Increase of Plasma Renin-Substrate Concentration after Infusion of Angiotensin in the Rat

1973 ◽  
Vol 44 (1) ◽  
pp. 87-90 ◽  
Author(s):  
M. Khayyall ◽  
J. MacGregor ◽  
J. J. Brown ◽  
A. F. Lever ◽  
J. I. S. Robertson
Keyword(s):  
Angiotensin Ii ◽  
Plasma Protein ◽  
Substrate Concentration ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Plasma Protein Concentration ◽  
Renin Substrate

1. Compared with sixteen control animals infused with saline, plasma renin-substrate concentration increased twofold (P < 0.001) in twenty-two rats following infusion of angiotensin II at a mean rate of 191 ng kg−1 min−1 for 13 h. 2. The change was not attributable to an overall increase of plasma protein concentration.

scholarly journals Effects of angiotensin II,thyroxine and estrogen on plasma renin substrate concentration and renin substrate production by the liver.

1981 ◽  
Vol 45 (9) ◽  
pp. 1078-1082 ◽  
Author(s):  
EIKI MURAKAMI ◽  
KUNIO HIWADA ◽  
TATSUO KOKUBU
Keyword(s):  
Angiotensin Ii ◽  
Substrate Concentration ◽  
Plasma Renin ◽  
Renin Substrate

MEASUREMENT OF PLASMA RENIN-SUBSTRATE IN MAN

1973 ◽  
Vol 56 (2) ◽  
pp. 159A-171 ◽  
Author(s):  
MALCOLM TREE
Keyword(s):  
Angiotensin Ii ◽  
Substrate Concentration ◽  
Plasma Renin ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Potential Sources ◽  
Sources Of Variation ◽  
Method Of Measurement ◽  
Inhibitor Solution

SUMMARY Values of plasma renin-substrate concentration in man vary widely according to the method of measurement used. Potential sources of variation have been tested and, as far as possible, excluded in the method described here. Blood was diluted rapidly in an angiotensinase-inhibitor solution containing EDTA and phenanthroline; plasma was separated by centrifugation and the renin-substrate in the specimen was hydrolysed by renin to angiotensin I which was identified as such by chromatography and radioimmunoassay. Angiotensin I was used as a standard to determine the amount of angiotensin formed on incubation. Use of angiotensin II for a standard, as in other methods, led to falsely low values of plasma renin-substrate concentration. Recovery of added substrate was 94%. Changes of plasma renin-substrate concentration in some physiological and pathological states are reported briefly.

Stimulation of angiotensinogen production: a dose-related effect of angiotensin II in the conscious dog

1980 ◽  
Vol 239 (6) ◽  
pp. E442-E446 ◽  
Author(s):  
C. Sernia ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Sampling Period ◽  
Minor Importance ◽  
Plasma Protein Concentration ◽  
Feedback Stimulus ◽  
Liver Slices

The hypothesis that angiotensin II (AII) provides a positive feedback stimulus for production of angiotensinogen was examined in conscious dogs. AII was infused intravenously for 24 h at 5, 20, and 50 ng x kg-1 x min-1 and blood pressure, plasma renin activity (PRA), and the concentrations of AII, angiotensinogen, corticosteroids, and total protein in plasma were measured 0, 2, 4, and 24 h after the start of infusion. In addition, the liver content of angiotensinogen and the release of angiotensinogen by liver slices in vitro were measured after the 24-h sampling period. AII infusion increased blood pressure in a dose-related manner. PRA was markedly decreased by all doses of AII. Plasma corticosteroids were increased only at the highest dose of AII and did not bear any relationship to changes in the concentration of angiotensinogen. Plasma protein concentration and hematocrit were unchanged. Plasma angiotensinogen concentration was unchanged at 2 and 4 h but was increased significantly at 24 h by the two highest doses of AII. A linear relationship was found between the dose of AII and plasma angiotensinogen concentration, the liver content of angiotensinogen, and the release from liver slices during a 2-h incubation. These results provide further evidence that AII has a role in angiotensinogen production but suggest that it is of minor importance in physiological conditions.

