Renal adaptation and gut hormone release during sodium restriction in ileostomized man

1985 ◽  
Vol 69 (3) ◽  
pp. 299-308 ◽  
Author(s):  
R. J. Unwin ◽  
S. Moss ◽  
W. S. Peart ◽  
Jane Wadsworth
Keyword(s):  
Test Meal ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Significant Rise ◽  
Plasma Aldosterone ◽  
Sodium Restriction ◽  
Gut Peptides ◽  
Plasma Aldosterone Concentration ◽  
Gut Hormone ◽  
Renal Adaptation

1. The renal excretion of water, electrolytes, aldosterone and kallikrein was monitored in 12 ileostomized patients before and during sodium deprivation. Changes in plasma renin activity (PRA), plasma aldosterone and plasma arginine vasopressin (AVP) concentrations were measured, together with aldosterone in ileal fluid. The pattern of gut peptide release in response to a test meal was also examined to assess whether a circulating gut peptide might be involved in the renal adaptation to sodium restriction, and compared with healthy normal subjects who were under no dietary constraint. 2. In each patient renal sodium excretion fell within 8–12 h of sodium deprivation and was associated with a prompt and significant rise in PRA; much later increases in plasma aldosterone concentration and renal aldosterone excretion occurred, and were established by day 2 of sodium restriction. No consistent change in renal kallikrein excretion was found. 3. Ileal sodium loss was little changed by sodium deprivation, but ileal potassium concentration rose steadily and became significantly correlated with PRA, and to a lesser extent with renal aldosterone excretion. 4. Of the gut peptides measured in plasma, only the insulin profile was altered by sodium deprivation, with an increase in the test meal response; insulin has previously been shown to have a significant antinatriuretic action at physiological concentrations. Plasma levels of pancreatic polypeptide and motilin were increased in ileostomized patients when compared with normal subjects, but were unaffected by the change to a low sodium diet. 5. An early increase in urine flow and water diuresis occurred during sodium deprivation, following a cyclical pattern with peaks each evening. There were no corresponding changes in measured plasma AVP concentration or creatinine clearance. This observation remains unexplained.

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.

Inhibition of the Renin-Angiotensin-Aldosterone System by l-Dopa with and without Inhibition of Extracerebral Dopa Decarboxylase in Man

1981 ◽  
Vol 61 (2) ◽  
pp. 187-190 ◽  
Author(s):  
C. Barbieri ◽  
R. Caldara ◽  
C. Ferrari ◽  
Rosa Maria Crossignani ◽  
M. Recchia
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Drugs Analysis ◽  
Catecholamine Levels

1. The present study was undertaken to investigate the possibility that central nervous system mono-aminergic pathways may play a role in the control of the renin-angiotensin-aldosterone system in man. 2. Eight normal subjects received in a randomized order placebo, l-dopa (500 mg, orally) and l-dopa (100 mg, orally) plus carbidopa (35 mg, orally) after pretreatment with carbidopa (50 mg every 6 h for four doses). 3. l-Dopa administration elicited a significant fall in plasma renin activity (PRA) (P < 0.01 at 120, 150 and 180 min) and in plasma aldosterone levels (P < 0.05 at 90, 120, 150 and 180 min); L-dopa plus carbidopa induced a decrease in PRA (P < 0.05 at 120 and 150 min, P < 0.01 at 180 min) and in plasma aldosterone concentration (P < 0.05 at 30 and 60 min, P < 0.01 at 90 and 120 min), in comparison with placebo administration; between-drugs analysis revealed no difference in the decreases in PRA and plasma aldosterone levels induced by the two regimens. 4. Since l-dopa, as well as l-dopa plus carbidopa, has been shown to augment catecholamine levels in the brain of various animal species, the present data suggest that in man PRA and plasma aldosterone concentration might be inhibited by increased central nervous system catecholamine levels.

THE EFFECT OF HEPARIN ON SODIUM CONSERVATION AND ON THE PLASMA CONCENTRATION, THE METABOLIC CLEARANCE AND THE SECRETION AND EXCRETION RATES OF ALDOSTERONE IN NORMAL SUBJECTS

1969 ◽  
Vol 60 (2) ◽  
pp. 249-264 ◽  
Author(s):  
Richard E. Bailey ◽  
Henry C. Ford
Keyword(s):  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Metabolic Clearance ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Heparin Administration ◽  
Aldosterone Production ◽  
Excretion Rates ◽  
Secretion Rates

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.

scholarly journals The Effects of Verapamil, Hydralazine and Doxazosin on Renin, Aldosterone and The Ratio Thereof

