title: Level and diurnal variations of hormones of interest to the cardiovascular system in patients with heart transplants.
abstract: The lack of a nocturnal decrease in blood pressure in cyclosporine-treated cardiac transplant recipients may indicate abnormalities in the mechanism(s) responsible for circadian variability in other physiologic parameters such as in circulating hormones. This possibility was addressed through repeated determinations of circulating catecholamines, neuropeptide Y, pancreatic polypeptide, calcitonin gene-related peptide, plasma renin activity, aldosterone, atrial natriuretic factor and cortisol. The results from 10 patients with heart transplants were compared with those of 12 age-matched, healthy control subjects. Both groups were studied during 24-hour supine rest. There was no difference between patients and control subjects in mean levels of catecholamines, neuropeptide Y, pancreatic polypeptide and aldosterone. Patients had higher levels (+/- SD) of plasma renin activity (6.4 +/- 1.3 vs 2.6 +/- 0.4 ng/ml/hour, p less than 0.001), calcitonin gene-related peptide (47.7 +/- 9.9 vs 33.3 +/- 5.7 pmol/liter, p less than 0.01) and atrial natriuretic factor (93.0 +/- 56.7 vs 20.7 +/- 8.9 pg/ml, p less than 0.001) than control subjects, respectively. Cortisol was not detected in patients. Abnormal diurnal profiles in patients were found for calcitonin gene-related peptide, aldosterone and atrial natriuretic factor, and for pancreatic polypeptide, together with decreased levels, in patients with greater than 6 months follow-up. Except for hormones reflecting sympathetic nervous activity, all hormonal systems studied showed abnormalities in level or circadian rhythmicity, or both. The pancreatic polypeptide results suggest that parasympathetic neuropathy could develop in cyclosporine-treated heart transplant recipients.
authors.affiliation: Deutsches Herzzentrum Berlin, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Sehested
authors.forename: F
authors.initials: F
authors.lastname: Thomas
authors.forename: M
authors.initials: M
authors.lastname: Thorn
authors.forename: S
authors.initials: S
authors.lastname: Schifter
authors.forename: V
authors.initials: V
authors.lastname: Regitz
authors.forename: S
authors.initials: S
authors.lastname: Sheikh
authors.forename: W
authors.initials: W
authors.lastname: Oelkers
authors.forename: U
authors.initials: U
authors.lastname: Palm
authors.forename: W
authors.initials: W
authors.lastname: Meyer-Sabellek
authors.forename: R
authors.initials: R
authors.lastname: Hetzer
mesh_terms: D000305:Adrenal Cortex Hormones / Q000097:blood*; D000328:Adult; D000450:Aldosterone / Q000097:blood; D000704:Analysis of Variance; D009320:Atrial Natriuretic Factor / Q000097:blood*; D001794:Blood Pressure; D015740:Calcitonin Gene-Related Peptide / Q000097:blood; D002395:Catecholamines / Q000097:blood*; D002940:Circadian Rhythm; D005260:Female; D006339:Heart Rate; D016027:Heart Transplantation / Q000502:physiology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008875:Middle Aged; D009478:Neuropeptide Y / Q000097:blood; D009479:Neuropeptides / Q000097:blood*; D010191:Pancreatic Polypeptide / Q000097:blood; D012083:Renin / Q000097:blood*
chemical_list: D000305:Adrenal Cortex Hormones; D002395:Catecholamines; D009478:Neuropeptide Y; D009479:Neuropeptides; D000450:Aldosterone; D010191:Pancreatic Polypeptide; D009320:Atrial Natriuretic Factor; D012083:Renin; D015740:Calcitonin Gene-Related Peptide; D006854:Hydrocortisone