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PubMed1983

Effects of metoclopramide, a dopamine antagonist, on secretion of aldosterone and renin release in patients with primary aldosteronism.

To assess the interaction between dopamine and aldosterone secretion in primary aldosteronism, the dopamine antagonist, metoclopramide (methoxy-2-chloro-5-procainamide), was given as an i.v. bolus (10 mg) to 5 patients with primary aldosteronism and 5 normal subjects treated with dexamethasone (2 mg/day) to eliminate an influence of ACTH. Metoclopramide increased plasma aldosterone concentration (PAC) in primary aldosteronism from 39.1 +/- 15.5 to 42.5 +/- 15.9 ng/100 ml (p less than 0.05) and also from 12.9 +/- 2.3 to 23.6 +/- 3.4 ng/100 ml (p less than 0.01) in normal subjects at 15 min. Plasma renin activity (PRA), and plasma concentrations of cortisol, potassium, and sodium did not significantly change with metoclopramide in either primary aldosteronism or normal subjects. Plasma prolactin increased by 12- and 20-fold in primary aldosteronism and in normal subjects, respectively, but there was no significant positive correlation between changes in PAC and in plasma prolactin in either primary aldosteronism or normal subjects. It is suggested that dopamine inhibits the secretion of aldosterone in primary aldosteronism as well as in normal subjects. It seems unlikely that dopamine affects the release of renin in primary aldosteronism.

Adrenocorticotropic Hormone↗
PubMed1982

Restoration of renin-aldosterone dynamics to normal following surgery in primary aldosteronism.

Little is known regarding the response of the renin-angiotensin-aldosterone system to dynamic maneuvers after surgical removal of an aldosterone-producing adenoma or whether normal renin-aldosterone relationships are restored following surgery. We utilized maneuvers designed to assess the adequacy of aldosterone suppression and renin stimulation to rapid changes in sodium and fluid volume status to examine these relationships in 21 patients before and after surgery for primary aldosteronism. All patients failed to suppress plasma aldosterone normally after intravenous saline infusion and failed to stimulate renin activity into the normal range following diuretic-induced sodium and volume depletion. No relationship between renin and aldosterone was discerned. The studies were repeated 6 mo. to 4 yrs. after unilateral adrenalectomy in all 21 patients. In every case the normal suppression of aldosterone and stimulation of renin was observed. Moreover a significant (p less than 0.001) relationship between renin and aldosterone was demonstrable. Thus in this population of patients with surgically responsive primary aldosteronism, no abnormality of aldosterone production persisted.

Adenoma↗
PubMed1997

Aldosterone to renin ratios in the evaluation of primary aldosteronism.

Primary aldosteronism, though an uncommon cause of hypertension, causes significant morbidity, making it important to diagnose and treat this condition. Its evaluation requires complex and time consuming investigative procedures in order to confirm the diagnosis and to differentiate between the subtypes of aldosterone producing adenoma and idiopathic hyperaldosteronism. Often, the values of renin and aldosterone are equivocal, and the diagnosis of primary aldosteronism is in doubt. In this study, we examine the use of aldosterone to renin ratios in confirming the diagnosis of primary aldosteronism when the usual criteria of suppressed renin and elevated aldosterone are not met. We have found that an aldosterone to renin ratio of 50 has a 100% specificity and 92% sensitivity for detecting primary aldosteronism. Also, an aldosterone to renin ratio of > 2000 is suggestive of an aldosterone producing adenoma.

Adrenocortical Adenoma↗
PubMed2026

Aldosterone fuels the progression of cardiovascular-kidney -metabolic syndrome: focus on primary aldosteronism spectrum.

