Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 52-year-old woman was admitted to our hospital for further examination of central obesity, hypertension and hirsutism suggesting Cushing's syndrome. Hirsutism had been remarkable for two years, and muscle weakness of the lower extremities gradually developed during the past year. CT scan revealed a tumor in the left adrenal gland which was 1 cm in diameter, round, well-circumscribed, homogeneous and not enhanced. Endocrine data disclosed increased urinary 17-OHCS (11.5-16.4 mg/day) and elevated plasma ACTH (125 pg/ml) and cortisol (19 micrograms/dl) with a lack of diurnal rhythm. Administration of the single-dose dexamethasone (1mg) did not suppress plasma cortisol. However, consecutive administration of either 2mg or 8mg of dexamethasone for 2 days suppressed both plasma cortisol and urinary 17-OHCS. Administration of metyrapone raised both urinary 17-OHCS and plasma ACTH levels. Rapid ACTH test resulted in a hyperresponse of plasma cortisol. CRF injection raised plasma ACTH and cortisol. Bilateral adrenal glands were well demonstrated by 19-iodocholesterol (I-131) scintigraphy during the administration of dexamethasone. MRI with Gd-contrast revealed a microadenoma in the sella turcica. With the diagnosis of Cushing's disease, the microadenoma was removed by the transsphenoidal approach and adrenal function was normalized. However, the left adrenal tumor remained on CT scan but was not demonstrated by scintigraphy. These findings indicate that this is a very rare case of Cushing's disease which was associated with an unilateral non-functioning adrenal tumor.
 ...
PMID:[A case of Cushing's disease associated with a non-functioning adrenal tumor]. 129 36

Altogether 16 persons with STH-producing hypophyseal adenoma were investigated by tacho-oscillography, total rheography, blood taken from the ulnar vein, a radioimmunoassay to determine the levels of STH, ACTH, cortisol, deoxycorticosterone, aldosterone, T3, T4, vasopressin, prostaglandin E2, 6-keto-prostaglandin F1 alpha, and plasma renin activity. Acromegalic patients demonstrated an elevated level of STH, and prostaglandin E2 secretion was inhibited. Two groups of patients were singled out according to the hemodynamic state: the 1st group was characterized by a hyperkinetic type of circulation and normotension of borderline hypertension; the 2nd group was characterized by hypokinetic circulation, increased vascular resistance, labile or stable arterial hypertension. The interrelationship of hemodynamic and hormonal indices was unnoticed. It has been assumed that of pathogenetic importance in the development of arterial hypertension is depletion of E2 production, and at early stages--body liquid retention resulting from hypersomatotropinemia.
 ...
PMID:[State of the endocrine and cardiovascular systems in patients with somatotropin-producing hypophyseal adenoma]. 130 90

Primary (partial) cortisol receptor resistance was previously reported in a total of 7 patients and 14 asymptomatic family members. Its occurrence is considered to be extremely rare. In the present study we report on 6 patients (2 males and 4 females) with the syndrome. The first male patient presented with mild hypertension. Hydrochlorothiazide therapy resulted in life-threatening hypokalemia. The second male patient had slight hypertension without hypokalemia. All four female patients presented between the age of 20-30 yr with acne, hirsutism, and irregular menstruations. Low dose dexamethasone therapy (1-1.5 mg/day) was of clinical benefit in these patients. All patients showed insufficient suppression of serum cortisol concentrations in the overnight 1-mg dexamethasone test. The diurnal rhythm of ACTH and cortisol was intact, albeit at an elevated level. There was a normal increase in ACTH, cortisol, and GH (except in one obese patient) in response to insulin-induced hypoglycemia, while cortisol production was elevated in three patients. Circulating adrenal androgen levels were increased in all patients. Glucocorticoid receptors were investigated in a whole cell dexamethasone binding assay in mononuclear leukocytes. In the first male patient, the number of receptors was very low, while the affinity was lower than that in controls. A lowered affinity to dexamethasone was found in one female patient, while a lowered number of receptors was found in three patients. In the second male patient, no abnormalities were found. As a bioassay for glucocorticoid action we also measured dexamethasone suppressibility of mitogen-stimulated incorporation of [3H]thymidine in mononuclear leukocytes. In the male patient with normal receptor status, dexamethasone suppressibility of [3H]thymidine incorporation was significantly lower than that in healthy controls with respect to both maximal suppression and IC50. Partial cortisol receptor resistance might be less rare than previously thought. In the six patients presented, at least three different forms can be recognized. Therapy with dexamethasone was successful in female patients with acne and hirsutism, as the secondary increase in the production of adrenal androgens was effectively controlled.
 ...
PMID:Cortisol receptor resistance: the variability of its clinical presentation and response to treatment. 1084 99

