Effects of routine heparin therapy on plasma aldosterone concentration

1991 ◽  
Vol 124 (3) ◽  
pp. 267-270 ◽  
Author(s):  
Yo Kageyama ◽  
Hiromichi Suzuki ◽  
Takao Saruta

Abstract. Changes in plasma aldosterone, plasma renin activity, plasma cortisol, serum sodium and potassium concentrations were studied in 9 patients with thromboembolic diseases treated with heparin. Heparin was administered at doses of 700-1000 units/h for 7-10 days. Plasma aldosterone decreased from 239±33 to 114±25 pmol/l during heparin therapy and returned to basal levels after discontinuation of the therapy. In addition, responses to a low sodium intake (3 g/day) and ACTH were examined in 5 patients during and 2 weeks after heparin therapy. The increase in plasma aldosterone caused by low sodium intake was significantly attenuated during heparin therapy (124±5% increase from baseline) as compared with that 2 weeks after heparin therapy (148±7%, p<0.05). On the other hand, ACTH stimulated plasma aldosterone similarly during and at 2 weeks after heparin therapy (increase from baseline: 190±20% vs 193±9%). These results suggest that heparin decreased plasma aldosterone owing to attenuation of the angiotensin Il-induced aldosterone production.

1992 ◽  
Vol 262 (5) ◽  
pp. F871-F877 ◽  
Author(s):  
W. V. Vieweg ◽  
J. D. Veldhuis ◽  
R. M. Carey

To investigate the pulsatile nature of basal and stimulated renin and aldosterone secretion, we sampled blood for plasma renin activity (PRA) and plasma aldosterone concentration at 10-min intervals for 24 h in nine normal supine human male subjects after equilibration in high- and low-sodium balance states. We evaluated serial hormonal measures by a quantitative waveform-independent deconvolution technique designed to compute the number, amplitude, and mass of underlying secretory bursts and simultaneously to estimate the presence and extent of basal secretion. For both PRA and aldosterone: 1) burstlike release accounted for greater than or equal to 60% of total secretion and tonic release for less than 40%; 2) there was an 80- to 85-min interpulse interval unchanged by sodium intake; 3) sodium restriction engendered an increase in plasma hormone concentrations by increasing the amount and maximal rate of hormone secreted per burst; 4) low dietary sodium also induced increases in basal hormone secretory rates, suggesting that there may be two regulatory processes driving renin and aldosterone secretion; and 5) PRA was significantly coupled to plasma aldosterone concentration by a 0-, 10-, or 20-min aldosterone lag time in both high- and low-sodium balance. We conclude that both renin and aldosterone are released via a predominantly burstlike mode of secretion; PRA and plasma aldosterone concentrations are positively coupled by a short time lag (0-20 min); and sodium restriction achieves an increase in mean PRA and plasma aldosterone concentration by selective amplitude enhancement of individual hormone secretory bursts and by increased tonic (interburst) basal secretory rates.


1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.


1975 ◽  
Vol 80 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Helmut Armbruster ◽  
Wilhelm Vetter ◽  
Rainer Beckerhoff ◽  
Jürg Nussberger ◽  
Hans Vetter ◽  
...  

ABSTRACT In order to investigate the role of renin secretion and of ACTH on the circadian rhythm of plasma aldosterone (PA), plasma renin activity (PRA), plasma cortisol (PC) and PA were determined at short-time intervals in 10 normal supine men. Six subjects were studied under a normal sodium intake and 4 under sodium restriction. In 4 subjects the secretion of ACTH was suppressed by dexamethasone. Under normal sodium intake changes in PA seemed to be more in parallel with changes in PC than by those in PRA as indicated by a higher significant correlation between PA and PC than between PA and PRA in 3 of the 4 subjects. In 1 subject no correlation was observed between PA and PC despite visual synchronism between the plasma concentrations of both hormones. Under dexamethasone medication fluctuations in PA were followed by those in PRA while PC was less than 2 μg/100 ml. In the sodium restricted state, changes in PA were closely paralleled and significantly correlated to PRA while no correlation was seen between PA and PC. Under dexamethasone medication the significant correlation between PA and PRA persisted. Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Under normal sodium intake ACTH seems to be the dominant factor controlling PA, whereas under sodium restriction changes in PA are mediated through the renin angiotensin system. When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake.


1987 ◽  
Vol 116 (2) ◽  
pp. 229-234 ◽  
Author(s):  
Takao Saruta ◽  
Hiromichi Suzuki ◽  
Takashi Takita ◽  
Ikuo Saito ◽  
Masaru Murai ◽  
...  

