Document Detail


Influence of neonatal sympathectomy on proximal renal resistance artery function in spontaneously hypertensive rats.
MedLine Citation:
PMID:  15480746     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Renal transplantation experiments have shown that the kidney contributes to chronic sympathectomy-induced arterial pressure reduction in spontaneously hypertensive rats (SHR). The underlying mechanisms are currently unclear but may include alterations in the function of small renal arteries. Neonatal SHR were sympathectomized by intraperitoneal guanethidine injections and removal of adrenal medullary tissue. Controls were sham- or hydralazine-treated. At 12 weeks of age, distal interlobar artery segments were investigated using small-vessel wire myography. Vessels from sympathectomized animals showed increased sensitivity to noradrenaline (NE). Vasopressin- and endothelin-1-induced vasoconstriction was similar in all groups (as reflected by the pD(2), i.e. -logEC(50), where EC(50) is the molar concentration of agonist eliciting a half-maximal response). Maximum vasopressin-induced tension was similar in all groups while endothelin-1-induced maximum tension was significantly higher in sympathectomized than in sham-treated SHR. The sensitivity of NE-induced vasoconstriction to extracellular Ca(2+) did not differ between groups while sensitivity to L-type Ca(2+) channel activation was significantly higher in both sympathectomized and hydralazine-treated animals than in sham-treated animals. Endothelium-dependent and independent vasodilation were similar in all groups. Sequential blockade of NO-synthase and cyclooxygenase had similar effects in all groups. In conclusion, neonatal sympathectomy does not induce any changes in the function of isolated proximal renal resistance arteries from SHR that could explain the blood pressure lowering effect of a kidney graft from sympathectomized SHR.
Authors:
Olaf Grisk; Ulrike Lother; Gert Gabriëls; Rainer Rettig
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-10-12
Journal Detail:
Title:  Pflügers Archiv : European journal of physiology     Volume:  449     ISSN:  0031-6768     ISO Abbreviation:  Pflugers Arch.     Publication Date:  2005 Jan 
Date Detail:
Created Date:  2005-02-28     Completed Date:  2005-05-16     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0154720     Medline TA:  Pflugers Arch     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  364-71     Citation Subset:  IM    
Affiliation:
Institut für Physiologie, Universität Greifswald, Greifswalder Strasse 11c, 17495 Karlsburg, Germany. grisko@uni-greifswald.de
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn / physiology*
Antihypertensive Agents / pharmacology
Blood Pressure / physiology
Calcium / pharmacology
Calcium Channels, L-Type / drug effects,  physiology
Catecholamines / pharmacology
Cyclooxygenase Inhibitors / pharmacology
Dose-Response Relationship, Drug
Endothelin-1 / pharmacology
Endothelium, Vascular / physiology
Hydralazine / pharmacology
Kidney Tubules, Proximal / innervation,  physiology*
Muscle Relaxation / drug effects
Muscle, Smooth, Vascular / physiology
Myography
Nitric Oxide Synthase / antagonists & inhibitors
Nitric Oxide Synthase Type III
Rats
Rats, Inbred SHR
Renal Artery / physiology*
Sympathectomy, Chemical
Vascular Resistance / physiology*
Vasodilation / drug effects
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Calcium Channels, L-Type; 0/Catecholamines; 0/Cyclooxygenase Inhibitors; 0/Endothelin-1; 7440-70-2/Calcium; 86-54-4/Hydralazine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, rat

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