Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was performed on seven patients with Cushing's disease and seven age and sex matched patients with essential hypertension. The patients maintained their usual diet and sodium intake and received the ACE inhibitor trandolapril at a dose of 2 mg daily for 8 days. Trandolapril treatment resulted in an increase in the active renin and decrease in the urinary kallikrein activity in both study groups. Blood pressure decreased significantly in patients with Cushing's disease and essential hypertension after 8 days of trandolapril treatment. The opposite responses of renin and kallikrein to ACE inhibition support a possible feed-back mechanism of regulation between the renin-angiotensin system and the kallikrein-kinin system.
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PMID:Trandolapril in Cushing's disease: short-term trandolapril treatment in patients with Cushing's disease and essential hypertension. 970 82

The aim of this presentation is evaluation of the renin-angiotensin-aldosterone system (RAA) in selected diseases of endocrine glands. In patients with acromegaly, Conn's syndrome, hyperparathyroidism, hyperthyroidism, hypothyroidism, phaeochromocytoma and Cushing's disease is possible to formulate the temporarily conclusions according to subsidiary meaning of angiotensin converting enzyme inhibitors (ACE I) in these endocrinopathies. Whereas the ACE I play an important role in the treatment of nephropathy and hypertension in diabetes mellitus.
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PMID:[The activity of renin-angiotensin-aldosterone system (RAA) and possibilities of application angiotensin converting enzyme inhibitors (ACE I) in selected diseases of endocrine glands]. 1049 33

It is difficult to predict the size of pituitary corticotroph tumors in dogs with Cushing's disease (pituitary-dependent hyperadrenocorticism [PDH]) without pituitary imaging techniques. The purpose of this study was to examine the relationship between plasma adrenocorticotropin hormone (ACTH) precursor concentration and pituitary size in dogs with Cushing's disease. Plasma concentrations of ACTH precursors (pro-opiomelanocortin [POMC]/pro-ACTH) and pituitary tumor height/brain area were measured in 36 dogs with pituitary corticotroph adenomas of various sizes. There was a correlation between tumor size (measured as the pituitary tumor height/brain area ratio [P/B]) and POMC/pro-ACTH concentration (r = .70; P < .0001). Dogs with P/B > or = 0.40 x 10(-2) mm(-1) had higher concentrations of ACTH precursors than dogs with P/B < 0.40 x 10(-2) mm(-1) (median concentration 85 pmol/L, range 15-1,350 pmol/L, n = 14 versus 15 pmol/L, range 15-108 pmol/L, n = 22; P < .0001). With a threshold of 35 pmol/L of POMC/pro-ACTH concentration, the estimated sensitivity and specificity of the kit were 93% (95% confidence interval [CI], 79-100%) and 86% (95% CI, 73-100%), respectively. We interpret these data as indicating that measurement of POMC and pro-ACTH might be of value in the characterization of tumor size in dogs with Cushing's disease. Low POMC/pro-ACTH concentrations make it unlikely that a large pituitary tumor exists in dogs with PDH.
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PMID:Plasma pro-opiomelanocortin, pro-adrenocorticotropin hormone, and pituitary adenoma size in dogs with Cushing's disease. 1571 43

Leukemia inhibitory factor (LIF) is a pleiotropic cytokine of the IL-6 family that activates the hypothalamic-pituitary-adrenal axis and promotes corticotrope cell differentiation during development. The aim of this study was to investigate the expression of LIF and its receptor (LIFR) in the canine pituitary gland and in corticotrope adenomas, and to perform a mutation analysis of LIFR. Using immunohistochemistry, immunofluorescence, and quantitative expression analysis, LIF and LIFR expression were studied in pituitary glands of control dogs and in specimens of corticotrope adenoma tissue collected through hypophysectomy in dogs with pituitary-dependent hypercortisolism (PDH, Cushing's disease). Using sequence analysis, cDNA was screened for mutations in the LIFR. In the control pituitary tissues and corticotrope adenomas, there was a low magnitude of LIF expression. The LIFR, however, was highly expressed and co-localized with ACTH(1-24) expression. Cytoplasmatic immunoreactivity of LIFR was preserved in corticotrope adenomas and adjacent nontumorous cells of pars intermedia. No mutation was found on mutation analysis of the complete LIFR cDNA. Surprisingly, nuclear to perinuclear immunoreactivity for LIFR was present in nontumorous pituitary cells of the pars distalis in 10 of 12 tissue specimens from PDH dogs. These data show that LIFR is highly co-expressed with adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) in the canine pituitary gland and in corticotrope adenomas. Nuclear immunoreactivity for LIFR in nontumorous cells of the pars distalis may indicate the presence of a corticotrope adenoma.
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PMID:Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas. 2003 83