Plasma 18-hydroxycorticosterone and aldosterone responses to angiotensin II and corticotropin in diabetic patients with hyporeninemic and normoreninemic hypoaldosteronism

1989 ◽  
Vol 121 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Ryoji Iwasaki ◽  
Toshikazu Kigoshi ◽  
Kenzo Uchida ◽  
Shinpei Morimoto
Keyword(s):  
Angiotensin Ii ◽  
Plasma Cortisol ◽  
Plasma Corticosterone ◽  
Zona Glomerulosa ◽  
Plasma Aldosterone ◽  
Diabetic Patients ◽  
Control Subjects ◽  
Normal Ranges ◽  
Baseline Levels

Abstract. To examine the nature of adrenal abnormalities in diabetic patients with hyporeninemic and normoreninemic hypoaldosteronism, responses of plasma 18-hydroxycorticosterone and plasma aldosterone to angiotensin II infusions and ACTH injection were investigated in 8 diabetic patients with hyporeninemic hypoaldosteronism and 9 diabetic patients with normoreninemic hypoaldosteronism compared to 11 control subjects. In both the patients with hyporeninemic and normoreninemic hypoaldosteronism, plasma 18-hydroxycorticosterone and plasma aldosterone were low, whereas plasma cortisol and plasma corticosterone were within normal ranges. Percent increments of plasma 18-hydroxycorticosterone and plasma aldosterone above their baseline levels after angiotensin II infusions were low or somewhat low in the patients with hyporeninemic hypoaldosteronism and low in the patients with normoreninemic hypoaldosteronism. Percent increments of plasma 18-hydroxycorticosterone and plasma aldosterone above their baseline levels after ACTH injection were similar in the three groups. These results suggest that in diabetic patients with isolated hypoaldosteronism, the adrenal abnormality, regardless of whether it is primary or secondary, is mainly due to impaired adrenal responsiveness to angiotensin II and atrophy of the zona glomerulosa.

The Control of Aldosterone Secretion in Nephrectomized Man

1974 ◽  
Vol 47 (3) ◽  
pp. 235-248 ◽  
Author(s):  
T. J. Goodwin ◽  
V. H. T. James ◽  
W. S. Peart
Keyword(s):  
Renal Transplantation ◽  
Angiotensin Ii ◽  
Plasma Cortisol ◽  
Extracellular Fluid ◽  
Renin Angiotensin System ◽  
Plasma Potassium ◽  
Zona Glomerulosa ◽  
Plasma Aldosterone ◽  
Clear Correlation ◽  
Sodium Depletion

1. The adrenal response to a reduction in extracellular fluid volume (ECFV), sodium depletion, intravenous adrenocorticotrophic hormone (ACTH) and angiotensin II was assessed from changes in plasma aldosterone and plasma cortisol in eleven nephrectomized patients. Five patients were also studied before nephrectomy and six after successful renal transplantation. 2. Before nephrectomy, the resting concentrations of plasma aldosterone were usually raised. In the three patients out of five tested, the response to intravenous ACTH was marked. In two out of four patients, there was a good response to angiotensin II infusion. In one of two patients, there was a good response to a reduction in ECFV and sodium depletion. 3. After nephrectomy, the resting concentrations of plasma aldosterone were negligible or uniformly reduced and the response to ECFV reduction, sodium depletion, ACTH and angiotensin II was universally poor. 4. In all cases there was a normal plasma cortisol response to ACTH. 5. After renal transplantation in six patients, the four to whom an infusion of angiotensin II was given showed a return to a normal aldosterone response and all six showed a normal response to ACTH. 6. No clear correlation was shown between resting concentrations of plasma aldosterone and plasma potassium after nephrectomy. 7. It was concluded that the kidney, through the renin-angiotensin system, may play its main part by sensitizing the zona glomerulosa to other stimuli, but an alternative kidney-dependent mechanism cannot be excluded.

Selective Hypoaldosteronism: A Study of Steroid Biosynthetic Pathways under Adrenocorticotrophin and Angiotensin II Infusion

1976 ◽  
Vol 51 (s3) ◽  
pp. 335s-337s ◽  
Author(s):  
M. Lebel ◽  
J. H. Grose
Keyword(s):  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Plasma Aldosterone ◽  
Zona Fasciculata ◽  
Biosynthetic Pathways ◽  
Normal Functioning ◽  
Probable Consequence ◽  
Plasma Steroids ◽  
Dose Dependent Increase ◽  
Dose Dependent

1. The functional integrity of the adrenal cortex has been tested in a case of selective hypoaldosteronism by adrenocorticotrophin (ACTH) and angiotensin II (AII) infusion. 2. During ACTH infusion a normal functioning zona fasciculata was indicated by the impressive increase of the ACTH-dependent plasma steroids; the aldosterone response was moderate. 3. During AII infusion the plasma aldosterone response was blunted with an unexpected dose-dependent increase in pregnenolone, resulting in abnormal decreasing progesterone/pregnenolone ratios during the infusion, suggesting a slow-down in the conversion of pregnenolone into progesterone. 4. This defect, a probable consequence of chronic renin deficiency on the zona glomerulosa, could be a contributing factor to the hypoaldosteronism.

