The Responses of Active and Inactive Plasma Renin to Various Conditions in Normal Subjects and the Role of Renal or Plasma Kallikrein in Activation of Inactive Renin

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.

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Plasma and tissue kallikrein–kinin systems during acute administration of frusemide in normotensive and hypertensive humans

Clinical Science ◽

10.1042/cs0810305 ◽

1991 ◽

Vol 81 (3) ◽

pp. 305-311 ◽

Cited By ~ 5

Author(s):

K. Peter Öhman ◽

Bengt E. Karlberg

Keyword(s):

Plasma Level ◽

Urine Volume ◽

Plasma Renin ◽

Normal Subjects ◽

Primary Hypertension ◽

Plasma Kallikrein ◽

Acute Administration ◽

Tissue Kallikrein ◽

Kinin System ◽

Hypertensive Patients

1. This study aims to further elucidate the role of the tissue and plasma kallikrein-kinin systems in blood pressure, electrolyte and volume homoeostasis. Components thereof and of the renin-angiotensin-aldosterone system were measured in conjunction with frusemide administration, in normotensive subjects and in patients with primary hypertension. 2. Frusemide increased plasma pre-kallikrein, angiotensin II and aldosterone concentrations and plasma renin activity, whereas the plasma level of tissue kallikrein remained unchanged. Basal values and the induced changes were similar in both groups. 3. Frusemide increased the urine volume and the excretion of Na+, K+, Mg2+, Cl−, aldosterone, prostaglandin E2 and tissue kallikrein. These changes were similar in both groups, but the total tissue kallikrein excretion was significantly lower in the hypertensive patients. Excretion of electrolytes and hormones was also measured during three 24 h urine collection periods and did not differ between the two groups. 4. Thus, acute administration of frusemide to hypertensive patients and normal subjects increased the plasma level of pre-kallikrein, possibly indicating less activation to kallikrein and subsequently less kinin generation in the blood stream. This also suggests a role for the plasma kallikrein-kinin system in the regulation of vascular tone and blood volume. Circulating tissue kallikrein does not seem to be acutely involved. 5. Urinary excretion of kallikrein is reduced in patients with primary hypertension after the administration of frusemide, apparently without affecting the renal excretory response.

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The role of atrial natriuretic peptide in the development of arterial hypertension in patients with hypothalamic puberty syndrome

Problems of Endocrinology ◽

10.14341/probl199743421-22 ◽

1997 ◽

Vol 43 (4) ◽

pp. 21-22

Author(s):

T. P. Krivchenko ◽

N. I. Verbovaya

Keyword(s):

Atrial Natriuretic Peptide ◽

Arterial Hypertension ◽

Natriuretic Peptide ◽

Plasma Renin ◽

Normal Subjects ◽

Functional Relationships ◽

Hypothalamic Syndrome ◽

Serum Aldosterone ◽

Atrial Natriuretic

Fifty-two youths with the hypothalamic syndrome of puberty and 13 normal subjects aged 13 to 24 were examined in order to elucidate the contribution of the depressor system factor atrial natriuretic peptide (ANP) to the development of arterial hypertension in such patients. The disease standing was 2 to 11 years. Plasma ANP, plasma renin activity, and serum aldosterone were radioimmunoassayed. The level of ANP was reliably decreased in patients with borderline arterial hypertension and directly correlated with changes of the renin-aldosterone system. This permitted a conclusion on the insufficient role of the depressor system in patients with the pubertal hypothalamic syndrome and contribution of ANP to the development of arterial hypertension and of disorders in the functional relationships between the renin-aldosterone system and ANP.

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Catabolism of Human Fibrinogen Fragment D in Normal Subjects and Patients with Liver Cirrhosis

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650106 ◽

1980 ◽

Vol 44 (03) ◽

pp. 146-149 ◽

Cited By ~ 3

Author(s):

Nicole Ardaillou ◽

Jeannine Yvart ◽

Philippe Le Bras ◽

Marie-José Larrieu

Keyword(s):

Liver Cirrhosis ◽

Clearance Rate ◽

Plasma Clearance ◽

Normal Subjects ◽

Fractional Catabolic Rate ◽

Human Fibrinogen ◽

Plasma Pool ◽

Catabolic Rate ◽

Chloramine T

SummaryThe catabolism of human fragment D, (FgD), obtained by plasmin digestion of fibrinogen has been investigated in normal subjects and patients with liver cirrhosis and the results compared with those obtained for fibrinogen (Fg). Fg was labelled with I-125 and Fg D with I-131 using the chloramine T method. The plasma disappearance curves of both labelled proteins fitted a two exponential curve. In controls the plasma clearance rate of Fg D was greater than that of Fg as shown by the marked difference between the half-lives of these two tracers: 8,9 and 83,5 hours for Fg D and Fg respectively. The fractional catabolic rate of Fg D was 3.38 times the plasma pool per day. In nine patients with liver cirrhosis, catabolism of Fg was not modified. In contrast, catabolism of Fg D was significantly reduced with a half life of 13.0 hours and a low fractional catabolic rate. These results suggest the role of the liver in the catabolism of Fg D in man.

