Influence of neonatal sympathectomy on proximal renal resistance artery function in spontaneously hypertensive rats.
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.
Institut für Physiologie, Universität Greifswald, Greifswalder Strasse 11c, 17495 Karlsburg, Germany. grisko@uni-greifswald.de
Olaf
O
Grisk
Ulrike
U
Lother
Gert
G
Gabriëls
Rainer
R
Rettig
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000502:physiology; D002118:Calcium / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000502:physiology; D002395:Catecholamines / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D019332:Endothelin-1 / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology; D006830:Hydralazine / Q000494:pharmacology; D007687:Kidney Tubules, Proximal / Q000294:innervation / Q000502:physiology*; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D009213:Myography; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III; D051381:Rats; D011918:Rats, Inbred SHR; D012077:Renal Artery / Q000502:physiology*; D013563:Sympathectomy, Chemical; D014655:Vascular Resistance / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects
D000959:Antihypertensive Agents; D020746:Calcium Channels, L-Type; D002395:Catecholamines; D016861:Cyclooxygenase Inhibitors; D019332:Endothelin-1; D006830:Hydralazine; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D002118:Calcium