Feedback-mediated reduction in glomerular filtration during acetazolamide infusion in insulin-dependent diabetic patients

1991 ◽  
Vol 81 (s25) ◽  
pp. 457-464 ◽  
Author(s):  
T. Hannedouche ◽  
M. Lazaro ◽  
A. G. Delgado ◽  
C. Boitard ◽  
B. Lacour ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Feedback System ◽  
Diabetic Patients ◽  
Control Subjects ◽  
Before And After ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

1. A sustained high glomerular filtration rate in diabetes mellitus is associated with increased proximal reabsorption, suggesting alterations in the tubulo-glomerular feedback system. To test this hypothesis, renal function was studied in eight control subjects and 14 recent-onset euglycaemic insulin-dependent diabetic patients before and after infusion of the carbonic anhydrase inhibitor, acetazolamide (5 mg/kg body weight). 2. Acetazolamide induced a dramatic fall in glomerular filtration rate in both diabetic patients and control subjects (from 138 ± 5 to 114 ± 4 and from 127 ± 3 to 113 ± 2 ml min−1 1.73 m−2, respectively, P < 0.0001). This fall in glomerular filtration rate was strongly correlated with the acetazolamide-induced decrease in absolute proximal reabsorption calculated by using lithium clearance. 3. To further assess the potential role of angiotensin II in the acetazolamide-induced tubulo-glomerular feedback response, 11 additional diabetic patients were investigated before and after the administration of acetazolamide plus the angiotensin-converting enzyme inhibitor, enalaprilat (1.25 mg intravenously). Despite the effective blockade of angiotensin II formation and a slight decrease in renal vascular resistance, the glomerular filtration rate fell significantly and by a similar magnitude as seen with acetazolamide alone. 4. These results indirectly suggest that there is an altered basal tubulo-glomerular feedback system in diabetic patients but a normal response to the increase in distal delivery. No convincing role for an angiotensin II-mediated effect on the afferent limb of the tubulo-glomerular feedback response could be demonstrated.

Role of angiotensin II in aldosterone regulation in the Pekin duck

1989 ◽  
Vol 123 (3) ◽  
pp. 445-NP ◽  
Author(s):  
D. A. Gray ◽  
R. Gerstberger ◽  
E. Simon
Keyword(s):  
Angiotensin Ii ◽  
Physiological Role ◽  
Plasma Potassium ◽  
Plasma Corticosterone ◽  
Plasma Aldosterone ◽  
Pekin Duck ◽  
Plasma Sodium ◽  
Pekin Ducks ◽  
Angiotensin Iii

ABSTRACT The response of plasma aldosterone to increased plasma angiotensin II (AII) was evaluated in normally hydrated Pekin ducks as well as in birds in which plasma sodium had been acutely increased (+12 mmol/l) or reduced (−4 mmol/l) by the prior infusion of hypertonic saline or hypotonic glucose. In all cases, the i.v. infusion of AII at rates of 5, 15 and 45 pmol/kg per min for 1 h produced dose-dependent increases in the plasma concentration of aldosterone, with a potency that was inversely related to the sodium status. In addition, adrenal receptors for AII were demonstrated by in-vitro autoradiography and membranebinding techniques, suggesting that the AII effect on aldosterone secretion is direct. Angiotensin II produced no change in plasma corticosterone. The infusion of KC1 at 1, 2 and 5 mmol/l for 1 h increased plasma potassium by as much as 2 mmol/l, but had no influence on plasma aldosterone. Similarly, the heptapeptide angiotensin III, infused at 5, 15 and 45 pmol/kg per min for 1 h had no effect on circulating aldosterone. The results show that in ducks, AII has a physiological role in the control of aldosterone, whereas plasma potassium and angiotensin III have no such secretagogue function. Journal of Endocrinology (1989) 123, 445–452

Humoral responses to intracerebroventricularly administered angiotensin II in dogs

1984 ◽  
Vol 247 (3) ◽  
pp. E336-E342
Author(s):  
T. Eguchi ◽  
E. L. Bravo
Keyword(s):  
Angiotensin Ii ◽  
Plasma Cortisol ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Ang Ii ◽  
Angiotensin System ◽  
Artificial Cerebrospinal Fluid ◽  
Aldosterone Production ◽  
Humoral Responses

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.