2021 ◽  
Author(s):  
Gregory P Veldhuizen ◽  
Rawan M Alnazer ◽  
Peter W. de Leeuw ◽  
Abraham A Kroon
Keyword(s):  
Antihypertensive Medication ◽  
Plasma Renin ◽  
Significant Rise ◽  
Plasma Aldosterone ◽  
Limited Evidence ◽  
Endocrine Society ◽  
Plasma Aldosterone Concentration ◽  
Before And After ◽  
Aldosterone To Renin Ratio ◽  
Drug Cessation

Abstract PURPOSE Hydralazine, doxazosin and verapamil are currently recommended by the Endocrine Society as acceptable bridging treatment in those in whom full cessation of antihypertensive medication is infeasible during screening for primary aldosteronism (PA). This is under the assumption that they cause minimal to no effect on the aldosterone-to-renin ratio, the most widely used screening test for PA. However, limited evidence is available regarding the effects of these particular drugs on said ratio. METHODS In the present study, we retrospectively assessed the changes in aldosterone, renin and aldosterone-to-renin values in essential hypertensive participants before and after treatment with either hydralazine (n = 26), or doxazosin (n = 20) or verapamil (n = 15). All samples were taken under highly standardised conditions. RESULTS Hydralazine resulted in a borderline significant rise in active plasma renin concentration (19 vs 25 mIU/L, p = 0.067) and a significant fall in the aldosterone-to-renin ratio (38 vs 24, p = 0.017). Doxazosin caused declines in both plasma aldosterone concentration (470 vs 330 pmol/L, p = 0.028) and the aldosterone-to-renin ratio (30 vs 20, p = 0.020). With respect to verapamil, we found no statistically significant effect on any of these outcome variables. CONCLUSION We conclude that the assumption that these drugs can be used with little consequence to the aldosterone-to-renin cannot be substantiated. While it is possible that they are indeed the best option when full antihypertensive drug cessation is infeasible, the potential effects of these drugs must still be taken into account when interpreting the aldosterone-to-renin ratio.

scholarly journals The Effects of Verapamil, Hydralazine, and Doxazosin on Renin, Aldosterone, and the Ratio Thereof

2021 ◽  
Author(s):  
Gregory P. Veldhuizen ◽  
Rawan M. Alnazer ◽  
Peter W. de Leeuw ◽  
Abraham A. Kroon
Keyword(s):  
Antihypertensive Medication ◽  
Plasma Renin ◽  
Significant Rise ◽  
Plasma Aldosterone ◽  
Limited Evidence ◽  
Endocrine Society ◽  
Plasma Aldosterone Concentration ◽  
Before And After ◽  
Aldosterone To Renin Ratio ◽  
Drug Cessation

Abstract Purpose Hydralazine, doxazosin, and verapamil are currently recommended by the Endocrine Society as acceptable bridging treatment in those in whom full cessation of antihypertensive medication is infeasible during screening for primary aldosteronism (PA). This is under the assumption that they cause minimal to no effect on the aldosterone-to-renin ratio, the most widely used screening test for PA. However, limited evidence is available regarding the effects of these particular drugs on said ratio. Methods In the present study, we retrospectively assessed the changes in aldosterone, renin, and aldosterone-to-renin values in essential hypertensive participants before and after treatment with either hydralazine (n = 26) or doxazosin (n = 20) or verapamil (n = 15). All samples were taken under highly standardized conditions. Results Hydralazine resulted in a borderline significant rise in active plasma renin concentration (19 vs 25 mIU/L, p = 0.067) and a significant fall in the aldosterone-to-renin ratio (38 vs 24, p = 0.017). Doxazosin caused declines in both plasma aldosterone concentration (470 vs 330 pmol/L, p = 0.028) and the aldosterone-to-renin ratio (30 vs 20, p = 0.020). With respect to verapamil, we found no statistically significant effect on any of these outcome variables. Conclusion We conclude that the assumption that these drugs can be used with little consequence to the aldosterone-to-renin cannot be substantiated. While it is possible that they are indeed the best option when full antihypertensive drug cessation is infeasible, the potential effects of these drugs must still be taken into account when interpreting the aldosterone-to-renin ratio.

Temporal pattern of renin and aldosterone secretion in men: effects of sodium balance

1992 ◽  
Vol 262 (5) ◽  
pp. F871-F877 ◽  
Author(s):  
W. V. Vieweg ◽  
J. D. Veldhuis ◽  
R. M. Carey
Keyword(s):  
Sodium Intake ◽  
Time Lag ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium

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.

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