Banks R O
Department of Physiology and Biophysics, University of Cincinnati College of Medicine, Ohio 45267-0576.
Am J Physiol. 1988 Apr;254(4 Pt 2):F470-6. doi: 10.1152/ajprenal.1988.254.4.F470.
The role of histamine (H) and prostaglandins (PGs) in the renal vasoconstriction prompted by a 10-min intrarenal infusion of norepinephrine (NE, 0.2 micrograms), antidiuretic hormone (ADH, 10 mU), or angiotensin II (ANG II, 0.05 micrograms) was evaluated in anesthetized dogs (amounts are per min per kg). Renal blood flow (RBF, flow probe) decreased four- to fivefold during the 1st min of infusion with each agonist but then gradually returned toward base line. This "escape" was greatest with ADH, less with NE, and small with ANG II. There was a postinfusion reactive hyperemia (RH) only after NE; NE-RH was 4.26 +/- 0.75 (SE) ml/g. Meclofenamate (MFA) reduced NE-RH to 60 +/- 11% of control and decreased NE escape. The H1-receptor antagonist, chlorpheniramine (CP), decreased NE-RH to 24 +/- 5% of control and reduced NE escape. MFA slowed, but did not block, ADH escape and had little effect on ANG II escape. CP did not affect ADH or ANG II escape. The histidine decarboxylase inhibitor, p-toluenesulfonohydrazine, did not affect NE escape but decreased NE-RH to 22 +/- 6% of control. Bolus injections of ADH during a constant infusion of the hormone were not vasoactive, indicating a tachyphylaxis-like phenomenon; this was not found with ANG II or NE. Finally, the excretion of histamine-like material increased from a control value of 0.69 +/- 0.08 to 1.28 +/- 0.28 micrograms/min during NE-RH. These results indicate that NE releases histamine and PGs from the kidney and that PGs account, primarily, for NE escape, whereas histamine accounts, primarily, for NE-RH.
在麻醉犬中评估了组胺（H）和前列腺素（PGs）在肾内输注去甲肾上腺素（NE，0.2微克）、抗利尿激素（ADH，10 mU）或血管紧张素II（ANG II，0.05微克）10分钟所引发的肾血管收缩中的作用（剂量为每分钟每千克）。在每种激动剂输注的第1分钟内，肾血流量（RBF，流量探头）下降了四到五倍，但随后逐渐恢复至基线水平。这种“逃逸”现象在ADH时最为明显，NE时次之，ANG II时最小。仅在NE输注后出现了输注后反应性充血（RH）；NE-RH为4.26±0.75（SE）毫升/克。甲氯芬那酸（MFA）将NE-RH降低至对照值的60±11%，并减少了NE的逃逸。H1受体拮抗剂氯苯那敏（CP）将NE-RH降低至对照值的24±5%，并减少了NE的逃逸。MFA减缓了但未阻断ADH的逃逸，对ANG II的逃逸几乎没有影响。CP不影响ADH或ANG II的逃逸。组氨酸脱羧酶抑制剂对甲苯磺酰肼不影响NE的逃逸，但将NE-RH降低至对照值的22±6%。在持续输注激素期间推注ADH无血管活性，表明存在类似快速耐受的现象；ANG II或NE未出现这种情况。最后，在NE-RH期间，组胺样物质的排泄量从对照值0.69±0.08增加至1.28±0.28微克/分钟。这些结果表明，NE从肾脏释放组胺和PGs，PGs主要导致NE的逃逸，而组胺主要导致NE-RH。
