Grisk Olaf, Lother Ulrike, Gabriëls Gert, Rettig Rainer
Institut für Physiologie, Universität Greifswald, Greifswalder Strasse 11c, 17495 Karlsburg, Germany.
Pflugers Arch. 2005 Jan;449(4):364-71. doi: 10.1007/s00424-004-1349-3. Epub 2004 Oct 12.
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.
肾移植实验表明，在自发性高血压大鼠（SHR）中，肾脏有助于慢性交感神经切除诱导的动脉血压降低。其潜在机制目前尚不清楚，但可能包括肾小动脉功能的改变。新生SHR通过腹腔注射胍乙啶和切除肾上腺髓质组织进行交感神经切除。对照组接受假手术或肼屈嗪治疗。在12周龄时，使用小血管线肌动描记法研究叶间动脉远端节段。来自交感神经切除动物的血管对去甲肾上腺素（NE）的敏感性增加。血管加压素和内皮素-1诱导的血管收缩在所有组中相似（以pD(2)反映，即-logEC(50)，其中EC(50)是引起最大反应一半的激动剂的摩尔浓度）。所有组中血管加压素诱导的最大张力相似，而内皮素-1诱导的最大张力在交感神经切除的SHR中显著高于假手术治疗的SHR。NE诱导的血管收缩对细胞外Ca(2+)的敏感性在各组之间没有差异，而对L型Ca(2+)通道激活的敏感性在交感神经切除和肼屈嗪治疗的动物中均显著高于假手术治疗的动物。所有组中内皮依赖性和非依赖性血管舒张相似。一氧化氮合酶和环氧化酶的顺序阻断在所有组中具有相似的作用。总之，新生期交感神经切除不会诱导SHR分离的近端肾阻力动脉功能发生任何变化，而这些变化可以解释来自交感神经切除的SHR的肾移植的降压作用。