In 2023, the American Heart Association (AHA) introduced the Cardiovascular-Kidney-Metabolic (CKM) syndrome concept to address the substantial burden of interrelated cardiovascular, kidney, and metabolic disorders. The framework highlights that chronic kidney disease (CKD) significantly accelerates CKM syndrome progression and increases cardiovascular risk, an effect that may be closely paralleled by aldosterone excess. Excess aldosterone can arise from renin-dependent aldosteronism (RDA), a primarily physiological state (not discussed in this review), or from renin-independent aldosteronism (RIA). RIA is a pathophysiologically relevant condition characterized by persistent autonomous activation, bypassing normal renin-angiotensin-aldosterone system (RAAS) regulation. Its most recognized form is PA, a prevalent, multidimensional disorder spanning a continuum from subclinical to overt autonomous aldosterone production. This leads to inappropriately elevated aldosterone relative to suppressed renin and sodium levels. PA is a leading cause of secondary hypertension and elevates the risk of metabolic and cardiorenal disorders, showing substantial overlap with CKM syndrome. Despite its clinical significance, the specific relationship between PA and CKM syndrome remains insufficiently investigated. This review synthesizes evidence from three key perspectives: (1) Epidemiology and clinical data show that PA spans a spectrum from subclinical to overt stages and is strongly associated with driving and accelerating the progression of CKM syndrome; (2) Therapeutically, targeted treatment of PA mitigates the adverse effects of aldosterone on CKM syndrome progression; and (3) Pathophysiologically, inappropriately elevated aldosterone primarily interacts with widely distributed mineralocorticoid receptors in tissues relevant to CKM syndrome, exacerbating key pathogenic pathways akin to adding fuel to the fire. Building on this synthesis, we emphasize that inappropriately elevated aldosterone is not merely a simple biomarker but an active driver and accelerator of CKM syndrome progression. This review also proposes future directions for integrated PA-CKM screening and management. Incorporating PA into the CKM syndrome framework could not only refine CKM syndrome care but also address the critical underdiagnosis of PA, whose screening rate regrettably remains below 2% in high-risk populations.

Humans↗
PubMed1979

Dissociation in the excretion of different aldosterone metabolites and unmetabolized ('free') aldosterone in hypertension.

1. The determination of aldosterone-18-glucuronide (pH 1-labile aldosterone) was complemented by concomitant measurements of free urinary aldosterone and tetrahydroaldosterone in 307 patients, most of whom were hypertensive. In 38 cases (12.3%) the normal, aldosterone-18-glucuronide concentration was clinically misleading, but increased free aldosterone and/or tetrahydroaldosterone values suggested the presence of hyperaldosteronism, which in many of these cases was confirmed by elevated excretion of the possible major aldosterone precursor 18-hydroxycorticosterone (18-OH-B). 2. Of 224 patients with essential hypertension and normal or low plasma renin activity 18 had an elevated free aldosterone and/or tetrahydroaldosterone excretion without increased aldosterone-18-glucuronide. These cases may represent early or pre-symptomatic forms of primary hyperaldosteronism. In other cases, particularly when tetrahydroaldosterone was increased alone, abnormalities of aldosterone metabolism were suspected. 3. In two out of 15 patients with primary hyperaldosteronism, aldosterone-18-glucuronide values were frequently found to be normal, although elevations were noted in other variables. However, no relation to the morphological abnormality (adenoma versus hyperplasia) was seen.

18-Hydroxycorticosterone↗
PubMed1990

Pituitary peptides other than ACTH may not be aldosterone secretagogue in primary aldosteronism.

In order to elucidate whether pituitary peptides other than ACTH which are derived from the proopiomelanocortin (POMC) are involved for aldosterone secretion in primary aldosteronism, we administered ovine corticotropin releasing factor (CRF), beta-endorphin and naloxone to seven patients with aldosterone producing adenoma. One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients. An opioid antagonist, naloxone (10 mg, iv) produced no noticeable change in plasma aldosterone in normal subjects, while it caused a slight increase in patients with primary aldosteronism. Plasma cortisol increased to a similar degree in response to CRF and naloxone in normal subjects and patients. In three patients with isolated ACTH deficiency, neither aldosterone nor cortisol responded to these stimuli. The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism.

Adenoma↗
PubMed1986

The relationship between salivary aldosterone and plasma free aldosterone concentrations.

