Strandhoy J W
J Cardiovasc Pharmacol. 1985;7 Suppl 8:S28-33.
Postsynaptic binding sites for alpha 1 and alpha 2 adrenoceptor ligands are found in abundance in the renal cortex of several species, with reports of 2-3 times as many alpha 2 as alpha 1 sites. These alpha adrenoceptor subtypes can potentially influence salt and water excretion through both vascular and tubular effects. Renal vascular resistance in dogs is increased by both alpha adrenoceptor subtype agonists but alpha 1 agonists are more potent. In rats, alpha 2, agonists have almost no effect on the renal circulation whereas alpha 1 agonists are capable of intense renal vasoconstriction. The mechanisms by which alpha 2 agonists increase glomerular filtration rate are not yet clear and may involve the secondary release of hormones affecting glomerular dynamics and permeability. Thus, an abundance of alpha 2 adrenoceptor binding sites in whole cortical homogenate of rat kidneys with little demonstrable vascular effect of alpha 2 agonist suggests that the preponderance of these receptors lies instead on the tubular epithelium. Alpha-1 adrenoceptors are probably responsible for the increased Na reabsorption from the proximal tubule and the anti-natriuresis following low level renal nerve stimulation. In contrast, an alpha 2 agonist such as guanabenz produces a diuresis by reducing the release of vasopressin and by antagonizing its hydrosmotic effect on the nephron, and a modest natriuresis by decreasing medullary interstitial osmolality and reducing passive Na reabsorption.
在多个物种的肾皮质中大量存在α1和α2肾上腺素能受体配体的突触后结合位点，据报道α2位点的数量是α1位点的2至3倍。这些α肾上腺素能受体亚型可通过血管和肾小管效应潜在地影响盐和水的排泄。α肾上腺素能受体亚型激动剂均可增加犬的肾血管阻力，但α1激动剂的作用更强。在大鼠中，α2激动剂对肾循环几乎没有影响，而α1激动剂能够引起强烈的肾血管收缩。α2激动剂增加肾小球滤过率的机制尚不清楚，可能涉及影响肾小球动力学和通透性的激素的继发性释放。因此，大鼠肾脏全皮质匀浆中存在大量α2肾上腺素能受体结合位点，但α2激动剂几乎没有明显的血管效应，这表明这些受体主要位于肾小管上皮。α1肾上腺素能受体可能是肾神经低水平刺激后近端小管钠重吸收增加和抗利钠作用的原因。相比之下，胍那苄等α2激动剂通过减少血管加压素的释放并拮抗其对肾单位的渗透作用而产生利尿作用，并通过降低髓质间质渗透压和减少被动钠重吸收而产生适度的利钠作用。
