Studies on Aldosterone Responsiveness to Angiotensin II during Clinical Variations in Calcium Metabolism in Normal Man

1982 ◽  
Vol 63 (3) ◽  
pp. 325-328 ◽  
Author(s):  
M. G. Bianchetti ◽  
C. Beretta-Piccoli ◽  
P. Weidmann ◽  
K. Boehringer ◽  
L. Link ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Calcium Metabolism ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Minor Role ◽  
Dose Rates ◽  
Normal Man ◽  
A Minor ◽  
Clinical Conditions ◽  
Dependent Pathway

1. Angiotensin II was infused at stepwise increasing dose rates (2, 4 and 10 pmol min–1 kg–1) in 12 normal subjects. Infusions were performed in the presence of normocalcaemia, mild hypercalcemia induced by concomitant calcium gluconate infusion, and after 2 weeks of treatment with nifedipine. 2. Pre-infusion plasma levels of angiotensin II, renin or aldosterone were not altered by acute mild hypercalcaemia or administration of nifedipine. The angiotensin II-induced increases in plasma aldosterone were also similar under the three study conditions. 3. Variations in calcium metabolism occurring under clinical conditions appear to play a minor role in modulating the angiotensin II-dependent pathway of aldosterone regulation in normal man.

Effect of Converting Enzyme Inhibition on the Systemic and Renal Responses to Acute Isotonic Volume Expansion in Normal Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 285s-287s ◽  
Author(s):  
A. Mimran ◽  
J. Ribstein
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Volume Expansion ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Converting Enzyme ◽  
Volume Dependence ◽  
Converting Enzyme Inhibition ◽  
Normal Man ◽  
Renal Responses

1. Systemic, humoral and renal responses to isotonic volume expansion (1800 ml in 3 h) were assessed in normal subjects before and during captopril administration. 2. Captopril, which otherwise induced a decrease in pre-saline mean arterial pressure (MAP), unmasked the volume-dependence of MAP, which increased linearly during volume expansion (+ 18.7 ± 3.8% at the end of volume expansion). 3. Captopril prevented the fall in plasma aldosterone produced by volume expansion but did not modify the natriuretic response to saline. 4. These results suggest that intrarenal rather than circulating angiotensin II may be one of the determinants of the natriuretic response to volume expansion in normal man.

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

1980 ◽  
Vol 59 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M. Epstein ◽  
M. D. Lifschitz ◽  
R. Re ◽  
E. Haber
Keyword(s):  
Plasma Renin Activity ◽  
Volume Expansion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Plasma Aldosterone Concentration ◽  
Normal Man

1. The relationship of the renin-angiotensin-aldosterone axis with renal prostaglandin E is complex. Although studies have suggested that these two hormonal systems respond to experimental manipulations in a parallel manner, their interdependence has not been assessed fully during volume expansion. Since studies have demonstrated that in normal man the central hypervolaemia induced by water immersion to the neck produces a prompt and profound suppression of plasma renin activity and plasma aldosterone concentration without concomitant alteration of plasma composition, immersion afforded a unique opportunity to assess simultaneously the effects of central hypervolaemia on plasma renin activity, plasma aldosterone concentration and prostaglandin E excretion. 2. Seven normal subjects were studied twice while in balance on a diet containing 10 mmol of sodium/day, 100 mmol of potassium/day: with indomethacin administration (50 mg given every 6 h for five doses) and without indomethacin. Urinary prostaglandin E excretion was measured hourly and plasma renin activity and plasma aldosterone concentration at 30 min intervals. 3. Immersion was associated with a marked suppression of plasma renin activity (59 ± 7%) and plasma aldosterone concentration (55 ± 3%) with a return to pre-study values during the recovery hour. Concomitantly, urinary prostaglandin E excretion increased from 4.7 to a peak of 10.9 ng/min. Although administration of indomethacin lowered the basal rate of urinary prostaglandin E excretion and plasma renin activity, it did not prevent the subsequent augmentation of urinary prostaglandin E or the suppression of plasma renin activity and plasma aldosterone during the subsequent 4 h of immersion. 4. These results demonstrate a dissociation of renin-aldosterone and prostaglandin E during hypervolaemia and suggest that whereas prostaglandin E may constitute one of the major determinants of renin release clinically and experimentally, these two hormonal systems can be dissociated from each other in response to central volume expansion in man.