The proportion of aldosterone in plasma not bound to proteins (% plasma free aldosterone, %PFA) was measured using an equilibrium dialysis technique and was found to lie predominantly in the range 25-40% although extremes of 20% and 60% were encountered. From this value and the total concentration of aldosterone in plasma (plasma aldosterone, PA) the concentration of free aldosterone in plasma (PFA) was calculated. Percentage PFA was not affected by the in-vitro addition of aldosterone (up to the equivalent of 2000 pmol/l) but the incremental addition of cortisol (up to the equivalent of 550 nmol/l) resulted in a linear increase in % PFA from 26% to 34%. Percentage PFA was found to be significantly, negatively correlated with serum albumin concentration (r = -0.87; P less than 0.001) but it was only when this was less than 15 milligrams that % PFA was abnormally high. Salivary aldosterone concentration (SA) was more highly correlated with PFA (r = 0.84) than with PA (r = 0.75), which indicates that even modest variance in %PFA has a discernible effect upon the overall SA-PA relationship. We conclude that measurement of salivary aldosterone concentrations gives a useful estimate of plasma free aldosterone level. Variations in the latter are determined more by changes in the total concentration of aldosterone in plasma than by variations in the degree of binding by plasma proteins.

Albumins↗
PubMed2004

Aldosterone administration to mice stimulates macrophage NADPH oxidase and increases atherosclerosis development: a possible role for angiotensin-converting enzyme and the receptors for angiotensin II and aldosterone.

BACKGROUND: The renin-angiotensin-aldosterone system is involved in the pathogenesis of atherosclerosis, partially because of its pro-oxidative properties. We questioned the effect and mechanisms of action of administration of aldosterone to apolipoprotein E-deficient (E(0)) mice on their macrophages and aorta oxidative status and the ability of pharmacological agents to block this effect. METHODS AND RESULTS: Aldosterone (0.2 to 6 microg. mouse(-1) x d(-1)) was administered to E(0) mice alone or in combination with eplerenone (200 mg x kg(-1) x d(-1)), ramipril (5 mg x kg(-1) x d(-1)), or losartan (25 mg x kg(-1) x d(-1)). Mouse aortic atherosclerotic lesion area and macrophage and aortic oxidative status were evaluated. Aldosterone administration enhanced the mouse atherosclerotic lesion area by 32%. Mouse peritoneal macrophages and aortic segments from aldosterone-treated mice exhibited increased superoxide anion formation by up to 155% and 69%, respectively, and this effect was probably mediated by NADPH oxidase activation, because increased translocation of its cytosolic component p47phox to the macrophage plasma membrane was observed. THP-1 macrophages incubated in vitro with aldosterone (10 micromol/L) exhibited a higher capacity to release superoxide ions by 110% and increased ability to oxidize LDL by 74% compared with control cells. Aldosterone administration enhanced mouse peritoneal macrophage ACE activity and mRNA expression by 2.3-fold and 2.4-fold, respectively. Only cotreatment of eplerenone with ramipril or losartan completely blocked the oxidative effects of aldosterone. CONCLUSIONS: Aldosterone administration to E(0) mice increased macrophage oxidative stress and atherosclerotic lesion development. Blocking of the mineralocorticoid receptor and inhibition of tissue ACE and/or the angiotensin receptor-1 reduced aldosterone deleterious pro-oxidative and proatherogenic effects.

Aldosterone↗
PubMed2006

Evidence for a role of vasopressin in the control of aldosterone secretion in primary aldosteronism: in vitro and in vivo studies.

