Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-1-18
pubmed:abstractText
ANG II (angiotensin II) facilitates catecholamine release from the adrenal medulla and neuronal NE (noradrenaline) release. Since animal experiments point to specific sympatho-inhibitory properties of the AT1 (ANG II type 1)-receptor blocker EPRO (eprosartan), the primary aim of this study was to clarify if EPRO inhibits sympathetic reactivity in humans as determined by the effect of EPRO on insulin-induced catecholamine release. Sixteen healthy male volunteers were randomized in a double-blind cross-over study to receive a single dose of EPRO (600 mg) compared with placebo, followed by insulin-induced hypoglycaemia [0.15 IU (international unit)/kg of body weight; intravenous bolus] on two study days 1 week apart. From baseline to the end of hypoglycaemia (170 min), the sympatho-adrenal reactivity was mapped by invasive continuous blood pressure monitoring and repeated measurements of FBF (forearm blood flow), arterial and venous concentrations of glucose, catecholamines [EPI (adrenaline) and NE (noradrenaline)], renin, ANG II and aldosterone. EPRO induced an 8-10-fold increase in plasma renin and ANG II concentrations compared with placebo. Plasma glucose decreased equally during placebo and EPRO from baseline 5.9 mmol/l to 1.9 mmol/l and 2.1 mmol/l respectively, inducing a 17-fold increase in arterial EPI concentration at peak. The AUC (area under the curve) during hypoglycaemia for arterial EPI concentrations was 314+/-48 nmol.min.l-1 in placebo compared with 254+/-26 nmol.min.l-1 following EPRO treatment (P=0.14). EPRO attenuated the corresponding AUC for the EPI-induced pulse pressure response (4670+/-219 mmHg.min in EPRO compared with 5004+/-266 mmHg.min in placebo; P=0.02). Moreover, EPRO caused a less pronounced increase in FBF compared with placebo (402+/-30 compared with 479+/-46 ml.100 g-1 of body weight; P=0.04). Musculocutaneous NE release was not affected by EPRO and the AUC for NE release was 51.69+/-15.5 pmol.min-1.100 g-1 of body weight in placebo compared with 39.35+/-18.2 pmol.min-1.100 g-1 of body weight after EPRO treatment (P=0.57). In conclusion, EPRO did not significantly inhibit sympathetic reactivity compared with placebo; however, it blunted the haemodynamic responses elicited by the sympatho-adrenal stimulation which only tended to be attenuated by this drug.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0143-5221
pubmed:author
pubmed:issnType
Print
pubmed:volume
108
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
113-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:15383007-Acrylates, pubmed-meshheading:15383007-Administration, Oral, pubmed-meshheading:15383007-Adult, pubmed-meshheading:15383007-Angiotensin II Type 1 Receptor Blockers, pubmed-meshheading:15383007-Blood Pressure, pubmed-meshheading:15383007-Catecholamines, pubmed-meshheading:15383007-Cross-Over Studies, pubmed-meshheading:15383007-Double-Blind Method, pubmed-meshheading:15383007-Epinephrine, pubmed-meshheading:15383007-Forearm, pubmed-meshheading:15383007-Heart Rate, pubmed-meshheading:15383007-Hemodynamics, pubmed-meshheading:15383007-Humans, pubmed-meshheading:15383007-Hypoglycemia, pubmed-meshheading:15383007-Imidazoles, pubmed-meshheading:15383007-Insulin, pubmed-meshheading:15383007-Male, pubmed-meshheading:15383007-Norepinephrine, pubmed-meshheading:15383007-Thiophenes
pubmed:year
2005
pubmed:articleTitle
Effect of eprosartan on catecholamines and peripheral haemodynamics in subjects with insulin-induced hypoglycaemia.
pubmed:affiliation
Department of Clinical Physiology and Nuclear Medicine, Glostrup University Hospital, DK-2600 Glostrup, Denmark. macn@glostruphosp.kbhamt.dk
pubmed:publicationType
Journal Article, Clinical Trial, Randomized Controlled Trial, Research Support, Non-U.S. Gov't