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

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

1980 ◽  
Vol 17 (5) ◽  
pp. 547-553
Author(s):  
Mitsuaki Nakamaru ◽  
Toshio Ogihara ◽  
Takeshi Hata ◽  
Toru Naka ◽  
Hiroshi Mikami ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Effect Of Age

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.

Haemodynamic and Endocrine Responses of the Kidney to Frusemide in Mild Essential Hypertension

1985 ◽  
Vol 68 (2) ◽  
pp. 159-164 ◽  
Author(s):  
I. G. Mackay ◽  
K. Nath ◽  
A. D. Cumming ◽  
A. L. Muir ◽  
M. L. Watson
Keyword(s):  
Glomerular Filtration Rate ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Underlying Factor ◽  
Induced Changes

1. Prostaglandin-dependent, frusemide-induced changes in renal plasma flow, glomerular filtration rate and plasma renin activity were measured in 14 patients with mild essential hypertension. 2. The renal haemodynamic responses to frusemide were the same as in 10 normal subjects. 3. Frusemide-induced changes in urinary PGE and kallikrein excretion were also the same as in normal subjects. 4. Impaired renal release of vasodilator prostaglandins in essential hypertension is likely to be secondary to the hypertension rather than an underlying factor in its development.

Effect of Intravenous Frusemide on Plasma Renin Concentration: Suppression of Response in Hypertension

1975 ◽  
Vol 49 (4) ◽  
pp. 353-358 ◽  
Author(s):  
P. L. Padfield ◽  
M. E. M. Allison ◽  
J. J. Brown ◽  
A. F. Lever ◽  
R. G. Luke ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
High Blood Pressure ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Primary Hyperaldosteronism ◽  
Plasma Renin Concentration ◽  
Low Renin Hypertension ◽  
Renal Adaptation

1. Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. 2. The renin response to frusemide was suppressed in patients with primary hyperaldosteronism. 3. In patients with low-renin hypertension and normal renin essential hypertension, the renin response to frusemide was similarly suppressed. 4. Suppression of the renin response to frusemide is therefore a feature of hypertension not confined to patients with primary hyperaldosteronism and low-renin hypertension. 5. Thus low-renin hypertension does not appear to constitute a distinct diagnostic entity. 6. It is suggested that suppression of the renin response is part of a long-term renal adaptation to high blood pressure.

Orthostatic Changes of Haemodynamics, Renal Function, Plasma Catecholamines and Plasma Renin Concentration in Normal and Hypertensive Man

1972 ◽  
Vol 42 (2) ◽  
pp. 209-222 ◽  
Author(s):  
M. Molzahn ◽  
TH. Dissmann ◽  
S. Halim ◽  
F. W. Lohmann ◽  
W. Oelkers
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renovascular Hypertension ◽  
Negative Correlation ◽  
Positive Relationship ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Filtration Fraction ◽  
Plasma Renin Concentration

1. In eight normal subjects, ten patients with labile hypertension, six with advanced essential hypertension and six with renovascular hypertension, plasma renin concentration, cardiac output, mean arterial pressure, clearances of creatinine and p-aminohippurate (PAH), and sodium excretion were measured before and after 30 min of 45° upright tilting. Changes in plasma adrenaline and noradrenaline concentration were measured in addition in the normal subjects, and in plasma volume in normal subjects and patients with labile essential hypertension. 2. In patients with advanced essential hypertension, heart rate and calculated peripheral resistance increased significantly less than in normal subjects, and plasma renin increased by 15% in this group, in comparison to 37% in normal subjects, 48% in labile essential hypertension, and 57% in renovascular hypertension. There was a positive relationship between changes in renin and noradrenaline concentrations in normal subjects. 3. Apart from a negative correlation between the increases in plasma renin concentration and mean arterial pressure in patients with renovascular hypertension, there were no significant relationships between changes in plasma renin and haemodynamics. 4. A negative correlation between changes in plasma renin and filtration fraction and a positive relationship between changes in renin and sodium excretion were found in normal subjects and patients with labile hypertension. Plasma renin increase was directly related to changes in the tubular rejection fraction of sodium in patients with labile hypertension. In the same group there was a negative correlation between changes of sodium rejection fraction and filtration fraction. 5. The results suggest a role of the adrenergic system in orthostatic renin release, but the functional connection between renal haemodynamics, tubular sodium handling and renin release across orthostasis cannot fully be explained on the basis of our present knowledge of renin releasing mechanisms.