scholarly journals Mec1 and Rad53 Inhibit Formation of Single-Stranded DNA at Telomeres of Saccharomyces cerevisiae cdc13-1 Mutants

Genetics ◽  
2004 ◽  
Vol 166 (2) ◽  
pp. 753-764 ◽  
Author(s):  
Xindan Jia ◽  
Ted Weinert ◽  
David Lydall
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Budding Yeast ◽  
Minor Role ◽  
Clamp Loader ◽  
Checkpoint Proteins ◽  
Checkpoint Kinases ◽  
Sliding Clamp ◽  
Telomere Binding Protein ◽  
A Minor ◽  
Dependent Pathway

Abstract Here we examine the roles of budding-yeast checkpoint proteins in regulating degradation of dsDNA to ssDNA at unprotected telomeres (in Cdc13 telomere-binding protein defective strains). We find that Rad17, Mec3, as well as Rad24, members of the putative checkpoint clamp loader (Rad24) and sliding clamp (Rad17, Mec3) complexes, are important for promoting degradation of dsDNA in and near telomere repeats. We find that Mec1, Rad53, as well as Rad9, have the opposite role: they inhibit degradation. Downstream checkpoint kinases Chk1 and Dun1 play no detectable role in either promoting degradation or inhibiting it. These data suggest, first, that the checkpoint sliding clamp regulates and/or recruits some nucleases for degradation, and, second, that Mec1 activates Rad9 to activate Rad53 to inhibit degradation. Further analysis shows that Rad9 inhibits ssDNA generation by both Mec1/Rad53-dependent and -independent pathways. Exo1 appears to be targeted by the Mec1/Rad53-dependent pathway. Finally, analysis of double mutants suggests a minor role for Mec1 in promoting Rad24-dependent degradation of dsDNA. Thus, checkpoint proteins orchestrate carefully ssDNA production at unprotected telomeres.

RESPONSE OF PLASMA ALDOSTERONE TO ANGIOTENSIN II, ACTH AND POTASSIUM IN MAN

1973 ◽  
Vol 72 (2) ◽  
pp. 293-307 ◽  
Author(s):  
D. Scholer ◽  
M. Birkhäuser ◽  
A. Peytremann ◽  
A. M. Riondel ◽  
M. B. Vallotton ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Time Course ◽  
Sodium Intake ◽  
Fold Increase ◽  
Normal Subjects ◽  
Potassium Citrate ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Variable Degree ◽  
Low Sodium

ABSTRACT Plasma aldosterone, corticosterone, cortisol and renin activity have been measured in recumbent normal subjects (n = 3–4) following stimulation with angiotensin II, ACTH and potassium. Control studies on a regular sodium intake show that in the same subject aldosterone and renin activity exhibit no time dependent pattern from 7 a.m. to 11 a.m., while corticosterone and cortisol decrease continuously. Angiotensin II (infusion of 7 ng/kg/min over 1–3 h), ACTH (rapid iv injection of 0.5 mg β1-24 ACTH) and potassium (potassium citrate 30 mEq. po every hour for 3 h) on a regular Na intake induce a reproducible increase of aldosterone. The onset of this increase is observed within 10 min for angiotensin II and ACTH and within 60–90 min for potassium. The range of the rise in aldosterone is about 20–25 ng/100 ml for all 3 stimuli, corresponding to a 3–5 fold increase from basal values. Angiotensin II and potassium are, in the dose used, specific stimuli of aldosterone; ACTH however stimulates aldosterone, corticosterone and cortisol, but to a variable degree and with a different time-course response. On a low sodium intake, a similar aldosterone response pattern is found after stimulation with ACTH, but only exceptionally after stimulation with potassium; after both stimuli values of 55–75 ng/100 ml have been reached.

scholarly journals FP016DOWN-REGULATION OF MEGALIN-MEDIATED ENDOCYTOSIS PLAYS A MINOR ROLE IN ANGIOTENSIN II INDUCED PROTEINURIA

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i54-i54
Author(s):  
Sandra Hummelgaard ◽  
Louise Tran ◽  
Kasper Schmidt ◽  
Erik Christensen ◽  
Rikke Nielsen ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Minor Role ◽  
A Minor
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