INTENSE SYMPATHETIC-NERVE ACTIVITY IN ADULTS WITH HYPOPITUITARISM ANDUNTREATED GROWTH-HORMONE DEFICIENCY

Citation
Yb. Sverrisdottir et al., INTENSE SYMPATHETIC-NERVE ACTIVITY IN ADULTS WITH HYPOPITUITARISM ANDUNTREATED GROWTH-HORMONE DEFICIENCY, The Journal of clinical endocrinology and metabolism, 83(6), 1998, pp. 1881-1885
Citations number
49
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
83
Issue
6
Year of publication
1998
Pages
1881 - 1885
Database
ISI
SICI code
0021-972X(1998)83:6<1881:ISAIAW>2.0.ZU;2-G
Abstract
Perturbations in the sympathetic nervous system may be anticipated in adults with hypopituitarism and untreated GH deficiency, because the s yndrome is associated with both peripheral and central factors known t o modulate sympathetic traffic. The higher prevalence of hypertension and increased cardiovascular morbidity/mortality reported in GH-defici ent patients may suggest increased activity of the sympathetic nervous system. We recorded muscle sympathetic nerve activity (MSNA) in 10 hy popituitary adults with adequate hormonal replacement therapy except G H and in 10 healthy controls matched for age, gender, and body mass in dex to test whether hormonal aberrations in hypopituitarism and untrea ted GH deficiency are associated with an increase in sympathetic nerve traffic. Blood samples for insulin-like growth factor I, free T-4, an d TSH were taken after an overnight fast, followed by an oral glucose tolerance test. Direct intraneural recordings of MSNA were performed w ith a tungsten microelectrode from the peroneal nerve. The hypopituita ry subjects had markedly increased MSNA (54 +/- 4 bursts/min vs. 34 +/ - 4 in controls; P < 0.002), which was not related to abdominal obesit y or altered glucose metabolism. When assessed for the whole study gro up, MSNA was inversely correlated to serum insulin-like growth factor I(r = -0.59; P < 0.006) and TSH (r = -0.46; P < 0.04). MSNA was positi vely correlated to diastolic blood pressure (r = 0.80; P < 0.0005) in patients, but not in controls. The intense sympathetic discharge is su ggested to be of central origin and may be an important underlying mec hanism for the secondary hypertension and increased cardiovascular mor bidity/mortality in this patient group.