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Biomedical subjects

G Opocher

Publications and source records attributed to G Opocher.

71 records · Page 4Linked to original sources
PubMed1981

Mineralocorticoid hypertension due to a nasal spray containing 9 alpha-fluoroprednisolone.

The finding of hypokalemia and of low plasma renin activity (PRA) in a hypertensive patient suggests a diagnosis of primary hypermineralocorticoidism. Medications containing compounds with mineralocorticoid-like activity (licorice, carbenexolone) may also cause the same syndrome. Recently, we carried out detailed studies on 10 patients with severe hypertension and hypokalemic alkalosis, suppressed PRA and low aldosterone levels. Plasma levels of cortisol and ACTH were suppressed in most of the cases. Measurement of deoxycorticosterone and corticosterone (and in some patient of 18-hydroxydeoxycorticosterone and 18-hydroxycorticosterone) was not significantly higher than normal. Therapeutic trials of dexamethasone and aminoglutethimide were ineffective. In contrast, spironolactone and amiloride treatment resulted in substantial but incomplete amelioration of both hypertension and hypokalemia. All of the patients share a common history of chronic rhinitis and habitual use of large doses of nasal spray containing 9 alpha-fluoroprednisolone and vasoconstrictor agents. Withdrawal resulted in a complete remission of hypokalemia in one to two weeks in all patients. The hypertension and depressed levels of PRA, aldosterone and cortisol took longer to return to normal, varying from case to case; in all but one patient, the values returned to normal within two months. This report reveals another cause of factitious mineralocorticoid excess which may be considered in the differential diagnosis of hypokalemic hypertensive syndromes.

Administration, Intranasal↗
PubMed1981

Effect of angiotensin II and converting enzyme inhibitor (captopril) on blood pressure, plasma renin activity and aldosterone in primary aldosteronism.

1. Patients with idiopathic hyperaldosteronism (IHA) show a response of aldosterone to posture which is not present in patients with aldosterone-producing adenoma (APA). We have determined whether this could be explained by a different sensitivity to angiotensin II. 2. Angiotensin II was infused in gradually increasing doses in six patients with APA and in seven patients with IHA. No changes in aldosterone concentration were found at the end of each period in APA, whereas there was a significant increase in IHA; blood pressure rose by a similar extent in both groups. 3. In order to evaluate the role of endogenous angiotensin II, captopril, a converting enzyme inhibitor, was administered to six patients with APA and five patients with IHA at a dose of 75 mg/day for 1 week. There was a significant fall of mean blood pressure in IHA and only minimal changes in APA. Plasma renin activity and plasma in urinary aldosterone were unchanged in APA. In IHA there was a small increase in upright plasma renin activity and a slight decrease in both plasma and urinary aldosterone, but these changes were not significant. 4. These findings further support the idea that idiopathic hyperaldosteronism is a clinical state different from that occurring in primary aldosteronism due to adenoma, and may be more closely related to essential hypertension.

Aldosterone↗
PubMed1981

Effect of metoclopramide on plasma aldosterone in normal subjects, primary aldosteronism and hypopituitarism.

The behaviour of plasma renin, aldosterone, cortisol and prolactin after administration of a drug with antidopaminergic action, metoclopramide, was evaluated in 6 normal subjects, 8 patients affected by primary aldosteronism and in 5 patients affected by anterior hypopituitarism. In the first two groups, besides the predictable increase of prolactin under metoclopramide, a significant aldosterone increase was noted. Cortisol remained unchanged, and PRA was not significantly increased. A similar pattern of aldosterone, cortisol and PRA was also found in patients with hypopituitarism. However, the plasma prolactin did not increase in this group. The comparative examination of three groups of patients leads us to conclude that aldosterone increase is not imputable to ACTH, renin or to prolactin. This may be explained by a possible direct effect of the antidopaminergic drug at the adrenal level, which is more likely than an effect through some yet undetermined factor.

Aldosterone↗
PubMed1981

[Surgical and medical treatment of renovascular hypertension (author's transl)].