Between 1980 and 1989, 21 children suffering from intractable seizures other than infantile spasms were treated with intramuscular ACTH at the Children's Hospital Camperdown. Five patients had two courses of ACTH therapy, 24% of patients had a good response (group A), 56% responded transiently (group B) and 20% did not respond (group C). Group A had normal development and no neurological deficits prior to seizures. A favourable response was not observed in patients with partial seizures, 90% of the patients who responded had a recurrence of seizures. Mean time to recurrence was 9.0 +/- 7.3 months in group A and 1.6 +/- 2.0 months in group B. Hypokalaemia, hypertension and infection were found in 42.9%, 33.3% and 19.1% respectively. ACTH also had effects on concurrent anti-epileptic drug levels.
 ...
PMID:ACTH treatment in intractable seizures of childhood. 132 Mar 46

ACTH and adrenocortical steroids have been known to raise blood pressure since their introduction into clinical practice. Our experimental studies in normal subjects show that ACTH reproducibly increases blood pressure in association with a rise in cardiac output, plasma and extracellular fluid volumes and exchangeable sodium. The rise in pressure is adrenally dependent and appears due to ACTH-induced increases in cortisol secretion. When ACTH is given by constant intravenous infusion, rates as low as 50 micrograms/day raise pressure. The increase in blood pressure is not dependent on, but modified by, dietary sodium content. Synthetic steroids (prednisolone, methylprednisolone, triamcinolone, dexamethasone) raise pressure in the absence of any increase in plasma volume or urinary sodium retention. Cortisol increases pressor responsiveness to endogenous and exogenous catecholamines, without evidence of any increase in sympathetic nervous activity. The role of this increased pressor responsiveness in ACTH/steroid-induced hypertension remains to be determined. There is some evidence from human studies that steroids may raise pressure by a hypertensinogenic mechanism, distinct from classical mineralocorticoid or glucocorticoid effects.
 ...
PMID:Adrenocorticotrophin and steroid-induced hypertension in humans. 132 9

The TGR(mREN2)27 is a new monogenetic rat model in hypertension research. As the mouse Ren-2d renin gene is integrated into their genome, they develop fulminant hypertension between 5 and 15 weeks of age, with blood pressure maxima of 300 mm Hg. Their plasma renin-angiotensin system (RAS) is suppressed, but the transgene is highly expressed in the adrenal gland, so we investigated its possible role in steroid metabolism and the pathogenesis of hypertension. During the phase of hypertension development (between 6-18 weeks), the urinary excretion of deoxycorticosterone (DOC), corticosterone (B), 18-hydroxycorticosterone, and aldosterone is 1.5- to 2.5-fold elevated compared with that in Sprague-Dawley (SD) rats (P less than 0.0005) despite the suppressed plasma RAS. Moreover, the adrenal gland in TGR(mREN2)27 shows an increased maximal response to ACTH stimulation in regard to urinary excretion of DOC (after ACTH, 244 +/- 42 ng/24 h in TGR; 62 +/- 10 ng/24 h in SD; P less than 0.0005) and B (after ACTH, 5144 +/- 346 ng/24 h in TGR; 2607 +/- 324 ng/24 h in SD; P less than 0.0005). Additionally, plasma prorenin in TGR was stimulated more than 10-fold, indicating transgene regulation by ACTH. Since spironolactone treatment did not lower the blood pressure in TGR, hypertension solely due to hypermineralocorticoism is unlikely. Our results indicate that the adrenal steroid metabolism is markedly stimulated in young TGR, and the absolute increase in urinary DOC and B after ACTH injections is enhanced, possibly due to a stimulated local intraadrenal RAS.
 ...
PMID:The role of the adrenal gland in hypertensive transgenic rat TGR(mREN2)27. 132 84

Overall 146 females suffering from essential hypertension (borderline, stage I and II according to WHO, 1980) were examined for basal concentrations of estradiol, estriol, progesterone, testosterone, cortisol, ACTH, prolactin in plasma, LH and FSH in blood and urine. The patients and 69 control normotensive females were reproductive, premenopausal, menopausal, postmenopausal, postcastration. Latent hypertension was elicited at bicycle exercise. It was found that relationships between sex hormones and gonadotropins both in hypertensive and normotensive women did not differ noticeably in reproductive period and in menopause. Hormone defects due to primary and secondary infertility, castration, menopause did not raise the risk of arterial hypertension onset. An-Unfavorable course of hypertension was observed in premenopause, following operative castration, in climacteric syndrome. The severity of AH at reproductive age was associated with hyposecretion of progesterone, estrogens and gonadotropins LH, FSH. This relationship was absent in menopausal women. A conclusion is proposed on miner significance of sex hormones imbalance and gonadotropins in the onset of arterial hypertension in females varying by generative activity.
 ...
PMID:[Role of imbalance of sex hormones and gonadotropins in the development and course of essential hypertension in women]. 132 46

