PMID- 22508053
OWN - NLM
STAT- MEDLINE
DCOM- 20120809
LR  - 20190212
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 29
IP  - 3-4
DP  - 2012
TI  - Neuropeptide Y reverses chronic stress-induced baroreflex hypersensitivity in 
      rats.
PG  - 463-74
LID - 10.1159/000338500 [doi]
AB  - Chronic stress, as a risk factor for cardiovascular diseases, has been reported 
      to result in elevated plasma neuropeptide Y (NPY) and be highly associated with 
      abnormal cardiac autonomic function. This study aimed to explore the effect of 
      NPY on the chronic stress-induced abnormal baroreceptor reflex sensitivity (BRS). 
      Seven types of recognized stressors were used to develop chronic stress rat 
      model. Subcutaneously implanting ALZET mini-osmotic pumps containing NPY were 
      used to evaluate the action of NPY on the stressed male rats. We found that 
      chronic stress showed no influence on baseline systolic blood pressure (SBP) and 
      heart rate (HR), whereas NPY (85 mug for 30 days) could elevate baseline SBP and 
      induce bradycardia in rats intervened by various stimuli. NPY pretreatment could 
      preserve chronic stress-induced decreases in left ventricular systolic pressure 
      (LVSP) and the maximum rate of change in left ventricular pressure in the 
      isovolumic contraction period (+dp/dt(max)) but has shown no effect on left 
      ventricular end diastolic pressure (LVEDP) and the maximum rate of change in left 
      ventricular pressure in the isovolumic relaxation period (-dp/dt(max)). Notably, 
      chronic stress led to baroreflex oversensitivity indicated by the elevated ratio 
      of Deltaheart rate (HR)/ Deltamean arterial blood pressure (MABP) in rats followed by 
      vasoconstrictor (phenylephrine, PE) or vasodilator (sodium nitroprusside, SNP) 
      administration, which was almost completely reversed by NPY pretreatment. The 
      expressions of substance P (SP) and gamma aminobutyric acid A receptor (GABA(A)R) 
      in nucleus tractus solitarius were increased in chronic stress rats, which were 
      counteracted by NPY pretreatment. We conclude that chronic stress-induced 
      baroreflex hypersensitivity could be blocked by NPY pretreatment. Furthermore, 
      the altered expressions of neurotransmitters and receptors in the brainstem might 
      contribute to this process.
CI  - Copyright (c) 2012 S. Karger AG, Basel.
FAU - Xie, Fang
AU  - Xie F
AD  - Department of Pharmacology, Harbin Medical University (the State-Province Key 
      Laboratory of Biomedicine-Pharmaceutics of China), Harbin, China.
FAU - Sun, Lihua
AU  - Sun L
FAU - Su, Xiaolin
AU  - Su X
FAU - Wang, Ying
AU  - Wang Y
FAU - Liu, Jing
AU  - Liu J
FAU - Zhang, Rong
AU  - Zhang R
FAU - Wang, Ning
AU  - Wang N
FAU - Zhao, Jing
AU  - Zhao J
FAU - Ban, Tao
AU  - Ban T
FAU - Niu, Huifang
AU  - Niu H
FAU - Ai, Jing
AU  - Ai J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120403
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (Neuropeptide Y)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, GABA-A)
RN  - 169D1260KM (Nitroprusside)
RN  - 1WS297W6MV (Phenylephrine)
RN  - 33507-63-0 (Substance P)
RN  - JHB2QIZ69Z (Calcitonin Gene-Related Peptide)
SB  - IM
MH  - Animals
MH  - Baroreflex/*drug effects
MH  - Blood Pressure
MH  - Body Weight
MH  - Bradycardia/chemically induced
MH  - Calcitonin Gene-Related Peptide/genetics/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Heart Rate
MH  - Heart Ventricles/metabolism/pathology
MH  - Myocardial Contraction
MH  - Neuropeptide Y/administration & dosage/*pharmacology
MH  - Nitroprusside/pharmacology
MH  - Phenylephrine/pharmacology
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, GABA-A/genetics/metabolism
MH  - *Stress, Physiological
MH  - Substance P/genetics/metabolism
EDAT- 2012/04/18 06:00
MHDA- 2012/08/10 06:00
CRDT- 2012/04/18 06:00
PHST- 2012/02/21 00:00 [accepted]
PHST- 2012/04/18 06:00 [entrez]
PHST- 2012/04/18 06:00 [pubmed]
PHST- 2012/08/10 06:00 [medline]
AID - 000338500 [pii]
AID - 10.1159/000338500 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2012;29(3-4):463-74. doi: 10.1159/000338500. Epub 2012 Apr 
      3.