renal Na handling and that the suppression of renal kallikrein—kinin and prostaglandin E in essential hypertension may be an etiological factor in essential hypertension.

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

1980 ◽  
Vol 59 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M. Epstein ◽  
M. D. Lifschitz ◽  
R. Re ◽  
E. Haber
Keyword(s):  
Plasma Renin Activity ◽  
Volume Expansion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Plasma Aldosterone Concentration ◽  
Normal Man

1. The relationship of the renin-angiotensin-aldosterone axis with renal prostaglandin E is complex. Although studies have suggested that these two hormonal systems respond to experimental manipulations in a parallel manner, their interdependence has not been assessed fully during volume expansion. Since studies have demonstrated that in normal man the central hypervolaemia induced by water immersion to the neck produces a prompt and profound suppression of plasma renin activity and plasma aldosterone concentration without concomitant alteration of plasma composition, immersion afforded a unique opportunity to assess simultaneously the effects of central hypervolaemia on plasma renin activity, plasma aldosterone concentration and prostaglandin E excretion. 2. Seven normal subjects were studied twice while in balance on a diet containing 10 mmol of sodium/day, 100 mmol of potassium/day: with indomethacin administration (50 mg given every 6 h for five doses) and without indomethacin. Urinary prostaglandin E excretion was measured hourly and plasma renin activity and plasma aldosterone concentration at 30 min intervals. 3. Immersion was associated with a marked suppression of plasma renin activity (59 ± 7%) and plasma aldosterone concentration (55 ± 3%) with a return to pre-study values during the recovery hour. Concomitantly, urinary prostaglandin E excretion increased from 4.7 to a peak of 10.9 ng/min. Although administration of indomethacin lowered the basal rate of urinary prostaglandin E excretion and plasma renin activity, it did not prevent the subsequent augmentation of urinary prostaglandin E or the suppression of plasma renin activity and plasma aldosterone during the subsequent 4 h of immersion. 4. These results demonstrate a dissociation of renin-aldosterone and prostaglandin E during hypervolaemia and suggest that whereas prostaglandin E may constitute one of the major determinants of renin release clinically and experimentally, these two hormonal systems can be dissociated from each other in response to central volume expansion in man.

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.

Effects of thyroid hormones on urinary and renal kallikreins

1992 ◽  
Vol 263 (3) ◽  
pp. E430-E434
Author(s):  
S. Avigdor ◽  
F. Alhenc-Gelas ◽  
J. Bouhnik
Keyword(s):  
Thyroid Hormones ◽  
Urinary Excretion ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Single Measurement ◽  
Kidney Weight ◽  
Plasma Aldosterone Concentration ◽  
Renal Kallikrein ◽  
Enzyme Changes ◽  
Intact Rats

The effects of thyroid hormones on the urinary excretion of kallikrein and on renal kallikrein were studied in rats. Total and active urinary kallikrein was decreased after thyroidectomy, but renal kallikrein content remained unchanged. Diuresis increased, and kidney weight and plasma aldosterone concentration decreased. Treatment with 3,5,3'-triiodo-L-thyronine restored the urinary kallikrein in thyroidectomized rats to normal and increased it in intact rats. It also produced increases in kidney weight and plasma aldosterone and a decrease in diuresis. The effect of thyroid hormones on the urinary kallikrein response to mineralocorticoids was also tested. Deoxycorticosterone acetate increased urinary kallikrein more in normal than in thyroidectomized rats. These results suggest that thyroidectomy decreases renal kallikrein synthesis and lowers the turnover rate of the enzyme, changes not detectable by a single measurement of the renal kallikrein content but reflected by an alteration in the urinary excretion of the enzyme. Thyroid hormones participate in the control of urinary kallikrein. This effect, however, is probably indirect and may be mediated by mineralocorticoids since thyroid function affects both the plasma level of aldosterone, which is known to influence renal kallikrein, and the kallikrein response to exogenous mineralocorticoids.

scholarly journals The effect of age on active and cryoactivatable inactive plasma renin in normal subjects and patients with essential hypertension.

1981 ◽  
Vol 45 (11) ◽  
pp. 1231-1235 ◽  
Author(s):  
MITSUAKI NAKAMARU ◽  
TOSHIO OGIHARA ◽  
TAKESHI HATA ◽  
ANNA MARUYAMA ◽  
HIROSHI MIKAMI ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Effect Of Age

Effect of Age on Active and Inactive Plasma Renin in Normal Subjects and in Patients with Essential Hypertension*

1981 ◽  
Vol 29 (8) ◽  
pp. 379-382 ◽  
Author(s):  
Mitsuaki Nakamaru ◽  
Toshio Ogihara ◽  
Jitsuo Higaki ◽  
Takeshi Hata ◽  
Anna Maruyama ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Effect Of Age

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.

scholarly journals Studies on sympathetic nerve, renin-angiotensin and renal kallikrein-kinin systems, and water-sodium balance in essential hypertension.

1980 ◽  
Vol 44 (5) ◽  
pp. 411-421 ◽  
Author(s):  
OSAMU IIMURA ◽  
KENJIRO KIKUCHI ◽  
MIYAMA AKIYOSHI ◽  
TAKASHI NAKAO ◽  
AKIFUMI KONDO ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Sympathetic Nerve ◽  
Sodium Balance ◽  
Renin Angiotensin ◽  
Renal Kallikrein
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