BIOSYNTHESIS OF ALDOSTERONE FROM 18-HYDROXYLATED PRECURSORS BY RAT ADRENAL TISSUE IN VITRO

1977 ◽  
Vol 75 (2) ◽  
pp. 187-195 ◽  
Author(s):  
D. I. FATTAH ◽  
B. J. WHITEHOUSE ◽  
G. P. VINSON
Keyword(s):  
Adrenal Glands ◽  
Specific Activity ◽  
Alternative Pathway ◽  
Control Diet ◽  
High Specific Activity ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Aldosterone Production

Rat adrenal capsules incubated with [3H]18-hydroxydeoxycorticosterone (18-OH-DOC) and [3H]18-hydroxycorticosterone gave appreciable yields of aldosterone from both precursors, similar in size to those obtained from labelled corticosterone, deoxycorticosterone and progesterone under the same conditions. After feeding rats for 14 days on a flour diet deficient in sodium, aldosterone production from endogenous precursors in vitro was increased twofold compared with that by adrenal glands from animals receiving the flour diet with 1% sodium chloride added (control diet). When adrenal capsules from animals on the low-sodium flour diet were incubated with high specific activity [3H]18-OH-DOC (sp. act. 40 Ci/mmol), the yield of [3H]aldosterone was increased two- to threefold compared with that produced by capsules from animals on the control diet. When capsules were incubated with low specific activity [3H] 18-OH-DOC and [14C]corticosterone (sp. act. 52 mCi/mmol) only the yield of [14C]aldosterone was increased. Yields of labelled 18-hydroxycorticosterone from all precursors tested were increased three- to fourfold in animals receiving the low-sodium diet relative to the controls. The results show that 18-OH-DOC can be an effective precursor for aldosterone formation by rat adrenal capsules, and that production of aldosterone and 18-hydroxycorticosterone from this precursor can be stimulated by a low-sodium diet. This suggests the existence of an alternative pathway for aldosterone biosynthesis involving 18-OH-DOC as an intermediate.

Increased Renal Sensitivity to Aldosterone in the Potassium-Loaded Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder
Keyword(s):  
Sodium Intake ◽  
Control Diet ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High K ◽  
And Control

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.

Alterations in Cerebrospinal Fluid Angiotensin II by Sodium Intake in Patients with Essential Hypertension

1989 ◽  
Vol 77 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Minoru Kawamura ◽  
Yuhei Kawano ◽  
Kaoru Yoshida ◽  
Masahito Imanishi ◽  
Satoshi Akabane ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Ang Ii ◽  
Sodium Depletion ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 ± 0.38 (sem) to 1.83 ± 0.43 fmol/ml (P < 0.01) and of ANG III from 0.65 ± 0.11 to 0.86 ± 0.15 fmol/ml (P < 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

In vivo stimulation of apical P2 receptors in collecting ducts: evidence for inhibition of sodium reabsorption

2005 ◽  
Vol 288 (6) ◽  
pp. F1243-F1248 ◽  
Author(s):  
D. G. Shirley ◽  
M. A. Bailey ◽  
R. J. Unwin
Keyword(s):  
Control Diet ◽  
P2 Receptors ◽  
Sodium Reabsorption ◽  
Receptor Subtype ◽  
Recovery Ratio ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Collecting Ducts

In vitro evidence suggests that intraluminal nucleotides, acting on apical P2 receptors, may influence amiloride-sensitive sodium reabsorption in collecting ducts. The present study has assessed this possibility directly in anesthetized rats, by determining the urinary recovery of 22Na relative to that of [14C]inulin (Na/inulin recovery ratio) during in vivo microperfusion of late distal tubules with artificial tubular fluid containing various P2 agonists (all at 1 mM). In animals maintained on a control diet, in which amiloride-sensitive 22Na reabsorption was modest, the poorly hydrolysable, broad-spectrum P2 agonist ATPγS had no significant effect on the Na/inulin recovery ratio. In contrast, in rats maintained on a low-sodium diet, in which amiloride-sensitive 22Na reabsorption was considerably enhanced, ATPγS caused a significant increase in the Na/inulin recovery ratio (control: 14 ± 3%; ATPγS: 28 ± 4%; n = 32 pairs; P < 0.001, paired t-test). No change in the Na/inulin recovery ratio was seen in time controls (13 ± 3 vs. 14 ± 4%; n = 15 pairs). In subsequent experiments in rats maintained on a low-sodium diet, we used more selective agonists in an attempt to identify the receptor subtype responsible for the effect of ATPγS. The P2Y1 agonist 2meSADP, the P2Y2/4 agonists Ap4A and Cp4U, and the P2X agonist BzATP were all without significant effect on the Na/inulin recovery ratio. These findings constitute the first in vivo evidence for a functional role for apical P2 receptors in collecting ducts, but the identity of the receptor subtype(s) involved remains elusive.

