Patel K P
Department of Physiology and Pharmacology, University of South Dakota, Vermillion 57069.
J Auton Nerv Syst. 1991 Oct;36(1):47-54. doi: 10.1016/0165-1838(91)90129-q.
To determine whether central alpha-2 adrenergic mechanisms are involved in the renal nerve mediated natriuresis and diuresis produced by acute volume expansion, urine flow and sodium excretion from innervated and denervated kidneys were measured before and after acute volume expansion (1 ml/min for 20 min) in the presence or absence of intracerebroventricular yohimbine (8 micrograms/kg/min), an alpha-2-antagonist, in Inactin-anesthetized Sprague-Dawley rats. The innervated to denervated (I/D) ratio for urine flow and sodium excretion indicated that acute volume expansion caused a greater natriuresis and diuresis from the intact kidney compared to the denervated kidney. However, these I/D ratios during acute volume expansion were significantly reduced in the presence of yohimbine i.c.v. Furthermore, central administration of clonidine, an alpha-2 agonist, produces a renal nerve mediated natriuresis. These data suggest that central alpha-2 adrenergic mechanisms may be involved in producing the renal sympatho-inhibition, which subsequently produces natriuresis and diuresis, in response to acute volume expansion.
为了确定中枢α2肾上腺素能机制是否参与急性容量扩张所产生的肾神经介导的利钠和利尿作用，在Inactin麻醉的Sprague-Dawley大鼠中，于急性容量扩张（1 ml/分钟，持续20分钟）前后，在有或无脑室注射育亨宾（8微克/千克/分钟）（一种α2拮抗剂）的情况下，测量了支配肾和去神经肾的尿流量和钠排泄量。尿流量和钠排泄量的支配肾与去神经肾（I/D）比值表明，与去神经肾相比，急性容量扩张使完整肾脏产生更大的利钠和利尿作用。然而，在脑室注射育亨宾的情况下，急性容量扩张期间的这些I/D比值显著降低。此外，中枢给予α2激动剂可乐定可产生肾神经介导的利钠作用。这些数据表明，中枢α2肾上腺素能机制可能参与产生肾交感抑制，进而在急性容量扩张时产生利钠和利尿作用。
