|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Hypertension occurred in 34/77 children (44%) during treatment with ACTH and 4/11 children (36%) during treatment with prednisolone.
|
31769329 |
2020 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Bolus, bolus along with continuous infusion or continuous infusion of ACTH did not affect both indices.The absence of clinical success (i.e. unchanged or increased blood pressure) was 33% and absence of biochemical success (persistent hypokalaemia or persistently raised aldosterone-to-renin ratio, or both) was 15%.
|
30601318 |
2019 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Retrospective data confirm the efficacy of ACTH or the synthetic analogue Synacthen in the treatment of acute gout in patients with comorbidities such as cardiovascular disease, chronic kidney disease, and hypertension, including those who were hospitalised, with all patients responding after 1-3 doses.
|
30183601 |
2019 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Identifying the mechanism of ACTH-dependent proliferation of VSMCs may help to provide new therapeutic targets for hypertension.
|
29943847 |
2018 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Hypertension and severe hypokalaemia associated with ectopic ACTH production.
|
30115708 |
2018 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
ACTH = adrenocorticotropic hormone; AIx@75 = augmentation index corrected for a heart rate of 75 beats per minute; BMI = body mass index; CVD = cardiovascular disease; DBP = diastolic blood pressure; FSH = follicle-stimulating hormone; GH = growth hormone; HT = hypertension; IGF-1 = insulin-like growth factor 1; LH = luteinizing hormone; MBP = mean blood pressure; MRI = magnetic resonance imaging; NFPA = nonfunctioning pituitary adenoma; PP = pulse pressure; PWA = pulse wave analysis; PWV = pulse wave velocity; SBP = systolic blood pressure; TSH = thyroid-stimulating hormone.
|
29975581 |
2018 |
|
Hypertensive disease
|
0.400 |
AlteredExpression
|
group |
BEFREE |
In this review we discuss the importance of the brain POMC-MC4R system in regulating SNS activity and BP in obesity and other forms of hypertension.
|
28274841 |
2017 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Peripheral LPH concentrations mediated the effect of hypertension on deep, but not periventricular, WMH volumes.
|
28756941 |
2017 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Adrenocorticotropic hormone (ACTH)-secreting tumors account for 2% to 6% of adenomas and are associated with obesity, hypertension, diabetes, and other morbidity.
|
28170483 |
2017 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
The consequent cortisol deficiency results in a compensatory increase in adrenocorticotropic hormone (ACTH) drive, which stimulates the production of deoxycorticosterone and corticosterone leading to hypertension and hypokalaemia.
|
28487303 |
2017 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
These findings expand on the clinical spectrum of phenotypes associated with KCNJ5 mutations and implicate these mutations in the pathogenesis of hypertension associated with increased aldosterone response to ACTH stimulation.
|
27293068 |
2016 |
|
Hypertensive disease
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Specific mutations in the leptin and the melaninocortin receptor genes in animal models of obesity without hypertension, the actions of α-melanocyte stimulating hormone, and SNS activity in obesity-related hypertension may promote recognition of protective and promoting factors for hypertension in obesity.
|
26103132 |
2015 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
This group had no difference in basal ACTH/renin (REN) concentrations compared with controls and the 83 patients with hypertension (73%) without an ALD hyper-response to ACTH stimulation.
|
25974737 |
2015 |
|
Hypertensive disease
|
0.400 |
Therapeutic
|
group |
CTD_human |
Effects of sepiapterin supplementation and NOS inhibition on glucocorticoid-induced hypertension.
|
20186125 |
2010 |
|
Hypertensive disease
|
0.400 |
Therapeutic
|
group |
CTD_human |
The glucocorticoid receptor is required for experimental adrenocorticotrophic hormone-induced hypertension in mice.
|
20659135 |
2010 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
CTD_human |
The glucocorticoid receptor is required for experimental adrenocorticotrophic hormone-induced hypertension in mice.
|
20659135 |
2010 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
CTD_human |
Effects of sepiapterin supplementation and NOS inhibition on glucocorticoid-induced hypertension.
|
20186125 |
2010 |
|
Hypertensive disease
|
0.400 |
Therapeutic
|
group |
CTD_human |
Cushing's disease in dogs and humans.
|
19153526 |
2009 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
CTD_human |
The role of 20-hydroxyeicosatetraenoic acid in adrenocorticotrophic hormone and dexamethasone-induced hypertension.
|
19458537 |
2009 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
CTD_human |
Cushing's disease in dogs and humans.
|
19153526 |
2009 |
|
Hypertensive disease
|
0.400 |
Therapeutic
|
group |
CTD_human |
The role of 20-hydroxyeicosatetraenoic acid in adrenocorticotrophic hormone and dexamethasone-induced hypertension.
|
19458537 |
2009 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
CTD_human |
Overall, the data establish that the alpha(2)-Na(+)-K(+)-ATPase ouabain-binding site is of central importance in the development of ACTH-induced hypertension.
|
18487447 |
2008 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
These novel data support the suggestion that chronic aldosterone excess, in genetically susceptible individuals, may be a consequence of increased ACTH drive to the adrenal and identify novel molecular mechanisms that may lead to the development of hypertension within the general population.
|
17980006 |
2008 |
|
Hypertensive disease
|
0.400 |
Therapeutic
|
group |
CTD_human |
Overall, the data establish that the alpha(2)-Na(+)-K(+)-ATPase ouabain-binding site is of central importance in the development of ACTH-induced hypertension.
|
18487447 |
2008 |
|
Hypertensive disease
|
0.400 |
Therapeutic
|
group |
CTD_human |
Arachidonic acid metabolism in glucocorticoid-induced hypertension.
|
18067589 |
2008 |