We have studied a group of 47 patients with unilateral or bilateral renal artery stenosis; 27 of them have been operated, while 20 have been subjected to medical treatment. Among the surgically treated patients, 18 out of the 22 cases with an unilateral stenosis had satisfactory results and didn't assume any treatment after surgical cure. All the 5 cases of bilateral stenosis presented a regular blood pressure after surgery. Nine among the 12 patients affected by unilateral stenosis and 3 among the 8 patients presenting bilateral forms who received medical treatment had successful results with the conventional therapy. The parameters that seems give a better prognostic indication for the surgical cure are either significant renal veins renin ratios (Ra/Rc and Rc/P), either high peripheral PRA values combined with a renal artery stenosis greater than or equal to 70%, in all the cases without evident damages in the opposite kidney, even if the renin ratios are not significant. The results of the medical treatment may be predicted from the entity of the renal stenosis. Failures are more likely to occur in the bilateral forms. In these cases the most satisfactory results can be obtained using minoxidil or the inhibitor of the converting enzyme of angiotensin I.

Adolescent↗
PubMed1979

[Diaxozide-induced acute stimulation of plasma renin activity in renal veins for diagnosis and prognosis in hypertensive patients (author's transl)].

Vena cava and renal veins PRA were measured and their ratios calculated (Ra/Rc and Rc/P) in 15 hypertensive patients before and after diazoside infusion (300 mg i.v.). Among the 4 patients with unilateral renal artery stenosis, 3 had both ratios significant in basal conditions. After diazoxide infusion, the ratios became significant in the 4th case, successfully operated. Surgery induced normalization of blood pressure also in 2 of 3 cases affected by renoparenchimal alterations: of these patients 1 had ratios significant in basal conditions and both after diazoxide. One patient had unilateral renal artery stenosis and controlateral small kidney: his ratios was significant in favour of small kidney both before and after diaxozide infusion. The correction of renal artery stenosis gave no results in blood pressure. In patients with essential hypertension the PRA values in renal veins were not significantly different either before and after diazoxide. In conclusion the acute diazoxide stimulation seems to improve the prognostic value of renal veins PRA and their ratios for the detection of surgically curable forms of renal hypertension.

Adolescent↗
PubMed1976

Aldosterone regulation in primary aldosteronism: differences between adenoma and bilateral hyperplasia.

1. The diurnal patterns of plasma aldosterone, plasma renin activity (PRA), cortisol and adrenocorticotrophic hormone (ACTH) in the supine and in the upright position have been studied in fourteen patients with primary aldosteronism, five with adenoma and nine with bilateral hyperplasia. Blood samples were drawn at intervals from 6 h to 30 min. 2. Supine patients with an adenoma showed marked diurnal variations of aldosterone, with maximal values at 08.00 hours and minimal values of 18.00 hours and secretory spurts beginning after 02.00 hours. Plasma cortisol paralleled aldosterone, and ACTH seemed to anticipate aldosterone and cortisol variations; PRA remained unchanged. In patients with hyperplasia, aldosterone was significantly lower than in the adenoma group at 08.00 hours, and its decline during the day was less marked; fluctuations rather than secretory episodes were seen. 3. After patients assumed the upright posture, aldosterone remained unchanged or decreased in patients with adenoma, whereas it significantly increased in hyperplasia; PRA remained low, although a slight increment was seen in the latter group. The different response of aldosterone in the two groups was not modified by the administration of propranolol, apparently excluding a renin-dependent mechanism. On the other hand, dexamethasone seemed to affect the response of aldosterone to the upright posture in both groups; in adenoma there was a slight but significant increase, and in hyperplasia the usual rise was partially suppressed. 4. It is concluded that ACTH has a predominant role in regulating aldosterone secretion in primary aldosteronism due to adenoma, whereas its action in bilateral hyperplasia is only permissive.

Adenoma↗
PubMed1976

[Effect of diazoxide on blood pressure, PRA and plasma aldosterone in hypertensive patients (author's transl)].

