Cryoactivation of Plasma Renin

1978 ◽  
Vol 55 (s4) ◽  
pp. 139s-141s ◽  
Author(s):  
A. Hara ◽  
M. Matsunaga ◽  
J. Yamamoto ◽  
K. Morimoto ◽  
H. Nagai ◽  
...  
Keyword(s):  
Low Temperature ◽  
Human Plasma ◽  
Trypsin Inhibitor ◽  
Plasma Renin ◽  
Haemorrhagic Shock ◽  
Rat Plasma ◽  
Renin Activity ◽  
Plasma Samples ◽  
Renin Substrate

1. The mechanism of increased renin activity after human plasma had been kept at −5°C for 4 days (cryoactivation) was investigated. 2. The increase in renin activity of human plasma by cryoactivation was closely correlated to the increase obtained by incubation with trypsin (r = 0·88, P < 0·001, n = 10). 3. An inhibitor of thiol enzyme, N-ethylmaleimide did not inhibit cryoactivation. 4. Soyabean trypsin inhibitor and di-isopropylfluorophosphate (DFP) inhibited cryoactivation, suggesting that the cryoactivation may be due to the action of a trypsin-like serine enzyme. 5. In an experiment in the rat haemorrhagic shock caused parallel increments of renin activity in non-cryoactivated and cryoactivated plasma, the renin activity being about two times higher in the latter. No significant differences were found in the concentrations of renin and renin substrate between the non-cryoactivated and cryoactivated plasma samples. 6. The results may indicate that a destruction of an inhibitor of the renin—renin substrate reaction is responsible for the increase of renin activity after exposure of rat plasma to low temperature. A trypsin-like enzyme in plasma might have destroyed the inhibitor during this procedure.

Elevation of plasma renin activity during avoidance performance in baboons

1976 ◽  
Vol 231 (3) ◽  
pp. 772-776 ◽  
Author(s):  
ML Blair ◽  
EO Feigl ◽  
OA Smith
Keyword(s):  
Plasma Renin Activity ◽  
Substrate Concentration ◽  
Avoidance Performance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sidman Avoidance ◽  
Papio Cynocephalus ◽  
Plasma Samples ◽  
Renin Substrate ◽  
Lever Pressing

The effect of a 3-h Sidman avoidance operant conditioning schedule (liver pressing to avoid an electric shock) on plasma renin activity and renin substrate concentration was examined in baboons (Papio cynocephalus). Plasma samples were drawn over a 24-h period on both the control and test days, and the avoidance session was presented on the morning of the test day. Plasma renin activity was significantly higher on the test day than at the corresponding hours of the control day at 1, 2, and 3 h after onset of the avoidance test and 30 min after its termination (P = .032). The magnitude of the increase in plasma renin activity was not correlated with either the rate of lever pressing or the number of shocks received. Renin substrate concentration was not changed during or after the avoidance session. These data demostrate that plasma renin activity can be increased by a psychological stimulus.

Immunochemical Differences between Angiotensin I-Forming Enzymes in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 41s-44s ◽  
Author(s):  
J. Menard ◽  
F.-X. Galen ◽  
C. Devaux ◽  
N. Kopp ◽  
Colette Auzan ◽  
...  
Keyword(s):  
Human Brain ◽  
Amniotic Fluid ◽  
Human Plasma ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Brain Extract ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Human Renin ◽  
Brain Extracts

1. Human plasma, amniotic fluid and acidified amniotic fluid were incubated at pH 5.5 with the same concentrations of human plasma renin substrate and rat plasma renin substrate. They produced three to eight times more angiotensin I with human than with rat renin substrate. By contrast, human brain extracts generated 20 times more angiotensin I when incubated with rat plasma renin substrate than with human plasma renin substrate. 2. Serial dilutions of anti-(human renin) antibody inhibited, in a dose-dependent manner, the production of angiotension I when plasma, amniotic fluid and brain extracts were incubated with human plasma renin substrate. They also inhibited the production of angiotensin I when plasma and amniotic fluid were incubated with rat plasma renin substrate. They were ineffective on the angiotensin I generation by human brain extracts acting on rat plasma renin substrate. 3. Affinity chromatography on an haemoglobin-Sepharose gel separated the fraction of brain extract acting on human renin substrate and inhibited by anti-(human renin) antiserum; this was not retained on the gel at pH 3.3. Part of the angiotensin I-forming activity detected by rat renin substrate hydrolysis was not retained on the gel and part was eluted at pH 8.5. These angiotensin I-forming activities did not hydrolyse human renin substrate, and were not neutralized by anti-(human renin) antibody. 4. These results demonstrate that a renin, immunochemically identical with renal, plasma and amniotic fluid renin, is present in the human brain. Other angiotensin I-forming activity, acting on an heterologous substrate at a more acidic pH, is also present in human brain.

