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Query: UMLS:C0020538 (
hypertension
)
170,190
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Salt resistant rats (R-strain of Dahl) accumulate large amounts of colloid in the pituitary cleft. Such colloid is largely absent in pituitaries of salt susceptible rats (S-strain of Dahl). Polyacrylamide gel electrophoresis of pituitary cleft colloid from R rats shows 4 proteins, designated R1, R2, R3 and R4 in order of decreasing electrophoretic mobility. These proteins have apparent molecular weights of 52,000, 63,000, 130,000 and greater than 235,000, respectively. Their apparent isoelectric points as determined by preparative isoelectric focusing are 4.82, 5.02, 5.54 and 4.35, respectively. Ferguson plots for R1, R2 and rat albumin suggest that R1 and R2 are size isomers of albumin. The molecular weights of R2, R3 and R4 suggest that R2 may polymerize to form a dimer and tetramer. Chronic feeding of 8% NaCl diet for 6 weeks does not influence pituitary accumulation of R1 protein in either R or S rats.
Pituitary
R1 accumulation does, however, segregate with resistance to salt-induced
hypertension
in genetic experiments. This strongly suggests that the accumulation of R proteins in the pituitary cleft reflects some genetically controlled change concerned with control of sodium metabolism.
...
PMID:Characteristics of pituitary colloid proteins and their correlation with blood pressure in the rat. 86 65
Altogether 24 adolescents with pubertal juvenile
dyspituitarism
(PJD) were investigated in the course of an oral GTT for 3 hours. The patients were divided into 3 groups: (1) with liver dysfunction and normal BP; (2) with normal liver and arterial
hypertension
; (3) with normal BP and normal liver function. The levels of glycemia, immunoreactive insulin, C-peptide and a molar C-peptide/insulin ratio were measured. All the examinees were characterized by basal and stimulated hyperinsulinemia against a background of a normal C-peptide value, the absence of a tendency to IRI reduction by the end of the GTT. A decrease in the C-peptide/IRI ratio was marked in the 1st group. One of the reasons of hyperinsulinemia in PJD in parallel with high insulin secretory pancreatic function can be a decrease in the metabolic clearance of liver insulin, especially noticeable in patients with hepatocyte dysfunction.
...
PMID:[C-peptide and insulin ratio in patients with juvenile dyspituitarism in varying symptomatology]. 151 65
The occurrence of pregnancy in the face of untreated Cushing syndrome is rare because of the high incidence of ovulatory disturbances experienced by patients with the disorder. A total of 58 patients with 65 pregnancies has been reported in the literature to date. Although pituitary-dependent adrenal hyperplasia is the most common etiology of Cushing syndrome in the general population, adrenal adenoma is more common in the pregnant population. Significant maternal morbidity is attributable to
hypertension
, congestive heart failure, and poor tissue healing. Prematurity and intrauterine growth retardation account for most of the perinatal morbidity; perinatal mortality is substantial. Treatment directed at relieving hypercortisolism has been instituted during pregnancy:
Pituitary
or adrenal surgery, chemotherapy, and pituitary irradiation have all been reported, with variable results. Information is lacking on any alteration of maternal morbidity after treatment. The impact of therapy on perinatal outcome appears limited to a reduction in the prematurity rate, but overall numbers are small and such a conclusion should be viewed with caution. No significant maternal or perinatal complications secondary to treatment itself were reported.
...
PMID:Cushing syndrome in pregnancy. 172 71
Pituitary
function studies were performed on 20 patients with benign intracranial
hypertension
. Abnormal results were only obtained in six cases and all of these findings could be attributed to sources other than the increased intracranial pressure. Once the disease as well as its cause had disappeared, a second study was carried out and the results for all the patients were then normal. Computerized tomographic scanning of the sella turcica detected an empty sella in one patient and a possible hypophyseal microadenoma without functional repercussions in another. No evidence was found that benign intracranial
hypertension
is provoked by an impairment in pituitary function, nor that it could be a secondary complication thereof.
...
PMID:[Pituitary study in benign intracranial hypertension]. 195 26
To study the regulation of hypothalamic vasopressin (VP) and oxytocin (OT) gene expression in relation to the development of
hypertension
, levels of VP mRNA and OT mRNA were determined in spontaneously hypertensive rats (SHR). Differences in VP and OT mRNA content of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of 4- and 10-week-old SHR and Wistar-Kyoto controls (WKY) were quantitated by dot-blot and Northern blot analysis. VP and OT pituitary content and VP plasma levels were measured by radioimmunoassays. VP mRNA levels were approximately 2-fold and 3-fold higher in the SON and PVN of 4-week-old SHR, respectively, as compared to controls. The OT mRNA levels were approximately 35% lower in both nuclei of the SHR. There was no difference in VP and OT pituitary content between 4-week-old SHR and WKY, but VP plasma levels were higher in SHR. In the 10-week-old SHR VP mRNA levels were still approximately 30-40% higher and the OT mRNA levels were approximately 40% lower in both nuclei when compared to age-matched WKY.