Intravenous diazoxide (300 mg) was administered to 29 hypertensive patients previously classified in subgroups according to their plasma renin and urinary aldosterone levels. The blood pressure was measured before and periodically after injection and plasma renin activity (PRA) and plasma aldosterone before and after 2 hours. The mean systolic and diastolic blood pressure fell notably from 193/118 to 155 93 mmHg; whereas PRA increased from 7.51 to 13.21 ng/ml/3 hrs and plasma aldosterone did not change significantly (71.3 and 102.8 ng%). Examining the individual sub-groups, a significant decrease in blood pressure was observed in 15 patients with low, posture unresponsive PRA, both in subjects with normal urinary aldosterone and those with surgically proven primary aldosteronism. In the former only the mean PRA showed a slight but sigificant increase, while in the latter the changes for both PRA and aldosterone were not significant. In the subgroups of patients with normal renin and urinary aldosterone the arterial pressure also significantly and promptly decreased. However, in this group the mean PRA substantially increased whereas the plasma aldosterone levels remained constant. The same blood pressure decline was observed in those patients with high PRA and aldosterone, including 1 case of pheocromocytoma. The mean PRA showed a further modest increase while the plasma aldosterone did not change significantly. These results indicate that the antihypertensive action of diazoxide is similar in the different types of hypertension (volume, vasoconstrictor or mixed form according to Laragh's classification), being independent of the basal plasma renin and aldosterone levels. Furthermore, the response of the blood pressure to diazoxide is not related in any way to the induced changes in PRA and plasma aldosterone values.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Natriuretic peptides receptors in human aldosterone-secreting adenomas.

Atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP) inhibit aldosterone secretion in humans both in vitro and in vivo. Unresponsiveness of aldosterone-secreting adenomas (aldosteronomas) to ANP in vitro and in vivo, might be due to reduced expression of the biologically-active natriuretic peptide receptor type A (NPr-A) and/or increased expression of the clearance receptor for natriuretic peptides (NPr-C). Therefore, we have analyzed NPr gene expression and ANP binding sites in human adrenals and aldosteronomas. Using reverse transcription and polymerase chain reaction, we cloned and characterized cDNAs for NPr-A, NPr-C, and the receptor (NPr-B) for the C-type natriuretic peptide (CNP). Total RNA from three normal human adrenals (obtained at surgery from patients with renal cancer) and five aldosteronomas were used for Northern analysis. NPr-A mRNA (approximately 4 kb) and NPr-B mRNA (approximately 4 kb) were expressed without significant differences in adrenals and in aldosteronomas except in an aldosteronomas that contained only very low amounts of NPr mRNAs. The gene expression of NPr-C was barely detectable both in adrenals and in aldosteronomas. ANP binding sites were analyzed by autoradiography with 125I-labeled ligand in other six aldosteronomas. Only one of the adenomas analyzed showed ANP binding sites with density of granules similar to nonadenomatous glomerulosa, whereas the others had significantly reduced densities. In summary, aldosteronomas express the genes encoding for NPr but mainly NPr-A, similarly to control adrenals. On the contrary, the binding sites for ANP are greatly reduced in most aldosteronomas. A somatic mutation or a post-transcriptional defect that reduces ANP binding sites might be present in some aldosteronomas.

Adenoma↗
PubMedDate not supplied

Plasma renin activity and urinary aldosterone in acromegaly.

The behaviour of the renin-angiotensin-aldosterone system was evaluated in 16 acromegalic patients, of whom 7 were hypertensive. The patients were studied in basal conditions, after suppression with 9alpha-fluorohydrocortisone, and after stimulation with furosemide. Baseline and after furosemide PRA were significantly lower in acromegalic hypertensive patients than in the normotensive group. Mean urinary aldosterone excretion was found at the upper limits of the normal range; it was occasionally elevated, but the values were not satistically different in the two groups. There was a suppression after 9 alpha fluorohydrocortisone in both groups, though it did not reached the 50%. These data show that there is a disorder of the renin-angiotensin-aldosterone system in acromegalic subjects. This defective regulation is sometimes similar to that present in primary aldosteronism. In fact in two patients a typical phlebographic and scintigraphic picture of primary aldosteronism has been found; surgery, performed in both patients, revealed a large cortical adenoma in one case and a macronodular hyperplasia in the second case. However, the relationship between this adrenal abnormalities and hypertension in acromegaly are not yet completely clarified.

