Increased nitric oxide synthase activity and expression in the hypothalamus of hindlimb unloaded rats

Patrick J. Mueller, C. Michael Foley, Cheryl M. Heesch, J. Thomas Cunningham, Hong Zheng, Kaushik P. Patel, Eileen M. Hasser

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Upon return from spaceflight or resumption of normal posture after bed rest, individuals often exhibit cardiovascular deconditioning. Although the mechanisms responsible for cardiovascular deconditioning have yet to be fully elucidated, alterations within the central nervous system have been postulated to be involved. The paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus are important brain regions in control of sympathetic outflow and body fluid homeostasis. Nitric oxide (NO) modulates the activity of PVN and SON neurons, and alterations in NO transmission within these brain regions may contribute to symptoms of cardiovascular deconditioning. The purpose of the present study was to examine nitric oxide synthase (NOS) activity and expression in the PVN and SON of control and hindlimb unloaded (HU) rats, an animal model of cardiovascular deconditioning. The number of neurons exhibiting NOS activity as assessed by NADPH-diaphorase staining was significantly greater in the PVN but not SON of HU rats. Western blot analysis revealed that neuronal NOS (nNOS) but not endothelial NOS (eNOS) protein expression was higher in the PVN of HU rats. In the SON, there was a strong trend for an increase in nNOS (p = 0.052) and a significant increase in eNOS expression in HU rats. Our results suggest that increased nNOS in the PVN contributes to autonomic and humoral alterations following cardiovascular deconditioning. In contrast, the functional significance of increases in nNOS and eNOS protein in the SON may be related to alterations in vasopressin release observed previously in HU rats.

Original languageEnglish (US)
Pages (from-to)65-74
Number of pages10
JournalBrain Research
Volume1115
Issue number1
DOIs
StatePublished - Oct 18 2006

Fingerprint

Cardiovascular Deconditioning
Supraoptic Nucleus
Paraventricular Hypothalamic Nucleus
Hindlimb
Nitric Oxide Synthase
Hypothalamus
Nitric Oxide
Neurons
NADPH Dehydrogenase
Space Flight
Bed Rest
Nitric Oxide Synthase Type III
Brain
Body Fluids
Vasopressins
Posture
Proteins
Homeostasis
Central Nervous System
Animal Models

Keywords

  • Body fluid regulation
  • Cardiovascular deconditioning
  • Paraventricular nucleus
  • Simulated microgravity
  • Supraoptic nucleus
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

Mueller, P. J., Foley, C. M., Heesch, C. M., Cunningham, J. T., Zheng, H., Patel, K. P., & Hasser, E. M. (2006). Increased nitric oxide synthase activity and expression in the hypothalamus of hindlimb unloaded rats. Brain Research, 1115(1), 65-74. https://doi.org/10.1016/j.brainres.2006.07.078

Increased nitric oxide synthase activity and expression in the hypothalamus of hindlimb unloaded rats. / Mueller, Patrick J.; Foley, C. Michael; Heesch, Cheryl M.; Cunningham, J. Thomas; Zheng, Hong; Patel, Kaushik P.; Hasser, Eileen M.

In: Brain Research, Vol. 1115, No. 1, 18.10.2006, p. 65-74.

Research output: Contribution to journalArticle

Mueller, PJ, Foley, CM, Heesch, CM, Cunningham, JT, Zheng, H, Patel, KP & Hasser, EM 2006, 'Increased nitric oxide synthase activity and expression in the hypothalamus of hindlimb unloaded rats', Brain Research, vol. 1115, no. 1, pp. 65-74. https://doi.org/10.1016/j.brainres.2006.07.078
Mueller, Patrick J. ; Foley, C. Michael ; Heesch, Cheryl M. ; Cunningham, J. Thomas ; Zheng, Hong ; Patel, Kaushik P. ; Hasser, Eileen M. / Increased nitric oxide synthase activity and expression in the hypothalamus of hindlimb unloaded rats. In: Brain Research. 2006 ; Vol. 1115, No. 1. pp. 65-74.
@article{37f9c635df184daf92ba709bde60e012,
title = "Increased nitric oxide synthase activity and expression in the hypothalamus of hindlimb unloaded rats",
abstract = "Upon return from spaceflight or resumption of normal posture after bed rest, individuals often exhibit cardiovascular deconditioning. Although the mechanisms responsible for cardiovascular deconditioning have yet to be fully elucidated, alterations within the central nervous system have been postulated to be involved. The paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus are important brain regions in control of sympathetic outflow and body fluid homeostasis. Nitric oxide (NO) modulates the activity of PVN and SON neurons, and alterations in NO transmission within these brain regions may contribute to symptoms of cardiovascular deconditioning. The purpose of the present study was to examine nitric oxide synthase (NOS) activity and expression in the PVN and SON of control and hindlimb unloaded (HU) rats, an animal model of cardiovascular deconditioning. The number of neurons exhibiting NOS activity as assessed by NADPH-diaphorase staining was significantly greater in the PVN but not SON of HU rats. Western blot analysis revealed that neuronal NOS (nNOS) but not endothelial NOS (eNOS) protein expression was higher in the PVN of HU rats. In the SON, there was a strong trend for an increase in nNOS (p = 0.052) and a significant increase in eNOS expression in HU rats. Our results suggest that increased nNOS in the PVN contributes to autonomic and humoral alterations following cardiovascular deconditioning. In contrast, the functional significance of increases in nNOS and eNOS protein in the SON may be related to alterations in vasopressin release observed previously in HU rats.",
keywords = "Body fluid regulation, Cardiovascular deconditioning, Paraventricular nucleus, Simulated microgravity, Supraoptic nucleus, Sympathetic nervous system",
author = "Mueller, {Patrick J.} and Foley, {C. Michael} and Heesch, {Cheryl M.} and Cunningham, {J. Thomas} and Hong Zheng and Patel, {Kaushik P.} and Hasser, {Eileen M.}",
year = "2006",
month = "10",
day = "18",
doi = "10.1016/j.brainres.2006.07.078",
language = "English (US)",
volume = "1115",
pages = "65--74",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Increased nitric oxide synthase activity and expression in the hypothalamus of hindlimb unloaded rats