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

1991 ◽  
Vol 69 (9) ◽  
pp. 1381-1384 ◽  
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.

Does heparin inhibit renin activity?

1991 ◽  
Vol 69 (9) ◽  
pp. 1360-1363 ◽  
Author(s):  
Masato Matsunaga ◽  
Yoko Yamanaka ◽  
Noriko Nagano ◽  
Yuki Iwasaki ◽  
Yumi Saito ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Substrate ◽  
Significant Difference ◽  
Inactive Renin

Although heparin was reported in the 1960s to inhibit renin activity, this has not always been confirmed by other investigators. Hence, we re-examined whether heparin really inhibits renin or not. Renin activities were determined by radioimmunoassay of angiotensin I generated at pH 7.4. (i) No significant difference was found between the two kinds of plasma samples obtained with heparin and with EDTA as anticoagulant, in ARC (renin activity with addition of sheep renin substrate), TRC (ARC after activation of inactive renin by trypsin), or PRA (plasma renin activity without additional substrate), (ii) Even in higher concentrations of heparin up to 500 U/mL, neither PRA, ARC, nor TRC of plasma was affected significantly. (iii) Heparin, in concentrations up to 500 U/mL, exerted no significant effect on TRC of the media of human vascular smooth muscle cell culture. In conclusion, heparin does not exert any significant inhibitory effect on human renin nor does it affect activation of inactive renin by trypsin in the range of concentration of practical use, under the conditions employed in this study.Key words: plasma renin, tissue renin, inactive renin, vascular smooth muscle cell, trypsin.

Absence of Activation in Vitro of Renin in Rat Plasma

1982 ◽  
Vol 62 (4) ◽  
pp. 435-437 ◽  
Author(s):  
M. H. De Keijzer ◽  
A. P. Provoost ◽  
F. H. M. Derkx
Keyword(s):  
Human Plasma ◽  
Active Form ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Plasma Renin Concentration ◽  
Inactive Form ◽  
Inactive Renin

1. Rat plasma was subjected at 4°C to various treatments known to convert inactive renin into its active form in human plasma. 2. No statistical differences in plasma renin concentration were found when the levels after the various treatments were compared with that of untreated rat plasma. 3. It is concluded that, in contrast to human plasma, no inactive form of renin is present in rat plasma.

Effect of temperature on plasma renin samples.

1978 ◽  
Vol 24 (7) ◽  
pp. 1202-1204 ◽  
Author(s):  
F Fyhrquist ◽  
L Puutula
Keyword(s):  
Plasma Renin Activity ◽  
Room Temperature ◽  
Plasma Renin ◽  
Renin Activity ◽  
Effect Of Temperature ◽  
Plasma Samples ◽  
Hypertensive Patients ◽  
Variable Extent ◽  
Venous Plasma

Abstract Plasma renin activity was measured in parallel in Na2EDTA-contained plasma samples after storage at -20, 4, and 24 degrees C, and in the lyophilized state. In peripheral venous plasma from 22 hypertensive patients, the activity (range, 0.08-46.7 microgram/liter per hour) remained stable during three days of storage at 4 degrees C, but decreased to a variable extent when plasma was kept at 24 degrees C: in one day by 9.2%, two days by 25.6%, and three days by 74.0%. Values were the same for samples handled at room temperature and chilled to 4 degrees C within 3 h and parallel samples immediately cooled in an icebath and kept at 4 degrees C. Freezing (-20 degrees C) and thawing of plasma was associated with a 22% mean increase in activity (range, 0-83%). Lyophilization resulted in a smaller increase of plasma renin activity (mean 12%, range 0-46%). Blood for renin analysis need not be cooled immediately, but must be cooled to 4 degrees C within 2-3 h. It then is stabe for at least three days. Freezing or lyophilization appears to be associated with some cold activation of "prorenin."

Cold Promoted Activation of Factor VII(CPA) and Plasma Renin Activity (PRA)

1979 ◽  
Author(s):  
E. van Royen ◽  
K. Hoekman ◽  
P. Elte ◽  
A. Schellekens
Keyword(s):  
Plasma Renin Activity ◽  
Pregnant Women ◽  
Plasma Renin ◽  
Special Care ◽  
Renin Activity ◽  
Factor Vii ◽  
Plasma Samples ◽  
Spontaneous Activation ◽  
Esterase Inhibitor

The CPA phenomenon occurs in about 20% of the population, 60% of women using contraceptive drugs and 90% of pregnant women. Cpa positive plasma samples show at 4°C spontaneous activation of prekallikrein and factor VII, shortening of the ThrombotestR Time (TT) and consumption of C4 esterase inhibitor. Since kalllkrein may activate prorenin, we related the CPA phenomenon to PRA.A highly significant correlation was found between the shortening of the TT at 4°C and an increase in PRA during storage of random plasma samples.It is concluded that special care should be taken when PRA is determined in CPA positive plasma samples in order to avoid erroneously high PRA levels.