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VARIATIONS IN PLASMA RENIN ACTIVITY AND URINARY ALDOSTERONE EXCRETION IN NORMAL SUBJECTS AFTER SALT RESTRICTION AND ACUTE PITUITARY INHIBITION WITH 6-DEHYDRO-16-METHYLENE HYDROCORTISONE

Acta Endocrinologica ◽

10.1530/acta.0.0670159 ◽

1971 ◽

Vol 67 (1) ◽

pp. 159-173

Author(s):

A. Peytremann ◽

R. Veyrat ◽

A. F. Muller

Keyword(s):

Plasma Renin Activity ◽

Salt Intake ◽

Plasma Renin ◽

Normal Subjects ◽

Inhibitory Effect ◽

Renin Activity ◽

Sodium Balance ◽

Experimental Conditions ◽

Salt Restriction ◽

Aldosterone Production

ABSTRACT Variations in plasma renin activity and urinary aldosterone excretion were studied in normal subjects submitted to salt restriction and simultaneous inhibition of ACTH production with a new synthetic steroid, 6-dehydro-16-methylene hydrocortisone (STC 407). At a dose of 10 mg t. i. d. this preparation exerts an inhibitory effect on the pituitary comparable to that of 2 mg of dexamethasone. In subjects maintained on a restricted salt intake, STC 407 does not delay the establishment of an equilibrium in sodium balance. The increases in endogenous aldosterone production and in plasma renin activity are also similar to those seen in the control subjects. A possible mineralocorticoid effect of STC 407 can be excluded. Under identical experimental conditions, the administration of dexamethasone yielded results comparable to those obtained with STC 407.

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The Renin Angiotensin System and Bipolar Disorder: A Systematic Review

Protein and Peptide Letters ◽

10.2174/0929866527666200127115059 ◽

2020 ◽

Vol 27 (6) ◽

pp. 520-528 ◽

Cited By ~ 2

Author(s):

Izabela Guimarães Barbosa ◽

Giulia Campos Ferreira ◽

Diomildo Ferreira Andrade Júnior ◽

Cássio Rocha Januário ◽

André Rolim Belisário ◽

...

Keyword(s):

Systematic Review ◽

Bipolar Disorder ◽

Cardiovascular Diseases ◽

Renin Angiotensin System ◽

Plasma Renin ◽

Angiotensin Receptors ◽

Angiotensin System ◽

Renin Angiotensin ◽

Search Terms

Bipolar Disorder (BD) is a chronic a multifactorial psychiatric illness that affects mood, cognition, and functioning. BD is associated with several psychiatric conditions as well clinical comorbidities, particularly cardiovascular diseases. The neurobiology of BD is complex and multifactorial and several systems have been implicated. Considering that the Renin Angiotensin System (RAS) plays an important role in cardiovascular diseases and that recently evidence has suggested its role in psychiatric disorders, the aim of the present study is to summarize and to discuss recent findings related to the modulation of RAS components in BD. A systematic search of the literature using the electronic databases MEDLINE and LILACS was conducted through March 2019. The search terms were: “Bipolar Disorder”; “Renin Angiotensin System”; “Angiotensin 2”; “Angiotensin receptors”; “Angiotensin 1-7”; “ACE”; “ACE2”; “Mas Receptor”. We included original studies assessing RAS in BD patients. Two hundred twenty-two citations were initially retrieved. Eleven studies were included in our systematic review. In the majority of studies (6 of 8), the ACE insertion/deletion (I/D) polymorphism did not differ between BD patients and controls. BD patients presented higher plasma renin activity in comparison with controls. The studies evaluating the RAS molecules in BD are very scarce and heterogeneous. The literature suggests a potential role of RAS in BD. Further studies are necessary to investigate this relationship.