CONTEXT: Arginine vasopressin (AVP) stimulates steroid secretion from the normal human adrenal gland and some cortisol-producing adrenocortical tumors or hyperplasia through activation of the V(1a) receptor. OBJECTIVE: The objective of the study was to investigate in vitro and in vivo the possible involvement of AVP in the physiopathology of primary aldosteronism. DESIGN: The design of the study included immunohistochemical, pharmacological, and molecular studies on aldosterone-producing adenoma (APA), followed by a monocentric, crossover trial of the orally active V(1a) receptor antagonist, SR 49059, in a double blind, randomized, and placebo-controlled fashion. SETTING: The study was conducted at a university hospital and research laboratory. PATIENTS: The study population included eight untreated patients with primary aldosteronism, four with APA and four with idiopathic hyperaldosteronism. MAIN OUTCOME MEASURES: Aldosterone secretion of APA cells in vitro and plasma aldosterone, renin, and ACTH were measured. INTERVENTION: SR 49059 (200 mg once daily) or placebo was administered during two 1-wk treatment periods separated by a 2-wk washout. RESULTS: We observed the occurrence of AVP-containing cells in APA tissues. Administration of AVP to perifused APA cells induced an increase in aldosterone production, which was inhibited by a specific V(1a) antagonist. RT-PCR analysis showed the expression of V(1a) receptor mRNA in most APAs studied. In APA patients, SR 49059 did not induce any effect on basal aldosterone secretion but provoked a plasma aldosterone response to orthostatism (P < 0.03) and strengthened the positive correlation between plasma aldosterone and ACTH. CONCLUSIONS: The present study indicates that functional V(1a) receptors are present in APA and suggests that AVP may exert an autocrine/paracrine control of aldosterone secretion in APA tissues.

Adenoma↗
PubMed1982

[The localization of aldosterone-producing adenoma on computed tomography--a comparative study with adrenal scintigraphy and plasma aldosterone concentration in the adrenal or renal vein].

The evaluation of computed tomography (CT) for detecting aldosterone-producing adenoma in primary aldosteronism was performed by comparison with adrenal scintiscan; determination of aldosterone in adrenal or renal veins, retroperitoneal pneumography and adrenal venography was reliable for diagnosis of adrenal tumors in pheochromocytoma or Cushing's syndrome, but not so effective for small adenoma of primary aldosteronism. An abdominal CT scan was performed on six patients with primary aldosteronism, one with idiopathic hyperaldosteronism and one with glucocorticoid responsive hyperaldosteronism; in an attempt to evaluate the utility of this noninvasive procedure. Diagnosis of hyperaldosteronism was made by demonstrating the elevated plasma aldosterone concentration and aldosterone secretion rate, normal excretion rate of urinary 17-OHCS and 17-KS, and low plasma renin activity. The CT scan correctly predicted unilateral adrenal adenoma in all the patients with primary aldosteronism of which the findings were identical to those demonstrated by surgery. The diameter of these tumors ranged from 10 X 7 X 6 to 19 X 17 X 14 mm. Also the CT scan in idiopathic hyperaldosteronism and glucocorticoid responsive hyperaldosteronism showed bilateral adrenal hyperplasia and bilateral normal adrenal glands, respectively. The pathological findings in these two cases disclosed the adrenal hyperplasia of zona glomerulosa and adrenal hyperplasia of zona subglomerulosa accompanied by a normal thickness of the adrenal gland, respectively. The precision of the CT scan, adrenal scintigraphy and determination of plasma aldosterone in the adrenal or renal veins were almost equal to the diagnosis of the localization of adrenal adenoma. It is concluded that the CT scan is a noninvasive and most useful method for the localization of aldosterone-producing adenoma and helpful in distinguishing adrenal adenoma from adrenal hyperplasia.

Adenoma↗
PubMed1987

Effects of aldosterone on intralymphocytic sodium and potassium in patients with primary aldosteronism.

In vitro effects of aldosterone have been described with regard to the intracellular sodium and potassium concentrations of human mononuclear leukocytes. In the present paper the in vitro effect of aldosterone on the intracellular sodium and potassium of human mononuclear leukocytes in 6 patients with primary aldosteronism was investigated. Except for one patient with elevated intracellular electrolytes, sodium and potassium in mononuclear leukocytes of patients with aldosteronism without incubation were within the range for normals. In the patients, no significant change of intracellular sodium or potassium was observed during incubation with or without aldosterone (1.4 nmol/l), whereas in normals, the loss of sodium and potassium during incubation without aldosterone was prevented by 1.4 nmol/l aldosterone. This insensitivity to aldosterone indicates that intracellular electrolytes in mononuclear leukocytes of patients with primary aldosteronism are kept in normal ranges by mechanism which are independent of mineralocorticoids and may represent the cellular correlate to the renal 'escape' phenomenon in aldosteronism.

