title: Exogenous glucocorticoid eliminates or reverses circadian blood pressure variations.
abstract: The effect of glucocorticoid on circadian variations of blood pressure was examined. In untreated patients with essential hypertension, a clear nocturnal fall in blood pressure and heart rate was observed and this was unaffected by combined treatment with antihypertensive drugs. The circadian blood pressure variation in patients with chronic glomerulonephritis (CGN) not receiving glucocorticoid treatment was essentially the same as that in patients with essential hypertension. In both groups there was a positive correlation between blood pressure and heart rate. On the other hand, in patients with CGN and systemic lupus erythematosus (SLE) who were treated with glucocorticoid, there was no nocturnal fall in blood pressure, and often a significant rise. In these patients the blood pressure was lowest in the afternoon and began to rise from then, and during the night, attaining a peak level in the morning. Despite this changed pattern of blood pressure variations, the heart rate in these patients was clearly reduced at night. In 10 patients with CGN and SLE, circadian rhythm of blood pressure and heart rate was examined before and during treatment with prednisolone (40.2 +/- 17.0 mg/day for 58.0 +/- 19.4 days, mean +/- s.d.). Prednisolone abolished the nocturnal fall of blood pressure, while the nocturnal fall of heart rate remained. There was no correlation between blood pressure and heart rate in patients with glucocorticoid treatment. These results suggest that the circadian blood pressure variation is influenced by the hypothalamo-pituitary-adrenal axis, probably through its action on the autonomic nervous system.
authors.affiliation: Department of Medicine, Tohoku University, Sendai, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Imai
authors.forename: K
authors.initials: K
authors.lastname: Abe
authors.forename: S
authors.initials: S
authors.lastname: Sasaki
authors.forename: N
authors.initials: N
authors.lastname: Minami
authors.forename: M
authors.initials: M
authors.lastname: Munakata
authors.forename: M
authors.initials: M
authors.lastname: Nihei
authors.forename: H
authors.initials: H
authors.lastname: Sekino
authors.forename: K
authors.initials: K
authors.lastname: Yoshinaga
mesh_terms: D000328:Adult; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects*; D002940:Circadian Rhythm / Q000187:drug effects*; D005921:Glomerulonephritis / Q000188:drug therapy* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D008180:Lupus Erythematosus, Systemic / Q000188:drug therapy* / Q000503:physiopathology; D008991:Monitoring, Physiologic; D010913:Pituitary-Adrenal System / Q000502:physiology; D011239:Prednisolone / Q000627:therapeutic use*
chemical_list: D000959:Antihypertensive Agents; D011239:Prednisolone