Document Detail

Nitric oxide in rostral ventrolateral medulla regulates cardiac-sympathetic reflexes: role of synthase isoforms.
MedLine Citation:
PMID:  19684188     Owner:  NLM     Status:  MEDLINE    
Our previous studies have shown that nitric oxide (NO) synthase (NOS)-containing neurons in the rostral ventrolateral medulla (rVLM) are activated during cardiac sympathoexcitatory reflexes (Refs. 12 and 13). However, the precise function of NO in the rVLM in regulation of these reflexes has not been defined. Three isoforms of NOS, including neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS), are located in the rVLM. We explored the role of NO, derived from different NOS isoforms in the rVLM, in processing cardiac-sympathetic reflexes using whole animal reflex and electrophysiological approaches. We found that, in anesthetized cats, increased mean arterial blood pressure and renal sympathetic nerve activity elicited by epicardial application of bradykinin (BK; 1-10 microg/ml, 50 microl) were significantly attenuated following unilateral rVLM microinjection of the nonselective NOS inhibitor, N(omega)-nitro-L-arginine methyl ester (50 nmol/50 nl), or a specific nNOS inhibitor, 7-nitroindazole (7-NI; 5-10 pmol/50 nl; both P < 0.05). In contrast, the responses of mean arterial blood pressure and renal sympathetic nerve activity to cardiac BK stimulation were unchanged by unilateral rVLM microinjection of N(omega)-nitro-D-arginine methyl ester (inactive isomer of N(omega)-nitro-L-arginine methyl ester, 50 nmol/50 nl), 3-6% methanol (7-NI vehicle), N(6)-(1-iminoethyl)-L-lysine (250 pmol/50 nl; iNOS inhibitor), or N(5)-(1-iminoethyl)-L-ornithine (250 nmol/50 nl; eNOS inhibitor). Furthermore, in separate cats, we noted that iontophoresis of 7-NI (0.1 mM) reduced the increased discharge of cardiovascular sympathoexcitatory rVLM neurons in response to cardiac stimulation with BK (P < 0.05). These neurons were characterized by their responses to inputs from baroreceptors, and their cardiac rhythmicity was determined through frequency and time domain analyses, correlating their discharge to arterial blood pressure and cardiac sympathetic efferent nerve activity. These data suggest that NO, specifically nNOS, mediates sympathetic cardiac-cardiovascular responses through its action in the rVLM.
Zhi-Ling Guo; Stephanie C Tjen-A-Looi; Liang-Wu Fu; John C Longhurst
Related Documents :
11093078 - Cardiovascular responses to nmda injected into nuclei of hypothalamus or amygdala in co...
24087988 - Kinetic study of the oh + glyoxal reaction: experimental evidence and quantification of...
3886138 - Role of sympathetic nerve activity in endotoxin induced hypotension in cats.
2892928 - Reflex pressor response to gastric mechanical stimulation in rats.
25107458 - Mechanical forces and lymphatic transport.
15703898 - Prone position improves mechanics and alveolar ventilation in acute respiratory distres...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-08-14
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  297     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-09-25     Completed Date:  2009-10-08     Revised Date:  2014-05-09    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1478-86     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Action Potentials
Baroreflex* / drug effects
Blood Pressure
Bradykinin / metabolism
Enzyme Inhibitors / administration & dosage
Heart / innervation*
Injections, Intraventricular
Kidney / innervation
Medulla Oblongata / cytology,  drug effects,  enzymology*
Nitrergic Neurons / drug effects,  enzymology*
Nitric Oxide / metabolism*
Nitric Oxide Synthase Type I / antagonists & inhibitors,  metabolism*
Nitric Oxide Synthase Type II / metabolism
Nitric Oxide Synthase Type III / metabolism
Pericardium / metabolism
Sympathetic Nervous System / drug effects,  enzymology*
Grant Support
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Isoenzymes; 31C4KY9ESH/Nitric Oxide; EC Oxide Synthase Type I; EC Oxide Synthase Type II; EC Oxide Synthase Type III; S8TIM42R2W/Bradykinin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Role of sarcoplasmic reticulum in mitochondrial permeability transition and cardiomyocyte death duri...
Next Document:  Postinfarction gene therapy with adenoviral vector expressing decorin mitigates cardiac remodeling a...