| Influence of neonatal sympathectomy on proximal renal resistance artery function in spontaneously hypertensive rats. | |
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MedLine Citation:
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PMID: 15480746 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Olaf Grisk; Ulrike Lother; Gert Gabriëls; Rainer Rettig |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2004-10-12 |
Journal Detail:
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Title: Pflügers Archiv : European journal of physiology Volume: 449 ISSN: 0031-6768 ISO Abbreviation: Pflugers Arch. Publication Date: 2005 Jan |
Date Detail:
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Created Date: 2005-02-28 Completed Date: 2005-05-16 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0154720 Medline TA: Pflugers Arch Country: Germany |
Other Details:
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Languages: eng Pagination: 364-71 Citation Subset: IM |
Affiliation:
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Institut für Physiologie, Universität Greifswald, Greifswalder Strasse 11c, 17495 Karlsburg, Germany. grisko@uni-greifswald.de |
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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