Adult↗
PubMed2004

Aldosterone-synthase overexpression in heart: a tool to explore aldosterone's effects.

Clinical observations indicate that elevated aldosterone impairs cardiovascular function. The mechanisms, however, are not totally understood although total and cardiovascular mortality are decreased by aldosterone antagonists. Experimentally, increased plasma aldosterone induces pericoronary inflammation and cardiac fibrosis. Our laboratory has discovered that aldosterone is synthesized in the rat heart, and has demonstrated that this cardiac aldosterone is involved in post-infarction cardiac remodeling. In man, activated cardiac aldosterone production has been described in patients with heart failure. In transgenic mice that overexpress aldosterone-synthase in the heart, we observe a normal cardiac function but a major coronary dysfunction, more pronounced in males. These observations converge to a potential physiological and pathological relevance of this system. Beneficial effects of anti-aldosterone treatment in heart failure may thus be secondary in part to blockade of cardiac aldosterone action.

Aldosterone↗
PubMed2002

Use of plasma aldosterone concentration-to-plasma renin activity ratio as a screening test for primary aldosteronism. A systematic review of the literature.

The aldosterone-renin ratio is widely used to screen for primary aldosteronism. We conducted a systematic review of the literature to establish the test characteristics (sensitivity, specificity, likelihood ratios at different cutoff values) of the aldosterone-renin ratio used in screening for primary aldosteronism in subjects with presumed essential hypertension. We searched Medline, EMBASE, and Current Contents databases, bibliographies of retrieved papers, and personal files for all reports published from January 1966 to October 2001. We consulted experts to identify additional published and unpublished reports. We included prospective studies of the ratio as a screening test for primary aldosteronism, without applying language or data availability restrictions. We excluded retrospective studies, case reports, and duplicate or preliminary reports. Working independently, we selected the articles, assessed their quality, and extracted their data. Data extracted included sample size and care setting, description of the testing conditions, description of the confirmatory tests, and the test characteristics of the ratio (sensitivity, specificity, likelihood ratios at different cutoff values). This review includes 16 studies with 3136 participants. None of the studies evaluated the aldosterone-renin ratio and the reference standard independently of each other; only two studies evaluated patients who had a "negative" ratio with the reference standard. Only 16.7% of the subjects had both the ratio and the confirmatory test performed. Ratio cutoff values ranged from 200 to 2774 pmol/L per ng/mL per hour. None of the studies provided valid estimates of the aldosterone-renin ratio test characteristics. There are no published valid estimates of the test characteristics of the aldosterone-renin ratio when used as a screening test for primary aldosteronism in patients with presumed essential hypertension.

Aldosterone↗
PubMed2002

Ratio of serum aldosterone to plasma renin concentration in essential hypertension and primary aldosteronism.

The ratio of serum aldosterone to plasma renin activity (PRA) has been proposed as sensitive screening method in the diagnosis of primary aldosteronism under random conditions. However, the method for determination of renin activity is hampered by the necessity of ice cooling during storage and transport. The present study was therefore conducted to examine the ratio of serum aldosterone to plasma renin concentration (ARR) and its usefulness in diagnosis of primary aldosteronism under ambulatory conditions and given antihypertensive medication. 146 patients with arterial hypertension who consecutively attended the outpatient clinic were studied prospectively. Patients with secondary hypertension besides primary aldosteronism were not included in the series. 37 normotensive patients served as control. Also, 17 patients with known primary aldosteronism were retrospectively examined. Among the hypertensive group 2 patients with Conn's syndrome were newly detected (1.4%). ARR was 7.92 +/- 6.04 [pg/ml]/[pg/ml] in normotensive controls (range from 2.03 to 26.98), 14.61 +/- 18.50 [pg/ml]/[pg/ml] in patients with essential hypertension (n = 144, range from 0.41 to 115.45) and 155.92 +/- 127.84 [pg/ml]/[pg/ml] in patients with primary aldosteronism (n = 19, range from 6.75 to 515). 17 of the 19 patients with Conn's syndrome had an ARR of more than 50. Under ongoing drug treatment this represents a sensitivity of 89% and a specificity of 96%. Sensitivity decreased to 84% and specificity increased to 100% when a second criteria (aldosterone > or = 200 pg/ml) was included. In summary, ARR using renin concentration is a useful screening parameter for primary aldosteronism.

