atrial-natriuretic-factor and Adrenal-Cortex-Neoplasms

The diagnosis of primary aldosteronism (PA) is based on the finding of the combination of elevated urinary and/or plasma aldosterone and suppressed renin activity in patients with hypertension and hypokalemia. However, PA consists in a number of subsets, and diagnostic criteria for a correct identification of surgically remediable forms are of great interest. The methods and the results concerning our series of 113 patients with primary aldosteronism are presented in this review. Aldosterone producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) were the most frequent forms, 51% and 44% respectively. They had similar BP levels, but hypokalemia was most frequently found in APA. Urinary and upright plasma aldosterone were similar, but supine plasma aldosterone was lower in IHA. Plasma aldosterone response to upright posture and angiotensin II infusion was absent in most cases of APA and present in IHA, but occasionally renin-responsive adenoma were found. Captopril failed to decrease plasma aldosterone in most patients with APA, and in a subgroup of patients with IHA. Patients with adenoma had also higher values of the aldosterone precursor 18-OH-B, and of atrial natriuretic peptide (ANP), probably as a consequence of a greater degree of volume expansion. Among morphological studies, CT scan and adrenal radio-cholesterol scintiscan provided similar results (85% accuracy): adrenal vein catheterization clarified almost all the remaining cases. Among the subsets of PA, 3 familiar cases of dex-suppressible hyperaldosteronism were recognized, with characteristically high levels of aldo, 18-OH-B, 18-OH-cortisol and 18-oxo-cortisol, due to the genetic abnormalities of the 11-18 hydroxylase system.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adenoma; Adrenal Cortex; Adrenal Cortex Neoplasms; Atrial Natriuretic Factor; Captopril; Carcinoma; Cytochrome P-450 CYP11B2; Cytochrome P-450 Enzyme System; Dexamethasone; Diagnostic Imaging; Humans; Hyperaldosteronism; Hyperplasia; Posture; Renin; Retrospective Studies; Steroid 11-beta-Hydroxylase

The first step in steroidogenesis is cholesterol mobilization from cytosolic lipid droplets to the initiating rate-limiting enzyme complex located on the inner mitochondrial membrane. Angiotensin II (AngII), the primary agonist of aldosterone secretion from adrenal glomerulosa cells, is known to induce cholesterol mobilization to mitochondria. However, the role of the protein kinase C (PKC) pathway in mediating cholesterol mobilization is unknown. To determine PKC's involvement, human adrenocortical carcinoma cells were incubated with or without PKC-activating phorbol 12-myristate 13-acetate (PMA) and mitochondrial cholesterol content assayed. Like AngII, PMA significantly elevated mitochondrial cholesterol content as well as aldosterone secretion. Thus, PKC may play a role in cholesterol mobilization to mitochondria and hence steroid production. Atrial natriuretic peptide (ANP) inhibited both AngII- and PMA-stimulated mitochondrial cholesterol content. These findings suggest that the ability of ANP to inhibit steroidogenesis induced by multiple agents may be related to its capacity to reduce cholesterol mobilization.

Topics: Adrenal Cortex Neoplasms; Adrenocortical Carcinoma; Angiotensin II; Atrial Natriuretic Factor; Biological Transport; Cell Line, Tumor; Cholesterol; Humans; Lipid Metabolism; Mitochondria; Phorbol Esters; Steroids