Abstract. The prognosis of hypertension was evaluated pre-operatively in 40 patients with primary aldosteronism owing to adenoma by examining the severity of hypertension, family history of hypertension, age of the patients, duration of hypertension, plasma renin activity, plasma aldosterone concentration, and efficacy of spironolactone (100 mg per day for 10 days) on blood pressure. In 30 of the 40 patients, the blood pressure was reduced to below 160/95 mmHg within a year after adrenalectomy (responders). In the other 10 patients, the blood pressure was not markedly reduced and remained above 160/95 mmHg (nonresponders). There were no significant differences in the age of the patients, family history of hypertension, plasma renin activity or plasma aldosterone concentration between these two groups. The severity of hypertension as judged by the WHO classification and the duration of hypertension prior to operation seemed to be of some use in assessing the postoperative prognosis of hypertension, but the efficacy of spironolactone was far more useful. That is to say, a reduction in mean blood pressure of more than 15 mmHg after administration of spironolactone was observed in 29 of the 30 responders. The remaining one patient showed an 11 mmHg reduction in mean blood pressure. On the other hand, none of the nonresponders revealed a reduction in mean blood pressure of more than 15 mmHg after spironolactone administration. From these results it is concluded that the pre-operative response of blood pressure to administration of 100 mg per day of spironolactone for 10 days represents a useful indicator of the postoperative prognosis of hypertension in patients with primary aldosteronism owing to adenoma.


1969 ◽  
Vol 60 (2) ◽  
pp. 249-264 ◽  
Author(s):  
Richard E. Bailey ◽  
Henry C. Ford

ABSTRACT The effects of heparin administration on various aspects of the response to Na restriction have been investigated in a group of carefully studied healthy subjects. Administration of heparin following the attainment of Na balance during Na restriction resulted in a decline in the plasma aldosterone concentration and in the aldosterone excretion and secretion rates; natriuresis and an increase in salivary Na/K ratio also occurred. No change in the metabolic clearance of aldosterone was observed. Plasma renin activity was increased during heparin administration and no change in plasma renin substrate concentration occurred (one subject). Administration of heparin both before and during Na restriction almost completely inhibited the increase in aldosterone production but the decline in urinary Na excretion during the adjustment period was not greatly altered when compared to that occurring in the absence of heparin.


1984 ◽  
Vol 247 (3) ◽  
pp. E336-E342
Author(s):  
T. Eguchi ◽  
E. L. Bravo

The mechanism(s) by which intracerebroventricularly administered angiotensin II (ANG II) regulates aldosterone production was investigated in dogs with chronically implanted cannula into a lateral cerebroventricle. In salt-replete and salt-depleted dogs, artificial cerebrospinal fluid (CSF) with or without ANG II (1, 10, 100 ng X kg-1 X min-1) was infused intracerebroventricularly for 2 h under pentobarbital anesthesia. Artificial CSF produced no significant humoral changes. Intracerebroventricular ANG II decreased plasma renin activity and increased both ACTH and plasma cortisol in both groups but decreased plasma aldosterone (PA) only in salt-depleted dogs. Dexamethasone pretreatment during intracerebroventricular ANG II decreased PA further in salt-replete but not in salt-depleted dogs. Moreover, the fall in PA during intracerebroventricular ANG II in salt-depleted dogs was prevented when intravenous infusion of ANG II (10 ng X kg-1 X min-1) was given simultaneously to maintain circulating ANG II levels. We conclude that PA response to intracerebroventricular ANG II is mediated primarily through the renin-angiotensin system in the salt-depleted state; however, in the salt-replete state, ACTH assumes a more important role.


1993 ◽  
Vol 265 (4) ◽  
pp. E648-E654 ◽  
Author(s):  
H. M. Siragy

Bradykinin (BK) is produced by the kidney, but the role of the renal kallikrein-kinin system (KKS) in the control of renal function is not understood. We studied the effects of intrarenal infusion of the BK antagonist, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-trifluoroacetic acid (BKA, n = 5) and BK (n = 4) alone or combined with antagonist (BKA 0.025 ng.kg-1 x min-1 + BK 0.25 ng.kg-1 x min-1, n = 4) in uninephrectomized conscious dogs in sodium balance at 10 and 80 meq/day. During low sodium intake, administration of BKA (infusions from 0.025 to 2.5 ng.kg-1 x min-1) caused a significant antidiuresis (P < 0.0001) and antinatriuresis (P < 0.0001) and a decrease in fractional sodium excretion (P < 0.0001). There were no changes in estimated renal plasma flow (RPF) or glomerular filtration rate during intrarenal administration of BKA at 0.025 and 0.25 ng.kg-1 x min-1. A dose of 2.5 ng.kg-1 x min-1 BKA caused a significant decrease in RPF. There were no changes in plasma aldosterone concentration, plasma renin activity, or systemic arterial pressure during intrarenal BKA administration. At 80 meq/day sodium balance (n = 5), intrarenal administration of BKA did not cause any systemic or renal effects. Intrarenal administration of BK at 0.25 ng.kg-1 x min-1 during low sodium balance caused an increase in urine flow rate and urinary sodium excretion. Coinfusion of BK with BKA completely abrogated the renal excretory changes induced by BKA. These data suggest that intrarenal KKS plays a role in control of renal function largely by a tubular mechanism during low sodium intake.