Adult↗
PubMed1989

Racial differences in aldosterone excretion and plasma aldosterone concentrations in children.

Blacks are more likely to have hypertension, have lower levels of plasma renin activity, and typically consume less potassium than whites. Whether blacks and whites secrete different amounts of aldosterone is less clear. We estimated aldosterone secretion indirectly in 715 children, 249 of whom were black, by measuring their nocturnal rates of urinary excretion of aldosterone. Dietary sodium and potassium intakes were estimated from their excretion rates. The mean (+/- SE) aldosterone-excretion rate was lower in the black children than in the white children (0.045 +/- 0.003 vs. 0.078 +/- 0.004 nmol per micromole of creatinine per kilogram of body weight; P less than 0.001). The potassium-excretion rate was also lower in the black children than in the white children (0.13 +/- 0.01 vs. 0.18 +/- 0.01 mmol per micromole of creatinine per kilogram; P less than 0.001). Aldosterone excretion was highly correlated with potassium excretion (P less than 0.001), but the lower aldosterone-excretion rate in blacks was explained only in part by their lower dietary intake of potassium. Systolic blood pressure was higher in black children (P less than 0.001), as was diastolic pressure (P = 0.037). In a second study of 99 children, the plasma aldosterone level was found to be significantly lower in black children than in white children (230 +/- 30 vs. 400 +/- 30 pmol per liter; P less than 0.001). Plasma renin activity and plasma cortisol levels were the same in both groups. In summary, we found that black children secrete about 40 percent less aldosterone than white children. The role of the lower aldosterone-secretion rate in the genesis of the higher blood pressures observed in black children is not known.

Aldosterone↗
PubMed2000

Intralymphocyte free magnesium in patients with primary aldosteronism: aldosterone and lymphocyte magnesium homeostasis.

It is known that hyperaldosteronism has been associated with magnesium deficiency, yet there are no data on the intracellular concentration of ionized magnesium ([Mg(2+)(i)]) in subjects with primary aldosteronism (PA). We measured intralymphocyte free magnesium ([Mg(2+)(i)]) and intralymphocyte free calcium ([Ca(2+)(i)]) in 16 patients with PA and 26 normotensive control subjects (NCs). [Mg(2+)(i)] and [Ca(2+)(i)] were also measured in blood lymphocytes incubated in vitro with aldosterone, according to a fluorimetric method. In subjects with PA, [Mg(2+)(i)] was significantly lower than that in NCs (mean+/-SD; PA 203+/-56 micromol/L, NCs 291+/-43 micromol/L, 95% confidence interval 57 to 119, P=0.001). In the patients, [Ca(2+)(i)] did not prove to be statistically different from that of NCs (mean+/-SD; PA 47.2+/-10.6 nmol/L, NCs 53.2+/-11 nmol/L). The lymphocytes exposed to the action of aldosterone showed a significant reduction in [Mg(2+)(i)] (n=15, NCs 271+/-28 micromol/L, aldosterone treatment 188+/-39 micromol/L, P=0.001, 95% confidence interval 57 to 108). The dose-effect curve of aldosterone on [Mg(2+)(i)] showed an EC(50) value of approximately 0.5 to 1 nmol/L aldosterone. The reduction in [Mg(2+)(i)] mediated by aldosterone is antagonized by the receptor inhibitor of aldosterone; it is inhibited by inhibitors of protein synthesis and is not measurable when the lymphocytes are incubated in an Na(+)-free medium. The data are consistent with the hypothesis that aldosterone affects the cellular homeostasis of magnesium, probably through modification of the activity of the Na(+)-Mg(2+) antiporter.

