Rudichenko V M, Beierwaltes W H
Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI 48202-2689, USA.
J Vasc Res. 1995 Mar-Apr;32(2):100-5. doi: 10.1159/000159082.
The vasoconstrictor vasopressin has been reported to induce paradoxical local vasodilation in the basilar vasculature through stimulation of the endothelium-derived relaxing factor nitric oxide (NO). We investigated the possibility that at subpressor doses, exogenous arginine vasopressin (AVP) might have a similar effect in the kidney. Ten Inactin-anesthetized rats were infused with sequential doses of AVP from 25 to 6,400 microU/min in 30-min increments. Subpressor infusion resulted in progressive renal vasodilation; renal blood flow (RBF) increased significantly going from 14 +/- 6% above basal at 200 microU/min (p < 0.02) to 27 +/- 5% (p < 0.01) at 1,600 microU/min accompanied by a 24 +/- 5% decrease in renal vascular resistance (RVR). At 6,400 microU/min, blood pressure (BP) increased 29 +/- 6 mm Hg and RVR increased. A second group of 8 rats were first given 10 mg/kg b.w. of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) before infusion of AVP. L-NAME increased BP 22 +/- 3 mm Hg (p < 0.001), and decreased RBF 16 +/- 3% (p < 0.005). After L-NAME, no dose of AVP had any further effect on either BP, RBF, or RVR. Continuous infusion of a single subpressor dose of 100 microU AVP resulted in a 26% increase in RBF (from 7.52 +/- 0.68 to 9.49 +/- 0.54 ml/min/g kidney weight, p < 0.001). AVP doubled urinary cyclic guanosine monophosphate excretion, a marker for renal NO synthesis, from 8.51 +/- 1.01 to 17.48 +/- 4.26 pM/min (p < 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
据报道，血管收缩剂血管加压素可通过刺激内皮源性舒张因子一氧化氮（NO），在基底血管系统中诱导反常的局部血管舒张。我们研究了在亚升压剂量下，外源性精氨酸血管加压素（AVP）在肾脏中是否可能有类似作用。给10只经Inactin麻醉的大鼠以30分钟为间隔，依次输注剂量从25至6400微单位/分钟的AVP。亚升压输注导致肾脏血管逐渐舒张；肾血流量（RBF）显著增加，从200微单位/分钟时比基础值高14±6%（p<0.02）增至1600微单位/分钟时的27±5%（p<0.01），同时肾血管阻力（RVR）降低24±5%。在6400微单位/分钟时，血压（BP）升高29±6毫米汞柱，RVR增加。第二组8只大鼠在输注AVP前先给予10毫克/千克体重的NO合成抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）。L-NAME使血压升高22±3毫米汞柱（p<0.001），使肾血流量降低16±3%（p<0.005）。给予L-NAME后，任何剂量的AVP对血压、肾血流量或肾血管阻力均无进一步影响。持续输注单一亚升压剂量的100微单位AVP使肾血流量增加26%（从7.52±0.68增至9.49±0.54毫升/分钟/克肾重，p<0.001）。AVP使尿中环磷酸鸟苷排泄量加倍，这是肾NO合成的一个标志物，从8.51±1.01增至17.48±4.26皮摩尔/分钟（p<0.025）。（摘要截短于250字）