Pituitary
VP and OT contents were respectively 1.5-fold higher and 20% lower in the 10-week-old SHR than in 10-week-old WKY. VP plasma levels were still elevated in the SHR. The data indicate that in the hypothalamo-neurohypophyseal system of the SHR the VP system is in a higher state of activity, while the OT system is lower in activity.
...
PMID:Vasopressin and oxytocin gene expression in the supraoptic and paraventricular nucleus of the spontaneously hypertensive rat (SHR) during development of hypertension. 323 90
Pituitary
cell reaggregates from 14-day-old and adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were cultured in serum-free, chemically defined medium supplemented with the thyroid hormone triiodothyronine and the glucocorticoid dexamethasone. After 1 wk in culture, aggregates were transferred into a perifusion system, and the effect of angiotensin II (ANG II) on prolactin (PRL) and growth hormone (GH) release was studied. In aggregates from adult SHR, ANG II displayed a significant and dose-dependent GH releasing activity, whereas a negligible effect or no effect was seen in aggregates from adult WKY. In contrast, no difference in the stimulation of PRL release by ANG II was found. To exclude the possibility that the enhanced GH responsiveness was secondary to longstanding
hypertension
, aggregates from animals in the prehypertensive stage were studied. Both the GH and PRL responses to ANG II were significantly higher in aggregates from 14-day-old SHR than in aggregates from 14-day-old WKY. These data indicate that abnormal GH and PRL responses to ANG II exist in pituitary cell aggregates from SHR long before
hypertension
develops. Because these differences were found in pituitary cells maintained in culture for 1 wk, they do not seem to be secondary to changes in brain regulation of pituitary function but rather are caused by factors intrinsic to the pituitary.
...
PMID:Enhanced ANG II activity in anterior pituitary cell aggregates from hypertensive rats. 341 35
Pubertal juvenile
dyspituitarism
(PJD) is one of the common types of obesity in adolescents. Literature data on the involvement of the renin-angiotensin-aldosterone, hypophysis-adrenal cortex system in the formation of this syndrome are of controversial nature, and the pathogenesis of the development of arterial
hypertension
in PJD is obscure in many respects. The purpose of the study was to investigate the activity of plasma renin, potassium and sodium in the blood serum as well as the excretion of potassium and sodium with daily urine in PJD patients. A total of 148 PJD patients aged 14 to 21 were examined, of them 22 had exogenous constitutional obesity. The control group was composed of 54 healthy persons of the same sex and age. Electrolyte metabolic derangement, an increase in the ACTH level and hyperaldosteronemia were shown to play a certain role in the development of arterial
hypertension
in PJD. The above changes developed in the presence of disordered interrelationships in the hypophysis-adrenal cortex, renin-angiotensin-aldosterone system.
...
PMID:[Pathogenesis of arterial hypertension in puberal juvenile dyspituitarism]. 390 40
Pituitary
glands removed from adult female normotensive Sprague-Dawley (S-D) rats were implanted beneath the renal capsule of 100-day male S-D rats. Female neonatal S-D rats were given a single sc injection of 1.25 mg of testosterone proprionate (TP) suspended in sesame oil. Systolic blood pressure and blood samples were taken at various time intervals postimplantation and TP treatment prio to autopsy. Both the TP treatment and pituitary implants caused hyperprolactinemia, increased adrenal weight concomitant with thymus gland involution, hypersecretion of corticosterone, but no increase in systolic blood pressure. It is suggested that the failure of these hyperprolactinemic S-D rats to develop
hypertension
was due to the absence of a genetically mediated hypertensinogenic factor present in this normotensive strain which is activated by chronic hyperprolactinemia.
...
PMID:Hyperprolactinemia and hyperadrenocorticism accompanied by normal blood pressure in Sprague-Dawley rats. 732 61
Pituitary
and adrenal glands removed from male and female spontaneously hypertensive (SH) rat donors with
high blood pressure
were implanted in normotensive, Sprague-Dawley (S-D) recipients which had been hypophysectomized or adrenalectomized. The transplants were accepted readily and after 90 days the animals were necropsied. Maintenance of organs and body weights suggested that the pituitary glands of SH rats have an adequate content of growth hormone but there may be an intrinsic deficiency of gonadotrophic hormones in this strain. The blood pressure of the hypophysectomized and adrenalectomized recipients was well maintained, particularly by the Sh-rat adrenal transplants, but the blood pressure of the recipients did not become abnormally elevated. SH-rat pituitary and adrenal glands caused fatty infiltration of the liver and hyperlipidaemia indicative of a lipotrophic factor in the SH rat strain. The histopathological changes in the transplanted pituitary and adrenal glands, and in intact pituitary and adrenal glands of the recipients, suggested that SH-rat pituitary glands secrete extra quantities of ACTH, that the pituitary-adrenal axis of this strain is extra sensitive to stressful stimuli, and that the spectrum of adrenal steroids secreted by this strain may be different from that of most normotensive strains.
...
PMID:Transplantation of pituitary and adrenal glands of spontaneously hypertensive rats into hypophysectomized or adrenalectomized, normotensive Sprague-Dawley rats. 742 92
Pituitary
adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion.
Pituitary
adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications,
hypertension
, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86
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