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NEUROPEPTIDE Y IN CORTISOL‐INDUCED HYPERTENSION IN MALE VOLUNTEERS
Author(s) -
Whitworth Judith A.,
Williamson Paula M.,
Brown Mark A.,
Morris Margaret J.
Publication year - 1994
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1994.tb02538.x
Subject(s) - neuropeptide y receptor , medicine , endocrinology , neuropeptide , psychology , receptor
SUMMARY 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.