AU - Mueller, Patrick J.

AU - Foley, C. Michael

AU - Heesch, Cheryl M.

AU - Cunningham, J. Thomas

AU - Zheng, Hong

AU - Patel, Kaushik P.

AU - Hasser, Eileen M.

PY - 2006/10/18

Y1 - 2006/10/18

N2 - Upon return from spaceflight or resumption of normal posture after bed rest, individuals often exhibit cardiovascular deconditioning. Although the mechanisms responsible for cardiovascular deconditioning have yet to be fully elucidated, alterations within the central nervous system have been postulated to be involved. The paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus are important brain regions in control of sympathetic outflow and body fluid homeostasis. Nitric oxide (NO) modulates the activity of PVN and SON neurons, and alterations in NO transmission within these brain regions may contribute to symptoms of cardiovascular deconditioning. The purpose of the present study was to examine nitric oxide synthase (NOS) activity and expression in the PVN and SON of control and hindlimb unloaded (HU) rats, an animal model of cardiovascular deconditioning. The number of neurons exhibiting NOS activity as assessed by NADPH-diaphorase staining was significantly greater in the PVN but not SON of HU rats. Western blot analysis revealed that neuronal NOS (nNOS) but not endothelial NOS (eNOS) protein expression was higher in the PVN of HU rats. In the SON, there was a strong trend for an increase in nNOS (p = 0.052) and a significant increase in eNOS expression in HU rats. Our results suggest that increased nNOS in the PVN contributes to autonomic and humoral alterations following cardiovascular deconditioning. In contrast, the functional significance of increases in nNOS and eNOS protein in the SON may be related to alterations in vasopressin release observed previously in HU rats.

AB - Upon return from spaceflight or resumption of normal posture after bed rest, individuals often exhibit cardiovascular deconditioning. Although the mechanisms responsible for cardiovascular deconditioning have yet to be fully elucidated, alterations within the central nervous system have been postulated to be involved. The paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus are important brain regions in control of sympathetic outflow and body fluid homeostasis. Nitric oxide (NO) modulates the activity of PVN and SON neurons, and alterations in NO transmission within these brain regions may contribute to symptoms of cardiovascular deconditioning. The purpose of the present study was to examine nitric oxide synthase (NOS) activity and expression in the PVN and SON of control and hindlimb unloaded (HU) rats, an animal model of cardiovascular deconditioning. The number of neurons exhibiting NOS activity as assessed by NADPH-diaphorase staining was significantly greater in the PVN but not SON of HU rats. Western blot analysis revealed that neuronal NOS (nNOS) but not endothelial NOS (eNOS) protein expression was higher in the PVN of HU rats. In the SON, there was a strong trend for an increase in nNOS (p = 0.052) and a significant increase in eNOS expression in HU rats. Our results suggest that increased nNOS in the PVN contributes to autonomic and humoral alterations following cardiovascular deconditioning. In contrast, the functional significance of increases in nNOS and eNOS protein in the SON may be related to alterations in vasopressin release observed previously in HU rats.

KW - Body fluid regulation

KW - Cardiovascular deconditioning

KW - Paraventricular nucleus

KW - Simulated microgravity

KW - Supraoptic nucleus

KW - Sympathetic nervous system

UR - http://www.scopus.com/inward/record.url?scp=33748928446&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33748928446&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2006.07.078

DO - 10.1016/j.brainres.2006.07.078

M3 - Article

C2 - 16938283

AN - SCOPUS:33748928446

VL - 1115

SP - 65

EP - 74

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -