Renin-angiotensin system: oral contraception and exercise in healthy female subjects

1985 ◽  
Vol 59 (6) ◽  
pp. 1690-1697 ◽  
Author(s):  
I. A. Huisveld ◽  
F. M. Derkx ◽  
B. N. Bouma ◽  
W. B. Erich ◽  
M. A. Schalekamp
Keyword(s):  
Oral Contraceptives ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Oral Contraception ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Active Renin ◽  
Healthy Female ◽  
Female Subjects

The effect of oral contraception and of exercise on the renin-angiotensin system was studied in 20 highly trained athletes, of whom 10 were ingesting oral contraceptives (users) and 10 were not (nonusers), and in 24 sedentary age-matched healthy female subjects, of whom 13 were users and 11 were nonusers. No training-related effects were observed with the exception of renin substrate, which was significantly higher in the athletes. The plasma concentrations of active renin and of trypsin-activatable prorenin were significantly lower in the subjects taking oral contraceptives. Renin substrate, however, was significantly higher in the oral contraceptives group. No difference in plasma renin activity (PRA) was observed between users and nonusers. The results demonstrate the well-known estrogen-induced stimulation of renin substrate synthesis by the liver and suggest a decreased secretion of renin by the kidney. Exhaustive exercise of short duration, performed by the trained athletes only, stimulated the renin-angiotensin system. An increase in PRA and in active renin concentration was observed. The prorenin concentration did not change significantly. The magnitude of the exercise-induced changes was considerably influenced by oral contraceptive medication. Nonusers showed a significantly greater increase in PRA and active renin and total renin concentration than users. Renin substrate decreased significantly during exercise in the nonusers only. These results demonstrate that oral contraceptives have a suppressive effect on renin secretion at rest, an effect that becomes more prominent during exercise, i.e., physiological stimulation.

Downregulation of the renin-angiotensin system in streptozotocin-diabetic rats

1992 ◽  
Vol 262 (1) ◽  
pp. E105-E109 ◽  
Author(s):  
L. A. Cassis
Keyword(s):  
Adipose Tissue ◽  
Replacement Therapy ◽  
White Adipose Tissue ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Brown Adipose ◽  
Insulin Replacement

To determine if insulin has the ability to regulate components of the renin-angiotensin system, renin and angiotensinogen mRNA and plasma concentrations were determined in 4-wk streptozotocin (STZ)-diabetic rats. In another group of STZ-diabetic rats, replacement insulin therapy was given over the 4-wk period, and the above parameters were examined. In STZ-diabetic rats, there was a significant regression of white adipose tissue that was accompanied by an increase in the yield of RNA obtained. Changes in white adipose tissue were reversed by insulin replacement therapy in STZ-diabetic rats. There were no changes in brown adipose tissue weight or RNA yield in STZ-diabetic rats. Plasma renin activity (PRA) was significantly decreased in STZ-diabetic rats; however, plasma angiotensinogen concentration was not significantly affected by diabetes. PRA was restored to control levels in STZ-diabetic rats with insulin replacement. Kidney renin mRNA as well as liver, epididymal, and interscapular fat angiotensinogen mRNA were significantly decreased in STZ-diabetic rats. Renin and angiotensinogen mRNA were not significantly different from control in all tissues examined in STZ-diabetic rats with insulin replacement therapy. Results from this study suggest a downregulation of the renin-angiotensin system in 4-wk STZ-diabetic rats at the level of mRNA expression that is restored by replacement therapy with insulin; therefore, insulin may directly or indirectly regulate the renin-angiotensin system.

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.

Active renin and angiotensinogen in cardiac interstitial fluid after myocardial infarction

1999 ◽  
Vol 276 (6) ◽  
pp. H1818-H1826 ◽  
Author(s):  
Alan T. Hirsch ◽  
John A. Opsahl ◽  
Mary M. Lunzer ◽  
Stephen A. Katz
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Hypertrophy ◽  
Infarct Size ◽  
Interstitial Fluid ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Left Ventricular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Active Renin