Adult↗
PubMed1979

Effects of metoclopramide and bromocriptine on the renin-angiotensin-aldosterone system in man. Dopaminergic control of aldosterone.

This study was designed to investigate the possible role of dopaminergic mechanisms in the control of the renin-angiotensin-aldosterone system in normal man. Six normal male subjects in metabolic balance at 150 meq sodium, 60 meq potassium constant intake received the specific dopamine antagonist, metoclopramide, 10 mg i.v. or placebo followed by angiotensin II infusion 1 h later on 2 consecutive days. Metoclopramide increased plasma aldosterone concentration from 8.2+/-2.2 to 21.0+/-3.3 ng/100 ml (P < 0.005) and plasma prolactin concentration from 18.0+/-4.0 to 91.7+/-4.0 ng/ml (P < 0.001) within 15 min of its administration. At 1 h, plasma aldosterone and prolactin concentrations remained elevated at 16.8+/-2.1 ng/100 ml (P < 0.01) and 86.8+/-15.9 ng/ml (P < 0.005), respectively. Angiotensin II at 2, 4, and 6 pmol/kg per min further increased plasma aldosterone concentration to 27.2+/-3.4, 31.9+/-5.7, and 36.0+/-6.7 ng/100 ml (P < 0.02), respectively. Placebo did not alter plasma aldosterone or prolactin concentrations, but angiotensin II increased plasma aldosterone concentration to 13.7+/-2.4, 19.0+/-1.9, and 23.3+/-3.2 ng/100 ml (P < 0.005). The increment of plasma aldosterone concentration in response to angiotensin II was similar after metoclopramide or placebo. The six subjects also received the dopamine agonist, bromocriptine, 2.5 mg or placebo at 6 p.m., midnight, and 6 a.m. followed by angiotensin II infusion on 2 consecutive d. Bromocriptine suppressed prolactin to <3 ng/ml. After placebo, plasma aldosterone concentration increased from 5.2+/-1.4 to 12.3+/-1.7, 17.2+/-2.2, and 21.8+/-3.5 ng/100 ml (P < 0.01) and after bromocriptine from 7.2+/-1.0 to 14.7+/-3.0, 19.8+/-3.2, and 23.4+/-1.6 ng/100 ml (P < 0.001) with each respective angiotensin II dose. No difference in the response to angiotensin II after bromocriptine or placebo was observed. Plasma renin activity, free 11-hydroxycorticoid concentration, and serum potassium concentration were unchanged by metoclopramide or bromocriptine. The results suggest that aldosterone production is under maximum tonic dopaminergic inhibition which can be overridden with stimulation by angiotensin II in normal man.

11-Hydroxycorticosteroids↗
PubMed1981

The plasma aldosterone response to angiotensin II infusion in aldosterone-producing adenoma and idiopathic hyperaldosteronism.

To determine if the adrenal sensitivity to angiotensin II in patients with an aldosterone-producing adenoma differs from that in patients with idiopathic hyperaldosteronism, we infused graded doses of angiotensin II into 17 patients with primary aldosteronism and measured their plasma aldosterone concentrations after each dose. At a rate of 0.5 ng angiotensin II/kg.min, the mean increase in the plasma aldosterone concentration in the 8 patients from whom an aldosterone-producing adenoma was subsequently removed was 4 +/ 2.4 ng/dl (mean +/- SE), which was significantly less (P less than 0.01) than the mean increase (23 +/- 4.8 ng/dl) in the 9 patients with idiopathic hyperaldosteronism. The threshold dose of angiotensin II in the patients with aldosterone-producing adenoma was 1.0 +/- 0.24 ng/kg.min, significantly greater (P less than 0.05) than the threshold dose (0.3 +/- 0.07 ng/kg.min) in the patients with idiopathic hyperaldosteronism. We conclude that the sensitivity of aldosterone-producing adenomas to angiotensin II is significantly less than that of the hypersecreting adrenal tissue in patients with idiopathic hyperaldosteronism. This difference in adrenal sensitivity might in part explain the difference in the response of plasma aldosterone concentrations to upright posture in these two subsets of aldosteronism with low renin activity.

Adenoma↗