Acromegaly↗
PubMedDate not supplied

Effect of indomethacin on urinary kallikrein excretion in Bartter's syndrome of the adult.

An elevated urinary kallikrein excretion was found in 3 out of 4 adult patients with Bartter's syndrome. After prostaglandin synthesis inhibition by indomethacin, serum potassium levels rose, plasma renin activity and urinary aldosterone excretion decreased. Urinary kallikrein excretion was reduced to within normal range in all patients. The fall of urinary kallikrein excretion after indomethacin may be partly due to plasma potassium and aldosterone variations, but more likely it is dependent on the reduced prostaglandin synthesis. These results support the hypothesis that renal prostaglandins activate renal kallikrein-kinin system, hence inducing an increase of renal blood flow, diuresis and natriuresis.

Adult↗
PubMedDate not supplied

Expression of type 1 angiotensin II receptors in human aldosteronomas.

Type 1 angiotensin II (AII) receptors (AT1 receptors), besides stimulation of aldosterone secretion, seem to transduce the growth factor-like activity of AII on glomerulosa cells. Although a local renin-angiotensin system and AII synthesis have been found in human adrenals and aldosteronomas, it is unclear whether aldosteronomas express AT1 receptors. Utilizing polymerase chain reaction (PCR) and reverse transcription-PCR (RT-PCR) with primers complementary to both genomic and cDNA sequences of human AT1 receptor, we have amplified and cloned a 734 bp fragment of the AT1 coding region. This DNA, after cloning and sequencing, was used for Northern analysis. Total RNA was extracted from 5 non-tumorous adrenals and 5 aldosteronomas. AT1 mRNA (approximately 2.4 kb) was expressed in all the aldosteronomas tested. Densitometric analysis of AT1 signals, corrected by beta actin expression, when compared to non-tumorous adrenals, did not show significant differences. AT1 receptor density and affinity in cell membrane obtained from 9 non-tumorous adrenal cortex and 8 aldosteronomas were also studied. 125I-AII was used as ligand and Dup 753 as AT1 antagonist: AT1 receptor density and affinity were not significantly different in aldosteronomas vs non-tumorous adrenal cortex. In conclusion, the expression of AT1 gene and the formation of an apparently normal receptor suggest that AT1 receptor should have a role in aldosteronoma cell biology.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

[Role of ketanserin in the treatment of primary hyperaldosteronism].

Ketanserin (Ket), a 5HT-2 serotoninergic receptor antagonist, is currently used as an antihypertensive agent. In our previous studies, both in vitro and in vivo when administered as bolus i.v. in subjects with primary aldosteronism (IAP), Ket exhibited an inhibitory action on aldosterone secretion. Therefore in the present study we investigated, in IAP patients, the effects of chronic treatment with Ket on blood pressure and mineralocorticoid secretion. Ket was administered at increased doses of 20 and 40 mg twice daily per os for 30 days and the following parameters were evaluated: blood pressure, heart rate, ur. aldosterone, pl. aldosterone both basal and after ACTH and angiotensin II (AII) stimulation, PRA, and atrial natriuretic factor (ANF). Our study demonstrated that Ket is a powerful blood pressure lowering agent with no relevant side effects and no variations of heart rate. Ur and pl aldosterone levels did not change during therapy; correspondingly, Ket did not modify ACTH or AII-induced stimulation. ANF levels, basally elevated in this syndrome, increased during Ket treatment. This new and interesting aspect deserves further evaluation. In conclusion Ket showed an effective antihypertensive effect in this syndrome, even if steroidogenesis inhibition does not seem to be a relevant component of its antihypertensive effect.

Administration, Oral↗