The renin-angiotensin system promotes cardiac hypertrophy after myocardial infarction. The purpose of this study was to measure renin and angiotensinogen in plasma and myocardium 10 days after myocardial infarction. Infarction involving 45 ± 4% of left ventricular circumference with accompanying hypertrophy was induced in rats ( n = 14). Plasma and myocardial renin were increased after infarction compared with sham controls ( n = 8) (27.4 ± 3.2 vs. 7.5 ± 1.8 ng ANG I ⋅ ml plasma ⋅ h−1, P < 0.0002; and 8.8 ± 1.6 vs. 2.5 ± 0.1 ng ANG I ⋅ g myocardium−1 ⋅ h−1, P < 0.008, respectively). After infarction, myocardial renin was correlated with infarct size ( r = 0.62, P < 0.02) and plasma renin ( r = 0.55, P < 0.04). Plasma angiotensinogen decreased in infarct animals, but myocardial angiotensinogen was not different from shams (1.1 ± 0.08 vs. 2.03 ± 0.06 nM/ml plasma, P < 0.002; and 0.081 ± 0.008 vs. 0.070 ± 0.004 nM/g myocardium, respectively). In conclusion, myocardial renin increased after infarction in proportion to plasma renin and infarct size, and myocardial angiotensinogen was maintained after infarction despite decreased plasma angiotensinogen and increased levels of myocardial renin.

AT1 antagonism and renin inhibition in mice: pivotal role of targeting angiotensin II in chronic kidney disease

2012 ◽  
Vol 303 (7) ◽  
pp. F1037-F1048 ◽  
Author(s):  
Christoph Fraune ◽  
Sascha Lange ◽  
Christian Krebs ◽  
Alexandra Hölzel ◽  
Jana Baucke ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Injury ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Pivotal Role ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renin Inhibition

The role of the renin-angiotensin system in chronic kidney disease involves multiple peptides and receptors. Exerting antipodal pathophysiological mechanisms, renin inhibition and AT1 antagonism ameliorate renal damage. However, it is unclear which mechanism exerts better nephroprotection. We compared the renin inhibitor aliskiren with the AT1 antagonist losartan in mice with chronic kidney disease due to renal ablation. Doses were adjusted to equipotent inhibition of the renin-angiotensin system, determined via a dose-response quantifying plasma and renal renin expression. Six-week treatment with either 500 mg/l drinking water losartan or 50 mg·kg−1·day−1 aliskiren significantly decreased albuminuria, glomerular damage, and transcription rates of renal injury markers to a similar extent. An array analysis comparing renal gene expression of losartan- and aliskiren-treated mice evaluating >34,000 transcripts demonstrated regulation for 14 genes only, with small differences. No superior nephroprotection was found by combining losartan and aliskiren. Compared with plasma concentrations, aliskiren accumulated ∼7- to 29-fold in the heart, liver, lung, and spleen and ∼156-fold in the kidney. After withdrawal, plasma concentrations dropped to zero within 24 h, whereas renal tissue concentrations declined slowly over days. Withdrawal of aliskiren in mice with chronic kidney disease revealed a significantly delayed re-increase in albuminuria compared with withdrawal of losartan. This study demonstrates equieffective nephroprotection of renin inhibition and AT1 antagonism in mice with chronic kidney disease without additional benefit of combination therapy. These observations underscore the pivotal role of targeting ANG II to reduce renal injury.

Renin-angiotensin system in hypothyroid rats: effects of potassium iodide and triiodo-L-thyronine

1984 ◽  
Vol 105 (4) ◽  
pp. 505-510 ◽  
Author(s):  
E. Jiménez ◽  
M. Montiel ◽  
J. A. Narváez ◽  
M. Morell
Keyword(s):  
Plasma Renin Activity ◽  
Potassium Iodide ◽  
Renin Angiotensin System ◽  
Kinetic Studies ◽  
Plasma Renin ◽  
The Other ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Previously Treated

Abstract. Kinetic studies of the renin-angiotensin system (RAS) were carried out by measuring plasma renin activity (PRA), plasma renin concentration (PRC) and plasma renin substrate (PRS). Changes in this system were studied during hypothyroidism, after administration of propylthiouracil (PTU), and in thyroidectomized rats. A significant decrease in PRA and PRC was observed in those animals previously treated with PTU. However, a significant increase in PRC, and a decrease in PRS, were found in T animals, but no changes in PRA were observed. In these animals, after daily administration of potassium iodide for I week (T+KI), no changes in RAS were observed in comparison with T rats. Nevertheless, administration of daily doses of triiodo-ithyronine (T+T3) induced a significant increase in PRA, leaving PRC unaltered. In this case the changes in PRA were related to the increase in PRS after T3 treatment. These results suggest that two different mechanisms were involved in renin release, one activated in T rats and the other in pharmacological hypothyroidism.

