Document Detail


Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep.
MedLine Citation:
PMID:  19439617     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The contribution of the paraventricular nucleus of the hypothalamus (PVN) in mediating cardiovascular, renal, hormonal, and sympathetic nerve responses to increased cerebrospinal fluid (CSF) [Na(+)] was investigated in conscious sheep. Intracerebroventricular hypertonic NaCl (0.5 mol/l, 20 microl/min for 60 min) increased arterial blood pressure [AP; +13.4 (sd 2.0) mmHg, P < 0.001] and central venous pressure [CVP; +2.8 (sd 1.3) mmHg, P < 0.001], but did not significantly change heart rate or cardiac output (n = 6). Elevated CSF [Na(+)] also lowered plasma ANG II levels [-3.3 (sd 1.6) pmol/l, P = 0.004] and increased creatinine clearance [+31.5 (sd 32.7) ml/min, P = 0.03] and renal sodium excretion [+9.2 (sd 9.2) mmol/h, P = 0.003]. Lidocaine injection (1 microl, 2%) into the PVN prior to the ICV infusion had no apparent effect per se, but it abolished the AP, CVP, creatinine clearance, and ANG II responses to hypertonic NaCl, as well as reducing the increase in renal sodium excretion (n = 6). Subsequent studies were performed in conscious sheep with chronically implanted electrodes for measurement of renal sympathetic nerve activity (RSNA). The effects of ICV hypertonic NaCl on AP and RSNA were measured before and after PVN-injection of glycine (250 nmol in 500 nl artificial CSF). ICV NaCl increased AP and decreased RSNA (P < 0.001). These effects were significantly reduced by glycine (P = 0.02-0.001, n = 5). Saline injected into the PVN (n = 5) or lidocaine injected outside the PVN (n = 6) had no effect on the response to ICV hypertonic NaCl. These results indicate that the PVN is an important mediator of cerebrally induced homeostatic responses to elevated sodium concentration/hyperosmolality.
Authors:
Robert Frithiof; Rohit Ramchandra; Sally Hood; Clive May; Mats Rundgren
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-05-13
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  297     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-07-03     Completed Date:  2009-08-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R185-93     Citation Subset:  IM    
Affiliation:
Karolinska Institutet, Dept. of Physiology and Pharmacology, S-17177, Stockholm, Sweden. robert.frithiof@ki.se
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MeSH Terms
Descriptor/Qualifier:
Anesthetics, Local / administration & dosage
Angiotensin II / blood
Animals
Blood Pressure
Cardiac Output
Central Venous Pressure
Consciousness
Creatinine / blood
Female
Glomerular Filtration Rate
Glycine / administration & dosage
Heart Rate
Hemodynamics* / drug effects
Homeostasis
Infusions, Parenteral
Injections
Kidney / innervation*
Lidocaine / administration & dosage
Natriuresis* / drug effects
Osmolar Concentration
Paraventricular Hypothalamic Nucleus / drug effects,  metabolism*
Saline Solution, Hypertonic / administration & dosage,  metabolism*
Sheep
Sodium / cerebrospinal fluid*
Sympathetic Nervous System / drug effects,  physiology*
Urodynamics
Chemical
Reg. No./Substance:
0/Anesthetics, Local; 0/Saline Solution, Hypertonic; 11128-99-7/Angiotensin II; 137-58-6/Lidocaine; 56-40-6/Glycine; 60-27-5/Creatinine; 7440-23-5/Sodium

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


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