Urinary kallikrein and systemic prostacyclin synthesis during sodium chloride infusion in normal man

1985 ◽  
Vol 68 (5) ◽  
pp. 537-543 ◽  
Author(s):  
M. L. Watson ◽  
A. D. Cumming ◽  
A. T. Lambie ◽  
J. A. Oates
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Plasma Protein ◽  
Sodium Excretion ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Urine Flow ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Plasma Protein Concentration

1. An intravenous infusion of 3 litres of sodium chloride solution (saline: 150 mmol/l) was given over 1 h to normal subjects. 2. During and immediately after the infusion, renal plasma flow increased in the majority of subjects, but the rise was not statistically significant. Significant increases in urine flow, sodium excretion, urinary kallikrein excretion and urinary excretion of dinor-6-keto prostaglandin (PG) F1α, a measure of systemic PGI2 synthesis, were noted. Plasma renin activity and plasma protein concentration were significantly lowered by the infusion. 3. At 2 h after the end of the infusion, although urine flow fell significantly, sodium excretion had not decreased. The reduction in plasma renin activity and plasma proteins persisted, and excretion of kallikrein and the PGI2 metabolite returned to control values. 4. Overall, urinary kallikrein excretion correlated significantly with urine flow and with sodium excretion. Peak kallikrein excretion occurred in the second 30 min of the infusion, and preceded maximal urine flow and sodium excretion. 5. The results suggest that increased systemic synthesis of PGI2 occurs in response to an acute infusion of sodium chloride, and may be an adaptive response of the vasculature to volume expansion. They support a role for the renal kallikrein-kinin system in the early diuretic and natriuretic response to saline infusion; the reduction in plasma renin activity and plasma protein concentration may be involved in both the early response and the persistent natriuresis 2 h after the infusion.

Effects of hypoproteinemia on fluid volumes and arterial pressure

1983 ◽  
Vol 245 (2) ◽  
pp. H284-H293 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Plasma Protein ◽  
Plasma Volume ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Protein Concentration

The effects of both moderate and large decreases in plasma protein concentration on arterial pressure and fluid volumes were studied in 23 conscious dogs. In experiment 1, plasma protein concentration decreased 33% during a 5-day plasmapheresis period. During this time sodium space increased 11%, mean arterial pressure decreased slightly, and neither blood volume nor plasma volume decreased. Experiment 2 was performed to see if blockade of the alpha-sympathetic and angiotensin systems could prevent the blood volume homeostasis during moderate hypoproteinemia. Sodium space increased; however, blood volume was unchanged. During experiment 3 plasma protein concentration decreased 68% over a 12-day plasmapheresis period. By the last day of plasmapheresis, plasma protein concentration was 2.4 g/100 ml, mean arterial pressure had decreased 26 mmHg, sodium space had increased 12%, plasma renin activity had increased 11-fold, and blood volume and plasma volume were 63.9 +/- 4.0 and 66.9 +/- 2.5% of control, respectively. We conclude that the maintenance of a normal blood volume during moderate hypoproteinemia does not require active participation of the renin-angiotensin and alpha-sympathetic systems and large decreases in plasma protein concentration are accompanied by marked hypovolemia, hypotension, and hyperreninemia.

Captopril Combined with Thiazide Lowers Renin Substrate Concentration: Implications for Methodology in Renin Assays

1981 ◽  
Vol 60 (5) ◽  
pp. 591-593 ◽  
Author(s):  
S. Rasmussen ◽  
M. Damkjaer Nielsen ◽  
J. Giese
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Substrate Concentration ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Renin Substrate ◽  
Activity Measurements ◽  
Captopril Treatment

1. We have measured plasma concentrations of renin, renin substrate and angiotensins I and II as well as plasma renin activity in nine patients with severe or malignant hypertension during treatment with captopril, hydrochlorothiazide and propranolol. 2. On captopril and hydrochlorothiazide the plasma concentrations of renin substrate and angiotensin II decreased markedly, while renin and angiotensin I levels were increased. 3. The changes in renin substrate concentration suggest a consumption of substrate induced by an increased renin release. Further, the positive feedback of angiotensin II on hepatic renin substrate synthesis may be inhibited. 4. The sequential changes in renin release during captopril treatment should be monitored by measuring plasma renin concentration since plasma renin activity measurements will be profoundly influenced by the marked changes in plasma renin substrate concentration.