Effect of angiotensin II on aldosterone and its precursor steroid production in adrenal zona glomerulosa cells from heparin-treated rats

1986 ◽  
Vol 111 (2) ◽  
pp. 222-227 ◽  
Author(s):  
K. Uchida ◽  
S. Azukizawa ◽  
N. Imaizumi ◽  
T. Kigoshi ◽  
I. Yamamoto ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Corticosterone Level ◽  
Plasma Renin ◽  
Plasma Corticosterone ◽  
Zona Glomerulosa ◽  
Threshold Dose ◽  
Lower Response ◽  
Aldosterone Production ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

Abstract. To assess the nature of the heparin-induced aldosterone deficiency, we investigated the stimulatory effect of angiotensin II (All) on aldosterone and its precursor steroids in adrenal zona glomerulosa cells from heparin-treated rats compared with those in the cells from vehicle-treated rats. Heparin-treated rats had low plasma aldosterone levels, high plasma renin activity and plasma All levels, and normal plasma corticosterone level 6 weeks after the treatment (1500 IU/kg, twice daily). Basal aldosterone production, when corrected to a uniform number of cells per group, was similar in the cells from heparin- and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to All; an increase by 4 orders of magnitude in the threshold dose for All and a decrease in the maximum All-stimulated level. The maximum All-stimulated levels, but not the basal levels, of pregnenolone, corticosterone and 18-OHB production were low in the cells from heparin-treated rats. ACTH caused a similar stimulatory effect on aldosterone production in the cells from heparin- and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to potassium; an increase by one order of magnitude in the threshold dose for potassium and a decrease in the maximum potassium-stimulated level, presumably because of the glomerulosa hyporesponsivness to AII. These results suggest that our heparin-treated rats have selective impairment of adrenal zona glomerulosa cells,

Aldosterone regulates salivary sodium secretion in cattle

1986 ◽  
Vol 108 (3) ◽  
pp. 405-411 ◽  
Author(s):  
F. Riad ◽  
J. Lefaivre ◽  
C. Tournaire ◽  
J.-P. Barlet
Keyword(s):  
Angiotensin Ii ◽  
Plasma Cortisol ◽  
Positive Relationship ◽  
Plasma Renin ◽  
Salivary Flow ◽  
Plasma Aldosterone ◽  
Parotid Glands ◽  
Plasma Aldosterone Concentration ◽  
Parotid Duct ◽  
Chronic Cannulation

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

Effect of Propranolol Therapy on Aldosterone Responses to Angiotensin II and Adrenocorticotropic Hormone in Essential Hypertension

1981 ◽  
Vol 61 (1) ◽  
pp. 107-110 ◽  
Author(s):  
M. S. Golub ◽  
M. L. Tuck ◽  
D. B. Fittingoff
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Before And After ◽  
Propranolol Therapy

1. The plasma aldosterone responses to exogenous angiotensin II and adrenocorticotropic hormone (ACTH) were studied before and after 1 month of propranolol therapy (120–240 mg/day) in eight patients with essential hypertension. 2. Basal supine plasma renin activity was decreased (P < 0.001) after propranolol, whereas plasma aldosterone was unchanged. After 3 h of upright posture the increases in both plasma renin activity and aldosterone were decreased (P < 0.05) after propranolol. 3. Plasma aldosterone responses to exogenous angiotensin II and ACTH were not significantly different after propranolol. Serum and urinary electrolytes and plasma cortisol were also unaffected by propranolol therapy. 4. It is concluded that changes in adrenal sensitivity are not responsible for maintaining unchanged supine plasma aldosterone concentrations after β-adrenoceptor antagonism in essential hypertension.

Effect of Spironolactone on Aldosterone Regulation in Man

1980 ◽  
Vol 58 (3) ◽  
pp. 227-233 ◽  
Author(s):  
R. C. Gaillard ◽  
A. M. Riondel ◽  
P. Chabert ◽  
M. B. Vallotton
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Corticosterone ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Minor Role ◽  
Corticosterone Concentration ◽  
Plasma Aldosterone Concentration ◽  
Normal Men

1. The action of spironolactone, a well-known antagonist of mineralocorticoids, on aldosterone regulation was investigated in normal young men to see whether it also acted as an inhibitor of biosynthesis in the adrenal gland. 2. The action of spironolactone was studied under three different conditions: (a) during 3 days of treatment with spironolactone; (b) during 1 day of combined administration with long acting adrenocorticotropic hormone (ACTH); (c) in the course of a continuous infusion of angiotensin II. 3. Spironolactone did not alter the metabolism of aldosterone or cortisol. 4. Spironolactone administration produced: (a) a marked increase in both aldosterone secretion and plasma renin activity, but no change in the plasma aldosterone/plasma renin activity ratio, the cortisol secretion rate or the plasma corticosterone concentration; (b) no blunting in the response of aldosterone to stimulation by ACTH; (c) no decrease in plasma aldosterone concentration when changes of the endogenous renin activity were prevented by an infusion of angiotensin II. 5. These results do not confirm the considerable inhibition of aldosterone excretion found by others after spironolactone administration to normal men. We observed no inhibition of aldosterone biosynthesis by spironolactone. However, a minimal, short-lived inhibition of biosynthesis cannot be excluded, but this possible action of spironolactone plays at best a minor role in the action of this drug.

Sign in / Sign up

Export Citation Format

Share Document