Fludrocortisone suppression test in normal subjects, in patients with essential hypertension and in patients with various forms of aldosteronism

1980 ◽  
Vol 93 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Jens Otto Lund ◽  
Meta Damkjær Nielsen
Keyword(s):  
Essential Hypertension ◽  
Primary Aldosteronism ◽  
Single Case ◽  
Plasma Renin ◽  
Normal Subjects ◽  
High Plasma ◽  
Significant Suppression ◽  
Control Value ◽  
Aldosterone Production ◽  
Aldosterone Producing Adenoma

Abstract. The response of urinary diurnal tetrahydroaldosterone (TH-aldo) excretion to fludrocortisone administration (0.3 mg q.i.d. for 3 days) was studied. In normal subjects (n = 13) and in patients with essential hypertension (n = 8), urinary TH-aldo decreased to 36 per cent (range 19–48) and to 51 per cent (range 33–61) of the control value, respectively. Twenty-four patients with primary aldosteronism were studied. Twenty-two of these showed no significant suppression of urinary TH-aldo in that the excretion of TH-aldo was 79 per cent of the control value or more. Nineteen of these patients were submitted to operation, and an adrenal aldosterone-producing adenoma was disclosed in every single case. Two patients with primary aldosteronism demonstrated a significant suppression of aldosterone production to 62 and 68 per cent, respectively. Adrenal micronodular hyperplasia was verified in one case and suspected in the other. A significant suppression of aldosterone production was observed in 4 of 5 patients with aldosteronism and normal or high plasma renin levels. The combination of low plasma renin and autonomy of aldosterone production offers a high degree of certainty for the presence of an aldosterone-producing adenoma.

Acute Effects of Captopril on Blood Pressure and Circulating Hormone Levels in Salt-Replete and Depleted Normal Subjects and Essential Hypertensive Patients

1981 ◽  
Vol 61 (1) ◽  
pp. 75-83 ◽  
Author(s):  
J. A. Millar ◽  
B. P. McGrath ◽  
P. G. Matthews ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Pulse Rate ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Primary Role ◽  
Ang Ii ◽  
Acute Effects ◽  
Mean Values ◽  
Plasma Renin Concentration

1. The acute effects of a single oral dose of captopril on blood pressure, pulse rate and circulating levels of angiotensin I (ANG I), angiotensin II (ANG II), renin, bradykinin and catecholamines were studied in three groups: eight normal subjects, six salt-depleted normal subjects and 16 patients with essential hypertension. 2. Captopril treatment did not cause any significant fall in supine blood pressure in salt-replete normal subjects or patients with untreated essential hypertension but was associated with a fall in mean blood pressure from 85 ± 2 to 75 ± 2 mmHg in salt-depleted normal subjects and from 131 ± 7 to 117 ± 5 mmHg in patients with essential hypertension treated with diuretics. There was no change in pulse rate in any group. 3. Hormonal responses to captopril were qualitatively similar in the three groups and consisted of significant falls in ANG II with corresponding increases in ANG I and plasma renin concentration. The changes in plasma renin concentration and ANG I were greater in salt-depleted normal subjects (mean values at 90 min were 1140% and 990% of basal levels respectively) than in salt-replete normal subjects (410%, 190%) and were blunted in patients with essential hypertension (140%, 120%). Blood bradykinin, noradrenaline and adrenaline concentrations did not change after captopril in any group. 4. The parallel fall in blood pressure and ANG II levels in salt-depleted normal subjects is consistent with maintenance of blood pressure by increased levels of ANG II in sodium depletion. 5. The failure of captopril to reduce acutely blood pressure in patients with essential hypertension despite suppression of plasma ANG II and without change in circulating bradykinin confirms that the renin-angiotensin system does not play a primary role in essential hypertension.

Sign in / Sign up

Export Citation Format

Share Document