Studies on the human ovarian renin-angiotensin system: optimization of assay methodology and effects of follicular stimulants

1990 ◽  
Vol 127 (3) ◽  
pp. 513-521 ◽  
Author(s):  
J. M. Brameld ◽  
F. Broughton Pipkin ◽  
E. M. Symonds
Keyword(s):  
Follicular Fluid ◽  
Ovarian Stimulation ◽  
Clomiphene Citrate ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
System Optimization ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Substrate Concentrations

ABSTRACT The renal and genital tracts share a common embryological origin; it is thus not surprising that tissues from both can synthesize renin. Preliminary studies showed extremely high concentrations of renin in follicular fluid (FRC) following ovarian stimulation for in-vitro fertilization. This necessitated complete revalidation of the renin assays and showed that data obtained using commercial kits were invalid. An assay protocol was developed using a 1:2 dilution of follicular fluid taken into EDTA (0·3 mol/l) and o-phenanthroline (0·05 mol/l). The assay was performed at pH 7·5 in the presence of excess exogenous (sheep) renin substrate, with incubation periods of 5, 10 and 15 min at 37 °C. This protocol resulted in the linear generation of angiotensin I (AI). Activation of inactive renin was performed using eightfold more trypsin than was required for plasma samples. Follicular renin substrate concentrations (FRS) were measured using the same assay methodology as used for measurement of plasma renin substrate concentrations (PRS). Storage of samples at −18 °C for up to 2 months was found not to affect the FRC, although repeated freeze-thaw cycles did. FRC and plasma renin concentrations (PRC) were very similar in 25 unstimulated control women, studied in the follicular phase of the menstrual cycle. Trypsin activation increased follicular total renin concentration (FTRC) more than plasma total renin concentration (PTRC) (P< 0·0001). FRS was slightly higher than PRS (P<0·02). Ovarian stimulation with clomiphene citrate (CC; six women) was without effect on these parameters. However, hyperstimulation with CC, human menopausal gonadotrophins (hMG) and human chorionic gonadotrophin (hCG) resulted in substantial increments in FRC and FTRC (P< 0·0001 for both) and somewhat smaller rises in PRC and PTRC (P<0·05; P < 0·0005). There was also a small rise in PRS (P< 0·0002), but no change in FRS. Treatment with buserelin, hMG and hCG was associated with similarly large increases in renin concentrations, and also increases in both FRS and PRS (P< 0·003; P<0·007) in comparison with samples from women stimulated with CC, hMG and hCG. Increased plasma renin activity has previously been reported in stimulated ovarian follicular fluid. Our data show clearly that this is primarily due to a rise in FRC and FTRC and not to a rise in FRS. The use of the anti-oestrogen CC alone for ovarian stimulation was without effect on the follicular renin-angiotensin system. Thus we suggest that it is the gonadotrophins themselves which stimulate renin production, presumably by the theca cells. The much smaller rise in PRC and PTRC may reflect the effects of an overspill into the systemic circulation or, less likely, effects of the gonadotrophins on renal renin production. There is no evidence for this latter suggestion. FRS was increased only slightly by ovarian stimulation and must be presumed to be rate-limiting in the generation of AI. Journal of Endocrinology (1990) 127, 513–521

scholarly journals Effect of captopril on the release of the components of the renin-angiotensin system into plasma and lymph.