1980 ◽  
Vol 239 (3) ◽  
pp. F271-F280 ◽  
Author(s):  
J. E. Hall ◽  
A. C. Guyton ◽  
M. J. Smith ◽  
T. G. Coleman

The present study was designed to quantitate the role of the renin-angiotensin system (RAS) in determining the chronic relationships between arterial pressure (AP), renal hemodynamics, and Na excretion. In six control dogs, Na balance was achieved during chronic step increases in Na intake from 5 to 500 meq/day with small increases in AP (<7 mmHg), moderate increases in GFR (19%), and decreases in filtration fraction (FF) and plasma renin activity. Similar increases in Na intake in six dogs with angiotensin II (AII) fixed, due to constant intravenous infusion of 5 ng . kg-1 . min-1 AII, caused large increases in AP (42%), GFR (31%) FF, and calculated renal Na reabsorption (TNa) above control. In six dogs with AII formation blocked with SQ 14,225, Na balance at intakes of 5-80 meq/day occurred at reduced AP, GFR, FF, and TNa, although plasma aldosterone concentration (PAC) was not substantially different from that in control dogs. At Na intakes above 240 meq/day, AP was not altered by SQ 14,225. These data indicate that during chronic changes in Na intake the RAS plays a major role, independent of changes in PAC, in allowing Na balance without large changes in GFR or AP. The mechanism whereby AII conserves Na chronically is through increased TNa, since steady-state TNa was increased by AII and decreased by SQ 14,225.


1986 ◽  
Vol 108 (3) ◽  
pp. 405-411 ◽  
Author(s):  
F. Riad ◽  
J. Lefaivre ◽  
C. Tournaire ◽  
J.-P. Barlet

ABSTRACT Intravenous infusion of aldosterone (10 μg/kg body wt per h for 5 h) in four 2-month-old calves decreased salivary and urinary sodium (Na+) concentration and increased salivary potassium (K+) concentration without modifying salivary flow or urinary K+ concentration. Intravenous angiotensin II infusion (0·3 μg/kg body wt per min for 1 h) in four Na+-replete 16-month-old bulls decreased salivary Na+ concentration and increased that of K+. It also increased plasma cortisol and plasma aldosterone concentrations, and decreased plasma renin activity (PRA). In four 16-month-old bulls Na+ deficiency (induced by chronic cannulation of the righ parotid duct and loss of saliva for 5 days) had similar effects to those observed following aldosterone infusion in calves: a decrease in salivary Na+/K+ ratio. This decrease was associated with an increase in PRA and an increase in plasma aldosterone concentration. In these animals a close positive relationship was observed between PRA and plasma aldosterone concentration (r = 0·91; n = 20; P < 0·01). Thus in cattle, during Na+ deficiency, the effect of aldosterone on parotid glands participates in the regulation of Na+ metabolism. J. Endocr. (1986) 108, 405–411


2019 ◽  
Vol 20 (3) ◽  
pp. 147032031987089
Author(s):  
Satoshi Kidoguchi ◽  
Naoki Sugano ◽  
Naomi Hayashi-Ishikawa ◽  
Norihiko Morisawa ◽  
Goro Tokudome ◽  
...  

Introduction: The captopril challenge test (CCT) is the major confirmatory test for primary aldosteronism (PA), and frequently carried out because of its convenience. However, it presents false-negative results with a certain probability, and as there are many criteria for CCT, it is not concluded yet which criteria to use. Materials and methods: A total of 71 PA patients were evaluated. We compared CCT-positive and CCT-negative patients in the following three criteria: plasma aldosterone/renin ratio (ARR) >200 after the CCT (criterion 1); plasma aldosterone concentration (PAC) >120 pg/ml after the CCT (criterion 2); and PAC suppression <30% of PAC before CCT (criterion 3). Results: The positive rate was 70.4%, 64.8% and 54.9% for criterion 1, criterion 2 and criterion 3, respectively. With criterion 1, the baseline plasma renin activity was lower, thus baseline ARR was higher in CCT-positive patients. With criterion 2, PAC was higher and estimated sodium intake and K were lower in CCT-positive patients. With criterion 3, K and PAC were lower in CCT-positive patients. Although it was not significant, in the patients with high sodium intake, the positive rate of criterion 1 was higher than that of the other criteria. Conclusions: ARR>200 is the valuable criterion for the diagnosis of PA.


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