We investigated the effect of long-term, low-dose ACTH in 13 patients (10 boys and 3 girls) with infantile spasms who were treated with low-dose ACTH (mean: 0.0081 mg/kg/day). Two patients (one boy and one girl) received this therapy twice because of relapse of tonic spasms. ACTH was injected intramuscularly every morning for 30 days, after which dosage was tapered. The mean observation period was 53.9 months. Complete cessation of seizures was attained in 13 of 15 treatment trials. In one trial, complete cessation was not attained but the number of attacks decreased to less than one-third of that before treatment. In only one trial was treatment not effective. EEG showed good response to this treatment. The side-effects of this therapy were hypertension in 6 patients, hypokalemia in 7, and emotional outburst in 7. Emotional outburst appeared during the early phase of therapy, while the other two side-effects appeared in the later phase and disappeared when ACTH-tapering was begun. Brain shrinkage observed on CT scan was mild in all trials. Five patients have had no relapse. The total dose of ACTH was significantly larger in the group with good outcome than in the group with poor outcome.
 ...
PMID:[Treatment of infantile spasms with long-term low dose ACTH]. 132 15

The most common ectopic production of a pituitary hormone is the one of ACTH leading to Cushing's syndrome. Ectopic ACTH-hypersecretion is the cause of Cushing's syndrome in 10-15% of all cases. The ACTH-secreting tumours are often oat-cell carcinomas of the lung, less frequently pancreatic cancers, hypernephromas, or C-cell carcinomas of the thyroid. Some of these tumours may be benign or semi-benign as the rare carcinoid tumours and cause great problems in the differential diagnosis of ACTH-dependent hypercortisolism. Out of 173 of our patients with Cushing's syndrome observed in the last 12 years 21 were caused by ectopic ACTH-production. Of these 21 patients 13 have a small cell carcinoma of the lung. The ectopic ACTH-syndrome often has typical clinical features caused by the levels of ACTH and cortisol leading to hypocalcemic alkalosis with muscle weakness and wasting, carbohydrate intolerance, and hypertension with oedema. The survival time in many of these patients is not long enough to allow them to develop typical signs of Cushing's syndrome though they are often highly pigmented. These patients are easily diagnosed. However, patients with small tumours which do not cause very elevated ACTH-levels and who have the more typical clinical signs of full-blown Cushing's syndrome are difficult to recognize. For the differential diagnosis of ACTH-dependent Cushing's syndrome the corticotropin-releasing hormone (CRH) stimulation test and dexamethasone suppression test with high doses are helpful. In special cases the venous sampling procedure for ACTH-measurements is necessary, also CT or NMR is helpful. Ectopic CRH-production is a rare cause of ACTH-dependent Cushing's syndrome. Patients with ectopic CRH-production and consecutive ACTH-hypersecretion from the pituitary have not been studied extensively. There are especially no well documented results of the use of the CRH-stimulation test in vivo in this group of patients with Cushing's syndrome. On the other hand, in the documented cases, not only CRH-, but also ACTH-production was found in the tumours. So far, this rare cause of ACTH-dependent Cushing's syndrome has to be excluded or confirmed by the measurement of endogenous CRH-levels. But until now we have not been able to detect one single case of ectopic CRH-production using a sensitive homologous CRH-radioimmunoassay over a period of more than 8 years in which we have seen nearly 120 newly diagnosed patients with ACTH-dependent Cushing's syndrome. Only in the plasma and tumour tissue of two patients of other groups have we found high CRH-levels.
 ...
PMID:Ectopic production of ACTH and corticotropin-releasing hormone (CRH). 132 73

1. The haemodynamic and metabolic effects of oral intake of approximately 30 mg/kg per day N-nitro-L-arginine (NOLA) were examined in sham and adrenocorticotrophin (ACTH, 0.5 mg/kg per day) treated conscious Sprague-Dawley rats (n = 33). 2. NOLA administration produced an increase in systolic blood pressure of 24 +/- 6 mmHg (P < 0.001), but did not alter food or water intake, urine volume or electrolyte excretion in rats not treated with ACTH. 3. Compared with sham injection, ACTH-treated rats demonstrated an increase in systolic blood pressure (water + sham, 3 +/- 1 mmHg; water + ACTH, 16 +/- 3 mmHg; P < 0.001), loss of bodyweight, and increases in water intake and urine volume. 4. The magnitude of the blood pressure rise in ACTH-treated rats was greater in those receiving NOLA than in those drinking water only (water + ACTH, 16 +/- 3 mmHg; NOLA + ACTH, 37 +/- 3 mmHg; P < 0.05). Metabolic changes were similar. 5. Inhibition of nitric oxide is unlikely to be a major determinant of ACTH-induced hypertension in the rat, since NOLA increased blood pressure whether or not ACTH was administered, indicating an additive effect of ACTH and NOLA administration.
 ...
PMID:Inhibition of NO synthesis has an additive effect on hypertension induced by ACTH in conscious rats. 133 Mar 90


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>