1992 ◽  
Vol 2 (7) ◽  
pp. 1241-1250 ◽  
Author(s):  
C S Wilcox ◽  
V J Dzau
Keyword(s):  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Lymph ◽  
Active Renin ◽  
Renal Interstitium ◽  
Arterial Plasma ◽  
Renal Vascular ◽  
Venous Plasma

The effects of captopril on the intrarenal renin-angiotensin system were assessed from measurements in arterial plasma, renal venous plasma, and renal lymph from salt-depleted dogs. In the basal state, immunoreactive angiotensin II (Ang II) in renal venous plasma averaged only 60 +/- 12% (P less than 0.01) of arterial plasma, although the concentration of Ang II in renal lymph was 2.0 +/- 0.4-fold (P less than 0.05) greater. The Ang II concentration of renal lymph incubated ex vivo at 37 degrees C doubled in 10 to 15 min, which was the time taken to collect renal lymph samples. Compared with arterial plasma, renal lymph contained lower concentrations (P less than 0.01) of renin substrate and angiotensin-converting enzyme but higher concentrations of active (5.3 +/- 2.1-fold) and inactive (8.9 +/- 3.2-fold) renin. Although captopril increased the secretion of active renin into renal venous plasma by six-fold, the secretion of total renin was unchanged because of a reciprocal fall in the secretion of inactive renin. The percent reduction in renal vascular resistance with captopril correlated with the percent fall in Ang II in renal lymph (r = 0.70). In conclusion: (1) all components of the renin-angiotensin system are represented in the renal interstitium, as reflected in lymph; (2) Ang II concentrations in renal lymph in vivo approximate arterial levels; (3) increased secretion of active renin into plasma during intrarenal infusion of captopril into denervated kidneys is due predominantly to renin activation; and (4) renal vascular resistance may depend on the concentration of Ang II in the renal interstitium.

CHANGES IN THE RENIN-ANGIOTENSIN SYSTEM INDUCED BY ORAL CONTRACEPTIVES

1972 ◽  
Vol 68 (3_Suppl) ◽  
pp. S31 ◽  
Author(s):  
R. Beckerhoff ◽  
J. A. Luetscher ◽  
W. Siegenthaler
Keyword(s):  
Oral Contraceptives ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Mediation of humoral catecholamine secretion by the renin-angiotensin system in hypotensive rainbow trout (Oncorhynchus mykiss)

1999 ◽  
Vol 160 (3) ◽  
pp. 351-363 ◽  
Author(s):  
NJ Bernier ◽  
H Kaiya ◽  
Y Takei ◽  
SF Perry
Keyword(s):  
Blood Pressure ◽  
Rainbow Trout ◽  
Enzyme Inhibitor ◽  
Plasma Concentrations ◽  
Plasma Catecholamines ◽  
Renin Angiotensin System ◽  
Adrenergic System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

The individual contributions of, and potential interactions between, the renin-angiotensin system (RAS) and the humoral adrenergic stress response to blood pressure regulation were examined in rainbow trout. Intravenous injection of the smooth muscle relaxant, papaverine (10 mg/kg), elicited a transient decrease in dorsal aortic blood pressure (PDA) and systemic vascular resistance (RS), and significant increases in plasma angiotensin II (Ang II) and catecholamine concentrations. Blockade of alpha-adrenoceptors before papaverine treatment prevented PDA and RS recovery, had no effect on the increase in plasma catecholamines, and resulted in greater plasma Ang II concentrations. Administration of the angiotensin-converting enzyme inhibitor, lisinopril (10(-4) mol/kg), before papaverine treatment attenuated the increases in the plasma concentrations of Ang II, adrenaline, and noradrenaline by 90, 79, and 40%, respectively and also prevented PDA and RS recovery. By itself, lisinopril treatment caused a gradual and sustained decrease in PDA and RS, and reductions in basal plasma Ang II and adrenaline concentrations. Bolus injection of a catecholamine cocktail (4 nmol/kg noradrenaline plus 40 nmol/kg adrenaline) in the lisinopril+papaverine-treated trout, to supplement their circulating catecholamine concentrations and mimic those observed in fish treated only with papaverine, resulted in a temporary recovery in PDA and RS. These results indicate that the RAS and the acute humoral adrenergic response are both recruited during an acute hypotensive stress, and have important roles in the compensatory response to hypotension in rainbow trout. However, whereas the contribution of the RAS to PDA recovery is largely indirect and relies on an Ang II-mediated secretion of catecholamines, the contribution from the adrenergic system is direct and relies at least in part on plasma catecholamines.

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