Postnatal development of the renin-angiotensin system in rats

1980 ◽  
Vol 238 (5) ◽  
pp. R432-R437 ◽  
Author(s):  
K. B. Wallace ◽  
J. B. Hook ◽  
M. D. Bailie
Keyword(s):  
Steady State ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Neonatal Rat ◽  
Postnatal Life ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Age Related

The purpose of this investigation was to correlate the development of the various enzyme activities associated with the renin-angiotensin system with age-related differences in the steady-state concentrations of angiotensin I (AI) and II (AII). Angiotensin was quantified by radioimmunoassay. Plasma renin activity and concentration increased between birth and 3 wk of age, and declined thereafter to adult values. Renal renin content, on the other hand, increased throughout the first 6 wk of postnatal life. The concentration of AII in plasma also increased following birth; however, maximum concentrations were not attained until 5 wk of age. In contrast, plasma AI did not increase between 3 and 6 wk of age. These data suggest that the steady-state concentration of AII in neonatal rat plasma may be partially limited by the low plasma renin substrate concentration. The increase in AII between 3 and 6 wk of age may reflect the increasing converting enzyme activity.

Plasma renin activity and plasma prorenin assays

1991 ◽  
Vol 37 (10) ◽  
pp. 1811-1819 ◽  
Author(s):  
J E Sealey
Keyword(s):  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Vascular Complications ◽  
Plasma Renin ◽  
Renin Activity ◽  
Blood Collection ◽  
Kinetic Assay ◽  
Renin Substrate ◽  
Patients With Diabetes ◽  
Commercial Kits

Abstract Sensitivity and accuracy are essential features of an assay of plasma renin activity (PRA) because the normal concentration of PRA is only 1 pmol/L, and subnormal concentrations have diagnostic relevance. Conditions for blood collection need to be standardized but the conditions are not difficult for outpatients. For routine diagnostic purposes blood should be collected from ambulatory (ideally, untreated) patients on moderate sodium intake. To avoid irreversible cryoactivation of plasma prorenin (which is present in 10-fold greater concentrations than renin), samples should be processed at room temperature and stored completely frozen. Cryoactivation occurs when plasma is liquid at temperatures less than 6 degrees C. PRA is commonly measured with an enzyme kinetic assay in which angiotensin I (Ang I) is formed by the reaction of plasma renin with endogenous renin substrate (angiotensinogen). The Ang I so formed is measured by RIA; results are expressed as an hourly rate (micrograms/L formed per hour). This method, which is provided by most commercial kits, has the potential for unlimited sensitivity because the step for Ang I generation can be prolonged as long as necessary, so that enough Ang I forms to be measured accurately. Unfortunately, that sensitivity is not always exploited. Dilution of plasma during pH adjustment should be kept to a minimum. The Ang I generation step should last at least 3 h. The step should last 18 h for samples with PRA less than 1.0 micrograms/L per hour, to eliminate the errors inherent in the measurement and subtraction of immunoreactive Ang I in the untreated plasma (blank subtraction). These changes actually simplify PRA measurements because they eliminate the need for ice in the clinic and reduce by almost half the number of samples to be assayed by RIA. I also describe the method for measurement of plasma prorenin, which may be an important marker for patients with diabetes mellitus who subsequently develop vascular complications.

Methods for serial study of renin-angiotensin system in the unanesthetized rat

1975 ◽  
Vol 228 (2) ◽  
pp. 369-375 ◽  
Author(s):  
JS Carvalho ◽  
R Shapiro ◽  
P Hopper ◽  
LB Page
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Angiotensin I ◽  
Ether Anesthesia ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Improved Technique

Micromethods for measurement of plasma renin concentration (PRC) and plasma renin-substrate concentration (PSC) have been developed for rat plasma with radioimmunoassay of angiotensin I. An improved technique for aortic implantation of plastic cannulas was developed for use in experiments 1-2 wk in duration. The effects on components of renin system of anesthesia and tail cutting were studied. Arterial blood was sampled through cannulas without animal manipulation. PRC varied little in unanesthetized rats, was moderately and variably increased during pentobarbital anesthesia, and was markedly and consistently elevated during ether anesthesia. PSC was unchanged during anesthesia. PRC was increased in blood obtained by tail cutting within 1-2 min after cutting. With the use of the methods and techniques described here serial studies of the renin system in plasma of unanesthetized rats are shown to be feasible. A role for the sympathetic nervous system in the mediation of renin secretion by ether is proposed.

Sign in / Sign up

Export Citation Format

Share Document