Clinical and Experimental Pharmacology and Physiology · 1994 · 16 citations · 23 references
Life SciencesEndocrinologyPhysiologyNeurochemistryNeuroendocrinologyNeuroimmunologyAdrenal HormonesAutonomic Nervous SystemAutonomic Nervous System ResponsesBlood Pressure RegulationHormonal InfluencesNeuroendocrine PhysiologyBlood PressureCortisol SignalingEosinophil CountHypertension Associated With CorticosteroidsSympathetic ActivationSympathetic InteractionsSympathetic Nervous System ResponsesSympathoadrenal Activation
1. Cortisol-induced blood pressure rises in men are not accompanied by increases in plasma catecholamines. The present study examines the effects of cortisol on the sympathetic co-transmitter, neuropeptide Y (NPY). 2. Eight normal men were given cortisol 200 mg/day over 5 days and haemodynamic, metabolic and hormonal measures were taken. Plasma NPY-like immunoreactivity (NPY-LI) concentrations were measured by direct radio-immunoassay. 3. Cortisol significantly increased systolic, diastolic and mean arterial pressure, bodyweight, plasma glucose and total white cell concentration and decreased plasma potassium and total eosinophil count, as in previous studies. Plasma NPY concentrations were not altered significantly during cortisol treatment, but increased following cessation of cortisol treatment (P = 0.006). 4. The essentially unchanged pattern for NPY concentration with cortisol treatment resembles that previously reported for adrenaline and noradrenaline, but the increase in NPY on cortisol withdrawal was not seen for adrenaline or noradrenaline. These data do not support a role for sympathetic activation in the genesis of cortisol-induced hypertension.
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On Methods in the Analysis of Profile Data
Samuel W. Greenhouse, Seymour Geisser · Psychometrika · 1959 · 5K citations