PMID- 11698067
OWN - NLM
STAT- MEDLINE
DCOM- 20020103
LR  - 20190624
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 430
IP  - 1
DP  - 2001 Oct 26
TI  - Intracerebroventricular administration of a glucocorticoid receptor antagonist 
      enhances the cardiovascular responses to brief restraint stress.
PG  - 87-91
AB  - Intracerebroventricular (i.c.v.) administration of the glucocorticoid receptor 
      antagonist 
      17beta-hydroxy-11beta(4-dimethylamino-phenyl)17alpha-(1-propynyl)estra-4,9dien-3one 
      (RU38486) in conscious rats slowly increased systolic blood pressure as assessed 
      with the indirect tail cuff method. However, direct measurement of blood pressure 
      in freely moving rats did not reveal changes in blood pressure after i.c.v. 
      injection of this antagonist either in the light or in the dark phase. In the 
      present study, the hypothesis is tested that aspects of the tail cuff procedure, 
      involving heat (30 min, 32 degrees C) and brief restraint stress, are necessary 
      conditions to detect the glucocorticoid receptor-mediated cardiovascular effect. 
      Freely moving rats equipped with a telemetric transmitter to directly measure 
      heart rate and blood pressure were injected i.c.v. with either the glucocorticoid 
      receptor or the mineralocorticoid receptor antagonist and were either left 
      undisturbed for 24 h, or were subjected to the tail cuff procedure at 1.5, 6.5 
      and 23.5 h after injection. Then after 30-min warming and during brief restraint, 
      blood pressure and heart rate showed a rapid increase. The mineralocorticoid 
      receptor antagonist administered i.c.v. did not affect these stress-induced 
      increases in cardiovascular responses. The glucocorticoid receptor antagonist 
      i.c.v. significantly increased the heart rate and pressor response at 24 h. In 
      the undisturbed rats, neither basal heart rate nor blood pressure were affected 
      by either antagonist during the circadian cycle. In conclusion, the blockade of 
      central glucocorticoid receptor causes a long-lasting facilitation of the 
      stress-induced pressor and heart rate response, which does not require a 2-week 
      training to the condition of heat and stress.
FAU - Van Acker, S A
AU  - Van Acker SA
AD  - Division of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, 
      Leiden University Medical Center, P.O. Box 9503, 2300 RA, Leiden, The 
      Netherlands.
FAU - Fluttert, M F
AU  - Fluttert MF
FAU - Sibug, R M
AU  - Sibug RM
FAU - De Kloet, E R
AU  - De Kloet ER
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Receptors, Glucocorticoid)
RN  - 27O7W4T232 (Spironolactone)
RN  - 320T6RNW1F (Mifepristone)
RN  - 76676-34-1 (RU 28318)
SB  - IM
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Circadian Rhythm
MH  - Heart Rate/drug effects
MH  - Hot Temperature
MH  - Injections, Intraventricular
MH  - Male
MH  - Mifepristone/*pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Glucocorticoid/*antagonists & inhibitors
MH  - Restraint, Physical
MH  - Spironolactone/*analogs & derivatives/pharmacology
MH  - Stress, Physiological/etiology/*physiopathology
MH  - Time Factors
EDAT- 2001/11/08 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/11/08 10:00
PHST- 2001/11/08 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/11/08 10:00 [entrez]
AID - S0014299901013413 [pii]
AID - 10.1016/s0014-2999(01)01341-3 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2001 Oct 26;430(1):87-91. doi: 10.1016/s0014-2999(01)01341-3.