The Effects of Haematocrit, Plasma Protein Concentration and Temperature of Drug-containing Blood In-vitro on the Concentrations of the Drug in the Plasma

1990 ◽  
Vol 42 (8) ◽  
pp. 577-580 ◽  
Author(s):  
AKIRA TAMURA ◽  
KAZUMOTO SUGIMOTO ◽  
TAKASHI SATO ◽  
TATSUZO FUJII
Keyword(s):  
Plasma Protein ◽  
Protein Concentration ◽  
Plasma Protein Concentration

Effects of hypoproteinemia-induced myocardial edema on left ventricular function

1998 ◽  
Vol 274 (3) ◽  
pp. H937-H944 ◽  
Author(s):  
M. Miyamoto ◽  
D. E. McClure ◽  
E. R. Schertel ◽  
P. J. Andrews ◽  
G. A. Jones ◽  
...  
Keyword(s):  
Plasma Protein ◽  
Protein Concentration ◽  
Systolic Dysfunction ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Control Group ◽  
Lv Function ◽  
Stroke Work ◽  
Plasma Protein Concentration ◽  
Total Plasma Protein

In previous studies, we observed left ventricular (LV) systolic and diastolic dysfunction in association with interstitial myocardial edema (IME) induced by either coronary venous hypertension (CVH) or lymphatic obstruction. In the present study, we examined the effects of myocardial edema induced by acute hypoproteinemia (HP) on LV systolic and diastolic function. We also combined the methods of HP and CVH (HP-CVH) to determine their combined effects on LV function and myocardial water content (MWC). We used a cell-saving device to lower plasma protein concentration in HP and HP-CVH groups. CVH was induced by inflating the balloon in the coronary sinus. Six control dogs were treated to sham HP. Conductance and micromanometer catheters were used to assess LV function. Contractility, as measured by preload recruitable stroke work, did not change in control or HP groups but declined significantly (14.5%) in the HP-CVH group. The time constant of isovolumic LV pressure decline (τ) increased significantly from baseline by 3 h in the HP (24.8%) and HP-CVH (27.1%) groups. The end-diastolic pressure-volume relationship (stiffness) also increased significantly from baseline by 3 h in the HP (78.6%) and HP-CVH (42.6%) groups. Total plasma protein concentration decreased from 5.2 ± 0.2 g/dl at baseline to 2.5 ± 0.0 g/dl by 3 h in the HP and HP-CVH groups. MWC of the HP (79.8 ± 0.25%) and HP-CVH groups (79.8 ±0.2%) were significantly greater than that of the control group (77.8 ± 0.3%) but not different from one another. In conclusion, hypoproteinemia-induced myocardial edema was associated with diastolic LV dysfunction but not systolic dysfunction. The edema caused by hypoproteinemia was more than twice that produced by our previous models, yet it was not associated with systolic dysfunction. CVH had a negative inotropic effect and no significant influence on MWC. IME may not have the inverse causal relationship with LV contractility that has been previously postulated but appears to have a direct causal association with diastolic stiffness as has been previously demonstrated.

Intrarenal renin inhibition increases renal function by an angiotensin II-dependent mechanism

1988 ◽  
Vol 255 (4) ◽  
pp. F749-F754 ◽  
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Competitive Inhibitor ◽  
Urinary Flow ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Renin Inhibition

ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +/- 1.4 to 15.1 +/- 5.1 and 19.9 +/- 3.2 mu eq/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +/- 2.5 to 35.6 +/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis.

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