Authors: Olaf Grisk Ulrike Lother Gert Gabriëls Rainer Rettig
Publish Date: 2004/10/12
Volume: 449, Issue: 4, Pages: 364-371
Abstract
Renal transplantation experiments have shown that the kidney contributes to chronic sympathectomyinduced 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 hydralazinetreated At 12 weeks of age distal interlobar artery segments were investigated using smallvessel wire myography Vessels from sympathectomized animals showed increased sensitivity to noradrenaline NE Vasopressin and endothelin1induced vasoconstriction was similar in all groups as reflected by the pD2 ie −logEC50 where EC50 is the molar concentration of agonist eliciting a halfmaximal response Maximum vasopressininduced tension was similar in all groups while endothelin1induced maximum tension was significantly higher in sympathectomized than in shamtreated SHR The sensitivity of NEinduced vasoconstriction to extracellular Ca2+ did not differ between groups while sensitivity to Ltype Ca2+ channel activation was significantly higher in both sympathectomized and hydralazinetreated animals than in shamtreated animals Endotheliumdependent and independent vasodilation were similar in all groups Sequential blockade of NOsynthase 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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