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Intense Sympathetic Nerve Activity in Adults with Hypopituitarism and Untreated Growth Hormone Deficiency¹

Institute for Clinical Neuroscience, Department of Clinical Neurophysiology (Y.B.S., M.E.), Department of Nephrology (H.H.), and Research Center for Endocrinology and Metabolism (G.J., B.-Å.B.), Sahlgren University Hospital, S-413 45 Goteborg, Sweden

Address all correspondence and requests for reprints to: Dr. Yrsa Bergmann Sverrisdóttir, Institute for Clinical Neuroscience, Department of Clinical Neurophysiology, Sahlgren University Hospital, S-413 45 Goteborg, Sweden. E-mail: yrsa.sverrisdottir{at}neuro.gu.se

Perturbations in the sympathetic nervous system may be anticipated in adults with hypopituitarism and untreated GH deficiency, because the syndrome is associated with both peripheral and central factors known to modulate sympathetic traffic. The higher prevalence of hypertension and increased cardiovascular morbidity/mortality reported in GH-deficient patients may suggest increased activity of the sympathetic nervous system.

We recorded muscle sympathetic nerve activity (MSNA) in 10 hypopituitary adults with adequate hormonal replacement therapy except GH and in 10 healthy controls matched for age, gender, and body mass index to test whether hormonal aberrations in hypopituitarism and untreated GH deficiency are associated with an increase in sympathetic nerve traffic.

Blood samples for insulin-like growth factor I, free T₄, and TSH were taken after an overnight fast, followed by an oral glucose tolerance test. Direct intraneural recordings of MSNA were performed with a tungsten microelectrode from the peroneal nerve.

The hypopituitary subjects had markedly increased MSNA (54 ± 4 bursts/min vs. 34 ± 4 in controls; P < 0.002), which was not related to abdominal obesity or altered glucose metabolism. When assessed for the whole study group, 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 positively correlated to diastolic blood pressure (r = 0.80; P < 0.0005) in patients, but not in controls.

The intense sympathetic discharge is suggested to be of central origin and may be an important underlying mechanism for the secondary hypertension and increased cardiovascular morbidity/mortality in this patient group.

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