Growth hormone-independent cardiotropic activities of growth hormone-releasing peptides in normal subjects, in patients with growth hormone deficiency, and in patients with idiopathic or ischemic dilated cardiomyopathy

Citation
F. Broglio et al., Growth hormone-independent cardiotropic activities of growth hormone-releasing peptides in normal subjects, in patients with growth hormone deficiency, and in patients with idiopathic or ischemic dilated cardiomyopathy, ENDOCRINE, 14(1), 2001, pp. 105-108
Citations number
18
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
ENDOCRINE
ISSN journal
1355008X → ACNP
Volume
14
Issue
1
Year of publication
2001
Pages
105 - 108
Database
ISI
SICI code
1355-008X(200102)14:1<105:GHCAOG>2.0.ZU;2-0
Abstract
Growth hormone releasing peptides (GHRPs) are synthetic molecules endowed w ith potent neuroendocrine activities mediated by specific receptors in the pituitary and in the central nervous system. GHRPs receptors have been repo rted even in perpheral tissues, particularly in the myocardium, where they probably mediate growth hormone (GH)-independent activities. We studied in humans the cardiac effects of hexarelin administration in 7 normal adults, in 7 severe CH-deficient patients, and in 12 patients with severe dilated c ardiomyopathy. Left ventricular ejection fraction (LVEF), mean blood pressu re (MBP), heart rate (HR), and CH levels were evaluated at baseline and eve ry 15 min up to 60 min after acute 2.0 mug/kg iv hexarelin administration. Basal LVEF in dilated cardiomyopathy was impaired and lower (p < 0.001) tha n in GH deficiency, in turn lower (p < 0.001) than in normal subjects. Hexa relin signficantly (p < 0.05) increased LVEF in normal and in GH-deficient subjects, but not in dilated cardiomyopathy, without significant variations in MBP and HR. Hexeralin significantly (p < 0.05) increased GH levels in n ormal subjects and in dilated cardiomyopathy but not in GH deficiency. Thes e findings suggest that, in humans, the acute administration of hexarelin e xerts a GH-independent positive inotropic effect likely mediated by specifi c GHRPs myocardial receptors.