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Measurement of inactive renin in normal, nephrectomized, and adrenalectomized rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y91-205 ◽

1991 ◽

Vol 69 (9) ◽

pp. 1381-1384 ◽

Cited By ~ 4

Author(s):

Knud Poulsen ◽

Arne Høj Nielsen ◽

Arne Johannessen

Keyword(s):

Animal Model ◽

Exchange Resin ◽

Cation Exchange Resin ◽

Plasma Renin ◽

Rat Plasma ◽

Angiotensin I ◽

Renin Substrate ◽

Suitable Animal Model ◽

Inactive Renin ◽

Adrenalectomized Rats

In a new method for measurement of inactive rat plasma renin, the trypsin generated angiotensin I immunoreactive material, which was HPLC characterized as similar to tetradecapeptide renin substrate, is removed by a cation exchange resin before the renin incubation step. The method also corrects for trypsin destruction of endogenous angiotensinogen by the addition of exogenous angiotensinogen. When measured with this method inactive renin in rat plasma decreased after nephrectomy and increased after adrenalectomy. This is in accordance with findings in humans. A sexual dimorphism of prorenin (inactive renin) in rat plasma, similar to that reported in humans and mice, was demonstrated. Thus, inactive renin in the rat is no exception among species, and the rat might be a suitable animal model for further studies dealing with the physiology of prorenin in plasma and tissues.Key words: angiotensinogen, inactive renin, renin.

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Ontogeny of neuronally released norepinephrine on renin secretion in sheep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1989.257.4.r765 ◽

1989 ◽

Vol 257 (4) ◽

pp. R765-R770 ◽

Cited By ~ 1

Author(s):

K. T. Nakamura ◽

J. M. Klinkefus ◽

F. G. Smith ◽

T. Sato ◽

J. E. Robillard

Keyword(s):

Renin Secretion ◽

Renal Nerves ◽

Nerve Terminals ◽

Norepinephrine Release ◽

Fetal Sheep ◽

Postnatal Maturation ◽

Active Renin ◽

Inactive Renin ◽

Cortical Slices

The role of renal nerves and norepinephrine release on renin secretion during fetal and postnatal maturation has not been studied. Experiments were performed to determine the effect of veratridine, a substance known to promote norepinephrine release from nerve terminals, on active and inactive renin secretion from renal cortical slices of fetal (134-138 days gestation; term is 145 days), newborn (4-9 days of age), and adult nonpregnant sheep. Veratridine (10-300 microM) significantly increased active renin secretion and produced a small but nonsignificant rise in inactive renin secretion in all three groups of animals (P less than 0.05). The percent rise in active renin secretion during veratridine stimulation was similar among all groups. Veratridine-stimulated (300 microM) active renin secretion was antagonized by tetrodotoxin (0.5 and 5.0 microM) and DL-propranolol (1 microM) in fetal renal cortical slices. However, neither tetrodotoxin nor propranolol completely inhibited the stimulatory effect of veratridine on active renin secretion. These results suggest that 1) norepinephrine released from nerve terminals may regulate active renin secretion early during development; 2) the effect of veratridine on active renin secretion was similar in fetal, newborn, and adult sheep; 3) veratridine had no significant effect on inactive renin secretion; and 4) active renin secretion due to depolarization of nerve terminals in fetal sheep is dependent on activation of beta-adrenoceptors as it is in adults.

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Comparison of the Renin Response to Dopamine and Noradrenaline in Normal Subjects and Patients with Autonomic Insufficiency

Clinical Science ◽

10.1042/cs0460481 ◽

1974 ◽

Vol 46 (4) ◽

pp. 481-488 ◽

Cited By ~ 3

Author(s):

C. S. Wilcox ◽

M. J. Aminoff ◽

A. B. Kurtz ◽

J. D. H. Slater

Keyword(s):

Autonomic Failure ◽

Sodium Intake ◽

Plasma Renin ◽

Normal Subjects ◽

Control Groups ◽

Autonomic Reflexes ◽

Fractional Increase ◽

The Mean ◽

Autonomic Insufficiency ◽

Stimulation Of

1. The effect on plasma renin activity (PRA) of dopamine and noradrenaline infusions was studied in three patients with Shy—Drager syndrome, three patients with Parkinson's disease and normal autonomic reflexes, and three healthy volunteers. The patients with the Shy—Drager syndrome had functional evidence of a peripheral lesion of the sympathetic nervous system and subnormal PRA on a controlled sodium intake. 2. In all subjects catecholamines were infused step-wise for 4 min until a 30% rise in systolic blood pressure occurred. 3. In each subject, PRA fell after noradrenaline but rose after dopamine. The mean fractional increase in PRA after dopamine was no less in the Shy—Drager patients than in the control groups. 4. The results suggest, first, that stimulation of dopamine receptors can release renin, and secondly, that inadequate renin stores cannot explain the low PRA found in our patients with autonomic failure.

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