Effects of Heparin Oligosaccharides with High Affinity for Antithrombin III in Experimental Venous Thrombosis

1982 ◽  
Vol 47 (03) ◽  
pp. 244-248 ◽  
Author(s):  
D P Thomas ◽  
Rosemary E Merton ◽  
T W Barrowcliffe ◽  
L Thunberg ◽  
U Lindahl
Keyword(s):  
Antithrombin Iii ◽  
Specific Activity ◽  
High Specific Activity ◽  
Factor Xa ◽  
Blood Levels ◽  
Thrombin Time ◽  
High Affinity ◽  
Very High

SummaryThe in vitro and in vivo characteristics of two oligosaccharide heparin fragments have been compared to those of unfractionated mucosal heparin. A decasaccharide fragment had essentially no activity by APTT or calcium thrombin time assays in vitro, but possessed very high specific activity by anti-Factor Xa assays. When injected into rabbits at doses of up to 80 ¼g/kg, this fragment was relatively ineffective in impairing stasis thrombosis despite producing high blood levels by anti-Xa assays. A 16-18 monosaccharide fragment had even higher specific activity (almost 2000 iu/mg) by chromogenic substrate anti-Xa assay, with minimal activity by APTT. When injected in vivo, this fragment gave low blood levels by APTT, very high anti-Xa levels, and was more effective in preventing thrombosis than the decasaccharide fragment. However, in comparison with unfractionated heparin, the 16-18 monosaccharide fragment was only partially effective in preventing thrombosis, despite producing much higher blood levels by anti-Xa assays.It is concluded that the high-affinity binding of a heparin fragment to antithrombin III does not by itself impair venous thrombogenesis, and that the anti-Factor Xa activity of heparin is only a partial expression of its therapeutic potential.

Time for a Renewed Focus on the DASH-Low Sodium Diet

2021 ◽  
Vol 77 (21) ◽  
pp. 2635-2637
Author(s):  
Neha J. Pagidipati ◽  
Laura P. Svetkey
Keyword(s):  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Taste Perception in Three Individuals on a Low Sodium Diet

Appetite ◽  
1981 ◽  
Vol 2 (1) ◽  
pp. 67-73 ◽  
Author(s):  
Mary Bertino ◽  
G.K. Beauchamp ◽  
D.R. Riskey ◽  
K. Engelman
Keyword(s):  
Taste Perception ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract 17541: An Education Intervention Focused on Self-monitoring for Symptom and Sodium Intake Improves Adherence to the Low Sodium Diet and Health Outcome in Patients with Heart Failure

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Eun Kyeung Song ◽  
Debra K Moser ◽  
Seok-Min Kang ◽  
Terry A Lennie
Keyword(s):  
Health Outcomes ◽  
Cox Regression ◽  
Sodium Intake ◽  
Control Group ◽  
Education Intervention ◽  
Self Monitoring ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Patients With Heart Failure

Background: Despite the clinical emphasis on recommending a low sodium diet (LSD), adherence to a LSD remains poor in patients with heart failure (HF). Additional research is needed to determine successful interventions to improve adherence to a LSD and health outcomes. Purpose: To determine the effect of an education intervention on adherence to a LSD and health outcomes. Method: A total of 109 HF patients (age 64±9 years, 29% female) who were non-adherent to LSD, indicating > 3g of 24-hour urinary sodium excretion (24hr UNa) at baseline, were randomly assigned to one of 3 groups: 1) symptom monitoring and restricted 3 gram sodium diet (SMART) group, 2) the telephone monitoring (TM) group, or 3) usual care control group. The SMART group received individualized teaching and guidance of self-monitoring for worsening symptom and sodium intake using symptom and food diary for 4 sessions over 8 weeks. Patients assigned to either of the 2 intervention groups (SMART or TM) received phone calls every 2 weeks over 8 weeks. At 6 months follow-up, adherence to a LSD was assessed using 24hr UNa. Patients were followed for 1 year to determine time to first event of hospitalization or death due to cardiac problems. Repeated measures ANOVA and Cox regression were used to determine the effect of intervention. Results: The SMART group (n=37) showed a significant reduction in sodium intake across time compared to the TM group (n=35) and control group (n=37) (p= .022). In the Cox regression, patients in the SMART group had longer cardiac event-free survival compared to the control group after controlling for age, gender, ejection fraction, angiotensin-converting enzyme inhibitor use, and better blocker use (p=.008). Conclusion: An education intervention focused on self-monitoring for symptom and sodium intake improved adherence to LSD and health outcomes in patients with HF. Helping patients engage in self-monitoring for symptom and sodium intake by themselves can promote better health outcome.

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