Nitric Oxide Is Formed in a Subpopulation of Rat Pineal Cells and Acts as an Intercellular Messenger

1998 ◽  
Vol 68 (1) ◽  
pp. 57-63 ◽  
Author(s):  
Rainer Spessert ◽  
Elisabeth Layes ◽  
Gabriele Hill ◽  
Lutz Vollrath
Keyword(s):  
Nitric Oxide ◽  
Intercellular Messenger

Nitric Oxide: A Novel Intercellular Messenger in the Striatum

1994 ◽  
pp. 163-169
Author(s):  
Piers C. Emson ◽  
Rosalinda Guevara Guzman ◽  
Rosa Señaris ◽  
Jiro Kishimoto ◽  
Weiming Xu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Intercellular Messenger

scholarly journals Modulation of swimming in the gastropod Melibe leonina by nitric oxide

2002 ◽  
Vol 205 (3) ◽  
pp. 397-403
Author(s):  
James M. Newcomb ◽  
Winsor H. Watson
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Marked Effect ◽  
Motor Program ◽  
No Donors ◽  
Histological Studies ◽  
The Central Nervous System ◽  
Oxide Synthase ◽  
Intercellular Messenger ◽  
Dependent Mechanism

SUMMARY Nitric oxide (NO) is a gaseous intercellular messenger produced by the enzyme nitric oxide synthase. It has been implicated as a neuromodulator in several groups of animals, including gastropods, crustaceans and mammals. In this study, we investigated the effects of NO on the swim motor program produced by isolated brains and by semi-intact preparations of the nudibranch Melibe leonina. The NO donors sodium nitroprusside (SNP, 1 mmol l–1) and S-nitroso-N-acetylpenicillamine (SNAP, 1 mmol l–1) both had a marked effect on the swim motor program expressed in isolated brains, causing an increase in the period of the swim cycle and a more erratic swim rhythm. In semi-intact preparations, the effect of NO donors was manifested as a significant decrease in the rate of actual swimming. An NO scavenger, reduced oxyhemoglobin, eliminated the effects of NO donors on isolated brains, supporting the assumption that the changes in swimming induced by donors were actually due to NO. The cGMP analogue 8-bromoguanosine 3′,5′-cyclic monophosphate (1 mmol l–1) produced effects that mimicked those of NO donors, suggesting that NO is working via a cGMP-dependent mechanism. These results, in combination with previous histological studies indicating the endogenous presence of nitric oxide synthase, suggest that NO is used in the central nervous system of Melibe leonina to modulate swimming.

scholarly journals Targeting Nitric Oxide with Natural Derived Compounds as a Therapeutic Strategy in Vascular Diseases

2016 ◽  
Vol 2016 ◽  
pp. 1-20 ◽  
Author(s):  
Maurizio Forte ◽  
Valeria Conti ◽  
Antonio Damato ◽  
Mariateresa Ambrosio ◽  
Annibale A. Puca ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Therapeutic Strategy ◽  
Therapeutic Potential ◽  
Vascular Diseases ◽  
Therapeutic Strategies ◽  
Vascular Homeostasis ◽  
The Family ◽  
No Signaling ◽  
Aggregation Control ◽  
Intercellular Messenger

Within the family of endogenous gasotransmitters, nitric oxide (NO) is the smallest gaseous intercellular messenger involved in the modulation of several processes, such as blood flow and platelet aggregation control, essential to maintain vascular homeostasis. NO is produced by nitric oxide synthases (NOS) and its effects are mediated by cGMP-dependent or cGMP-independent mechanisms. Growing evidence suggests a crosstalk between the NO signaling and the occurrence of oxidative stress in the onset and progression of vascular diseases, such as hypertension, heart failure, ischemia, and stroke. For these reasons, NO is considered as an emerging molecular target for developing therapeutic strategies for cardio- and cerebrovascular pathologies. Several natural derived compounds, such as polyphenols, are now proposed as modulators of NO-mediated pathways. The aim of this review is to highlight the experimental evidence on the involvement of nitric oxide in vascular homeostasis focusing on the therapeutic potential of targeting NO with some natural compounds in patients with vascular diseases.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Nitric Oxide Reduces Pressor Responsiveness During Ovine Hypoadrenocorticism

2001 ◽  
Vol 28 (5-6) ◽  
pp. 459-462
Author(s):  
Pini Orbach ◽  
Charles E Wood ◽  
Maureen Keller-Wood
Keyword(s):  
Nitric Oxide
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