The purpose of this study was to investigate the mechanisms of action of pituitary adenylate cyclase-activating polypeptide (PACAP) in stimulating aldosterone production in two different models: bovine adrenal zona glomerulosa (ZG) cells in primary culture and the human adrenocortical carcinoma cell line H295R. PACAP binds to two major groups of receptors: type I, which prefers PACAP38 and PACAP27 over vasoactive intestinal peptide (VIP); and type II, which has approximately equal affinity for PACAP38, PACAP27, and VIP. The type I subclass comprises multiple splice variants that can be distinguished by their specificity to PACAP38 and PACAP27 in their activation of adenylate cyclase and phospholipase C. Type II PACAP/ VIP receptors couple only to AC. In bovine ZG cells, PACAP38 and PACAP27 stimulated aldosterone production in a dose-dependent manner, whereas VIP was ineffective. In H295R cells, PACAP38, PACAP27, and VIP dose-dependently stimulated aldosterone production with roughly the same ED50. In bovine ZG cells, PACAP38 and PACAP27 stimulated cAMP production with similar efficacy, whereas VIP had no effect. In H295R cells, all three peptides stimulated cAMP accumulation. PACAP38 and PACAP27 also activated PLC in bovine ZG cells as they induced an increase in Ins(1,4,5)Ps production. In H295R cells, neither of these peptides was able to stimulate IP turnover. These results indicate that PACAP stimulation of aldosterone production is mediated by the PVR1s or the PVR1hop splice variants of the type I PACAP-specific receptor subtype in bovine ZG cells, whereas only type II PACAP/VIP receptors seemed to occur in the human H295R cell line. In addition, PACAP-stimulated aldosterone production was inhibited by atrial natriuretic peptide in bovine and human adrenocortical cells, however not by the same mechanism. This further supports species-specific and/or cell type-specific signaling pathways for PACAP in the regulation of aldosterone production.

Topics: Adrenal Cortex Neoplasms; Aldosterone; Animals; Atrial Natriuretic Factor; Cattle; Cells, Cultured; Cyclic AMP; Humans; Inositol 1,4,5-Trisphosphate; Neuropeptides; Pituitary Adenylate Cyclase-Activating Polypeptide; Vasoactive Intestinal Peptide; Zona Glomerulosa

The inhibitory effect of atrial natriuretic peptide (ANP) on angiotensin II (AII)-stimulated aldosterone secretion has been previously studied in rat and bovine adrenal zona glomerulosa cells in primary culture. However the understanding of the mode of action of ANP at the molecular level has been hampered by limitations of those primary cell culture systems and by the lack of cell lines from human adrenal cortex. Here we demonstrate the presence of fully functional ANP receptors in the recently characterized AII-responsive adrenocortical carcinoma cell line H295R. Specific saturable binding of 125I-rANP to H295R cell membrane preparations revealed a single class of high affinity binding sites with a density of 20 fmol/mg of protein. The pharmacological profile of this ANP receptor was documented by competitive binding of 125I-rANP with naturally occurring natriuretic peptides. rANP was the most potent with a Kd of 42 pM. pBNP32 was less potent with a Kd of 174 pM. 125I-rANP binding was not competed by pCNP (NPRB-specific ligand) nor by C-ANF (NPRC-specific ligand). Photoaffinity labeling of membrane preparations with 125I-BPA-ANP revealed a single specific protein of molecular weight around 130 kDa. This protein was further identified by immunodetection with a specific antibody directed to the human ANP-specific receptor NPRA. Natriuretic peptides stimulated cGMP production by the receptor-coupled guanylate cyclase with the same specificity. Aldosterone production by AII-stimulated H295R cells was dose-dependently inhibited by rANP with an ED50 of 1.5 nM. In addition, we used this model to test two chimeric analogs of ANP and BNP. pBNP1 and pBNP3 were, respectively, 4- and 2-fold more potent than rANP in competing for 125I-rANP binding with Kd of 10 and 20 pM. pBNP1 was 24-fold more potent in inhibiting AII-stimulated aldosterone production with ED50 of 63 pM. pBNP1 is therefore the most potent natriuretic peptide analog tested. In summary, the human H295R cell line contains NPRA receptors positively coupled to the particulate guanylate cyclase and that antagonize angiotensin II stimulation of aldosterone secretion.

Topics: Adrenal Cortex; Adrenal Cortex Neoplasms; Aldosterone; Atrial Natriuretic Factor; Biological Assay; Cyclic GMP; Humans; Receptors, Atrial Natriuretic Factor; Recombinant Proteins; Tumor Cells, Cultured

Previous studies have shown a significant association between allelic frequencies at the ANP gene locus and aldosterone responsiveness to angiotensin in aldosterone-producing adenoma (APA). We searched for any gross insertions or deletions in the ANP gene in APA and any associations between allelic frequencies at the Hpa II and Sca I RFLP sites within the ANP gene and angiotensin-responsive and unresponsive APA and normal subjects. We also searched for possible point mutations in the promoter region of the ANP gene (-595 to transcription start site) in peripheral blood and tumor DNA from 59 patients with APA and in peripheral blood DNA from 39 normal subjects by polymerase chain reaction and single strand conformation polymorphism (PCR-SSCP) analysis. No large alterations in the ANP gene were observed, and no difference in allelic frequencies at the RFLP sites were seen between the two tumor subtypes, angiotensin-responsive and angiotensin-unresponsive APA, or between the APA group and normal subjects. SSCP analysis, however, did reveal mutations in the promoter region of the ANP gene (-375 to -595) in both peripheral blood and tumor DNA from 8 of 59 (14%) patients with APA, compared with only one of 39 normal controls (2.6%). This study suggests that alterations in the proximal promoter region of the ANP gene in APA may be important in the regulation of ANP transcription and may be involved in the underlying pathophysiology of aldosterone-producing adenoma in at least some patients.

Topics: Adenoma; Adrenal Cortex Neoplasms; Aldosterone; Atrial Natriuretic Factor; Base Sequence; Deoxyribonucleases, Type II Site-Specific; DNA; Humans; Molecular Sequence Data; Mutation; Polymerase Chain Reaction; Polymorphism, Restriction Fragment Length; Polymorphism, Single-Stranded Conformational; Promoter Regions, Genetic

High level of urinary kallikrein excretion was observed in a 23-year-old man with primary aldosteronism. Unilateral adrenalectomy improved the clinical symptoms and normalized the urinary concentration of this vasoactive substance. Although plasma atrial natriuretic factor was not elevated, adrenal surgery lowered its concentration. Coexistence of an adrenal adenoma and lesions of nodular hyperplasia were detected in the removed adrenal gland. We summarize the clinical data of this patient and review the literature.

Topics: Adrenal Cortex; Adrenal Cortex Neoplasms; Adrenalectomy; Adrenocortical Adenoma; Adult; Atrial Natriuretic Factor; Humans; Hyperaldosteronism; Kallikreins; Male

The previous study demonstrated that the aldosterone secretion of aldosterone-producing adrenocortical adenoma failed to be suppressed by human atrial natriuretic peptide, based on the data in synthetic alpha-human atrial natriuretic peptide infusion in vivo and the effect on in vitro secretion from cultured adenoma cells. Using the membrane fractions prepared from human adrenal tissues and an aldosterone-producing adenoma tissues, we characterized the binding sites for [125I] alpha-human atrial natriuretic peptide by the binding study and affinity-labeling of [125I] alpha-human atrial natriuretic peptide. Both normal adrenal and adenoma tissue membrane fractions possessed specific binding sites, however the relative binding capacity for [125I] alpha-human atrial natriuretic peptide in the adenoma preparations was markedly lower than that in the normal adrenal tissue preparation. The specific binding sites for [125I] alpha-human atrial natriuretic peptide were detected at the region of 140 KD and 67-70 KD only in the normal adrenal membrane fractions. Our data suggest that the refractoriness to the effect of atrial peptide may be due to the reduced receptor sites in aldosterone-producing adenoma cells.

Topics: Adenoma; Adrenal Cortex Neoplasms; Aldosterone; Atrial Natriuretic Factor; Binding Sites; Humans; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface; Tumor Cells, Cultured

Human adrenal gland and aldosterone-producing adenoma (APA) obtained from adrenalectomy could be maintained in vitro for one to two months. The explants continued to secrete aldosterone for the duration of culture. This method was superior to monolayer cell culture. The influence of alpha-human atrial natriuretic factor (alpha-hANF) was investigated by treating cultures of normal adrenal cortex and APA with alpha-hANF (10(-8) mol/L and 3 x 10(-8) mol/L respectively). We measured aldosterone in culture media collected at 2h before alpha-hANF treatment and 0.5, 2, 4 and 24h after. It was found that alpha-hANF stimulated aldosterone secretion of normal adrenal tissue but slightly inhibited that of APA.

Topics: Adenoma; Adrenal Cortex; Adrenal Cortex Neoplasms; Adult; Aldosterone; Atrial Natriuretic Factor; Culture Techniques; Female; Humans; Hyperaldosteronism; Male; Middle Aged

In vitro studies have shown that glucocorticoids may increase atrial natriuretic-hormone (ANH) synthesis and/or release. This action of glucocorticoids has also been suggested in vivo in patients with Cushing's syndrome. However, in this circumstance, plasma AH elevation might be due to humoral disturbances associated with cortisol overproduction. We studied 16 patients with endogenous hypercorticism and 11 of them after successful treatment. Plasma levels of ANH, plasma renin activity (PRA), aldosterone, desoxycorticosterone (DOC), angiotensin II (AII), cortisol, osmolarity, sodium and potassium, urinary free cortisol (UFC), and blood pressure were measured. Before treatment the mean plasma ANH concentration in patients with Cushing's syndrome was significantly higher than in controls (11.3 +/- 2.6 vs. 4.9 +/- 2.3 pmol/l; p less than 0.001). ANH was correlated with cortisol and UFC (r = 0.715, r = 0.700; p less than 0.05). There was no significant correlation between plasma ANH, PRA, aldosterone, DOC, AII, osmolarity, sodium or blood pressure. After recovery, ANH concentration decreased in all patients and was not different from that of normal subjects (4.9 +/- 2.3 vs. 4.3 +/- 2.6 pmol/l). These results suggest that in Cushing's syndrome, ANH secretion is mainly dependent on the severity of hypercortisolism and independent of the other associated disturbances that we studied.

Topics: ACTH Syndrome, Ectopic; Adenoma; Adrenal Cortex Diseases; Adrenal Cortex Neoplasms; Adrenocortical Hyperfunction; Adult; Angiotensin II; Atrial Natriuretic Factor; Cushing Syndrome; Desoxycorticosterone; Humans

Primary aldosteronism is the principal disorder of the zona glomerulosa, and a number of subsets have been identified: unilateral adenoma, bilateral micro- or macronodular hyperplasia (idiopathic aldosteronism), primary hyperplasia, and aldosterone-producing carcinoma, either adrenal or ectopic. The diagnostic criteria for a correct differential diagnosis of these subsets are now quite reliable, and our experience is presented in detail. Unfortunately, the pathogenesis of most of these forms is still poorly recognized and requires further investigation. An extreme sensitivity to angiotensin II is present in patients with idiopathic aldosteronism, and a role of adrenal renin is now being advocated. A peculiar form of hyperaldosteronism is the glucocorticoid-remediable subtype. An unusual sensitivity of aldosterone to ACTH is present in this form. The qualitative biochemical abnormality in this disorder consists of a marked overproduction of products of the cortisol C-18-oxidation pathway, 18-hydroxycortisol and 18-oxocortisol, which are more abundant than aldosterone and 18-hydroxycorticosterone. A family with 3 affected sibs has been studied by our group. In other clinical situations, classical zona fasciculata mineralocorticoids (deoxycorticosterone [DOC], corticosterone, and their 18-hydroxy compounds) are secreted in excess. The hypertensive diseases of this zone are rare DOC-secreting tumors and two forms of congenital adrenal hyperplasia, the 11 beta-hydroxylase and 17 alpha-hydroxylase deficiency syndromes, which are identified by the presence of hypokalemia and suppressed renin activity. DOC is the only mineralocorticoid hormone (MCH) oversecreted in the 11-hydroxylase deficiency syndromes, while all ACTH-dependent MCH levels are very high in the 17-hydroxylase deficiency syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adenoma; Adrenal Cortex Neoplasms; Adrenal Gland Diseases; Adrenal Glands; Aldosterone; Atrial Natriuretic Factor; Blood Pressure; Dexamethasone; Diagnosis, Differential; Humans; Hyperaldosteronism; Hypertension; Mineralocorticoids; Potassium; Sodium

The effects of atrial natriuretic peptide (ANP) on adrenocortical fasciculata cells were examined in the ACTH-responsive Y-1 mouse adrenocortical tumor cell line. Y-1 cell membranes rapidly bound [125I]ANP, with equilibrium binding (22 C) reached within 45 min. Binding of [125I]ANP was inhibited in a concentration-dependent manner by unlabeled ANP and atriopeptin-I (IC50, approximately 1.2 X 10(-9) and 1.6 X 10(-8) M, respectively), but not by C- or N-terminal-deleted ANP fragments, ACTH, or arginine vasopressin (up to 10(-6) M). Scatchard analysis revealed a single class of high affinity binding sites with a Kd of 1.6 X 10(-10) M and a binding capacity of 560 fmol/mg protein. Photo-affinity labeling demonstrated the specific binding of ANP to two protein entities of 130 and 63 kDa. ANP stimulated both cGMP synthesis and secretion from Y-1 cells (EC50, approximately 3.5 X 10(-9) M). Release of the nucleotide was inhibited by probenecid (IC50, approximately 5 X 10(-5) M). The atrial peptide partially inhibited ACTH-stimulated cAMP formation (IC50, approximately 10(-8) M) and partially antagonized basal and ACTH-stimulated steroidogenesis. The data demonstrate the presence in Y-1 cells of specific and saturable ANP receptors, activation of which leads to changes in cyclic nucleotide metabolism and inhibition of steroidogenesis.

Topics: 8-Bromo Cyclic Adenosine Monophosphate; Adrenal Cortex Neoplasms; Adrenocorticotropic Hormone; Animals; Atrial Natriuretic Factor; Binding, Competitive; Cell Line; Cell Membrane; Corticosterone; Cyclic AMP; Cyclic GMP; Kinetics; Mice; Probenecid; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface

The effect of synthetic alpha-human atrial natriuretic peptide (ANP) on aldosterone secretion was studied in human aldosterone producing adrenocortical adenoma obtained surgically from a patient with primary aldosteronism and in human apparently normal adjacent adrenal cortical tissues obtained from a patient with pheochromocytoma, in vitro. Apparently normal adrenal cortical tissue responded to ANP with the known inhibition of aldosterone secretion. In contrast, the aldosterone producing adenoma did not respond to ANP. When stimulated by either ACTH or angiotensin II, there is no inhibition by ANP in the adenoma tissue, whereas normal tissue was inhibited. Immunohistochemical examination utilizing an ANP-receptor antiserum demonstrated that there was no evidence of binding site in the cortical adenoma, in contrast, zona glomerulosa cells in the cortical tissues adjacent to either aldosterone producing adenoma or pheochromocytoma were densely stained. This apparent lack of ANP-receptors is an associated finding with the hypersecretion of aldosterone in the aldosterone producing adenoma.

Topics: Adenoma; Adrenal Cortex; Adrenal Cortex Neoplasms; Adrenocorticotropic Hormone; Aldosterone; Atrial Natriuretic Factor; Humans; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface; Recombinant Proteins

The effects of synthetic alpha-human atrial natriuretic polypeptide (alpha-hANP) on cortisol secretion by adrenocortical adenoma cells from patients with Cushing's syndrome (CS cells) in primary monolayer cultures, compared to cultured normal adrenal cells, were studied. alpha-hANP significantly inhibited cortisol secretion by human normal adrenal cells in culture, but had no direct effect on cortisol secretion from CS cells, in the presence or absence of 10(-8) M ACTH. alpha-hANP enhanced the accumulation of intracellular cyclic GMP in normal adrenal cells in culture, but not in CS cells. Visualization of [125I] iodo-alpha-hANP-specific binding sites by an in vitro receptor autoradiographic technique showed that these sites were lacking in adrenocortical adenoma tissues. These results suggest that the loss of alpha-hANP inhibitory effect on cortisol secretion in CS cells may be due to the absence of alpha-hANP receptor sites.

Topics: Adenoma; Adrenal Cortex Neoplasms; Adrenal Glands; Adult; Aldosterone; Atrial Natriuretic Factor; Cells, Cultured; Cushing Syndrome; Cyclic GMP; Female; Humans; Hydrocortisone; Middle Aged; Peptide Fragments; Tumor Cells, Cultured

Rat adrenocortical carcinoma cells possess a high density of atrial natriuretic factor (ANF) receptors which are coupled with membrane guanylate cyclase and corticosterone production. Herein we show that pretreatment of these cells with phorbol 12-myristate 13-acetate (PMA), a known activator of protein kinase C, attenuates the ANF-stimulated cyclic GMP accumulation in a dose-dependent manner. The half maximum inhibitory concentration of PMA was 10(-10) M. When these cells were incubated with PMA in the presence of 1-(5-isoquinolinyl-sulfonyl)-2-methyl piperazine, a protein kinase C inhibitor, the PMA-mediated attenuation of ANF-stimulated cyclic GMP formation is blocked. These results suggest that protein kinase C negatively regulates the ANF-receptor coupled membrane guanylate cyclase system in these cells.

Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Adrenal Cortex Neoplasms; Animals; Atrial Natriuretic Factor; Cyclic GMP; Enzyme Activation; Guanylate Cyclase; Isoquinolines; Phosphorylation; Piperazines; Protein Kinase C; Rats; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface; Tetradecanoylphorbol Acetate

Topics: Adrenal Cortex Neoplasms; Adult; Atrial Natriuretic Factor; Blood Pressure; Heart Rate; Humans; Hyperaldosteronism; Middle Aged; Pituitary Hormones, Anterior

Low-dose angiotensin II (ANG II) infusion raised plasma atrial natriuretic peptide (ANP) levels only when endogenous renin-angiotensin levels were low, as in aldosterone-producing adenoma. When plasma renin activity (PRA) levels rose tenfold following removal of the tumour, low-dose ANG II infusion no longer stimulated ANP, but fivefold higher doses did. Indomethacin lowered both PRA and ANP in Bartter's syndrome and in normal subjects. The effect of indomethacin on ANP is probably not direct, since it did not lower ANP in aldosterone-producing adenoma. Neither did it lower PRA in aldosterone-producing adenoma, and in most studies ANP and PRA moved in parallel, consistent with positive regulation of ANP by ANG II. When ANG II infusion stimulated ANP, it also raised blood pressure, which could therefore be mediating the effects of ANG II on ANP. However, both PRA and ANP are high in Bartter's syndrome, while blood pressure is normal or low, and indomethacin lowers PRA and ANP in Bartter's syndrome and in normal subjects without lowering the blood pressure. The relative importance of regulatory factors such as central blood volume/atrial pressure and ANG II level probably varies in different situations. In aldosterone-producing adenoma, a high central blood volume appears to over-ride the effect of a low ANG II level. In Bartter's syndrome a high ANG II level appears to over-ride the effect of low central blood volume.

Topics: Adenoma; Adolescent; Adrenal Cortex Neoplasms; Adult; Aldosterone; Angiotensin II; Atrial Natriuretic Factor; Bartter Syndrome; Blood Pressure; Child; Child, Preschool; Humans; Hyperaldosteronism; Indomethacin; Middle Aged; Renin

Isolated fasciculata cells of rat adrenal cortex, when incubated with atrial natriuretic factor (ANF), stimulated the levels of cyclic GMP and corticosterone production in a concentration-dependent manner without a rise in the levels of cyclic AMP. The ANF-dependent elevation of cyclic GMP was rapid, with a detectable increment in 30 s. ANF also stimulated the particulate guanylate cyclase. These results not only indicate the coupling of cyclic GMP and corticosterone production with ANF signal, but also demonstrate that, like the ACTH signal, cyclic AMP is not the mediator of ANF-induced adrenocortical steroidogenesis.

Topics: Adrenal Cortex; Adrenal Cortex Neoplasms; Animals; Atrial Natriuretic Factor; Carcinoma; Corticosterone; Cyclic AMP; Cyclic GMP; Rats; Stimulation, Chemical

The effects of synthetic alpha-human atrial natriuretic polypeptide (alpha hANP) on aldosteronogenesis in normal and aldosterone-producing adenoma cells (APA cells) in primary monolayer cultures were studied. alpha hANP significantly inhibited aldosterone secretion from normal adrenal cells in culture, but had no inhibitory effect on aldosterone secretion from APA cells in the presence or absence of 10(-8) M ACTH. alpha hANP enhanced the accumulation of intracellular cGMP in normal adrenal cells in culture, but not in APA cells. Visualization of [125I]iodo-alpha hANP-specific binding sites in APA and adjacent normal adrenal tissues by an in vitro receptor autoradiographic technique showed that these sites were localized only in normal adrenal tissue, but not in APA tissue. These results suggest that the lack of an inhibitory effect of alpha hANP on aldosteronogenesis in APA cells may be due to the absence of alpha hANP-specific receptor sites in APA cells.

Topics: Adenoma; Adrenal Cortex Neoplasms; Adult; Aldosterone; Atrial Natriuretic Factor; Autoradiography; Cells, Cultured; Cyclic GMP; Female; Humans; Middle Aged; Radioligand Assay; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface