Bądzyńska Bożena, Baranowska Iwona, Sadowski Janusz
Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 Pawińskiego St., 02-106, Warsaw, Poland.
Pflugers Arch. 2021 Apr;473(4):623-631. doi: 10.1007/s00424-021-02534-1. Epub 2021 Mar 2.
Earlier evidence from studies of rat hypertension models undermines the widespread view that the rate of renal medullary blood flow (MBF) is critical in control of arterial pressure (MAP). Here, we examined the role of MBF in rats that were normotensive, with modest short-lasting pressure elevation, or with overt established hypertension. The groups studied were anaesthetised Sprague-Dawley rats: (1) normotensive, (2) with acute i.v. norepinephrine-induced MAP elevation, and (3) with hypertension induced by unilateral nephrectomy followed by administration of deoxycorticosterone-acetate (DOCA) and 1% NaCl drinking fluid for 3 weeks. MBF was measured (laser-Doppler probe) and selectively increased using 4-h renal medullary infusion of bradykinin. MAP, renal excretion parameters and post-experiment medullary tissue osmolality and sodium concentration were determined. In the three experimental groups, baseline MAP was 117, 151 and 171 mmHg, respectively. Intramedullary bradykinin increased MBF by 45%, 65% and 70%, respectively, but this was not associated with a change in MAP. In normotensive rats a significant decrease in medullary tissue sodium was seen. The intramedullary bradykinin specifically increased renal excretion of water, sodium and total solutes in norepinephrine-treated rats but not in the two other groups. As previously shown in models of rat hypertension, in the normotensive rats and those with acute mild pressure elevation (resembling labile borderline human hypertension), 4-h renal medullary hyperperfusion failed to decrease MAP. Nor did it decrease in DOCA-salt model mimicking low-renin human hypertension. Evidently, within the 4-h observation, medullary perfusion was not a critical determinant of MAP in normotensive and hypertensive rats.
早期对大鼠高血压模型的研究证据，削弱了普遍认为肾髓质血流量（MBF）速率在动脉压（MAP）控制中起关键作用的观点。在此，我们研究了MBF在血压正常、短期血压适度升高或明显已患高血压大鼠中的作用。所研究的组为麻醉的斯普拉格 - 道利大鼠：（1）血压正常组，（2）静脉注射去甲肾上腺素导致急性MAP升高组，以及（3）单侧肾切除后给予醋酸脱氧皮质酮（DOCA）和1%氯化钠饮用水3周诱导高血压组。通过激光多普勒探头测量MBF，并通过肾髓质4小时输注缓激肽选择性增加MBF。测定MAP、肾脏排泄参数以及实验后髓质组织渗透压和钠浓度。在三个实验组中，基线MAP分别为117、151和171 mmHg。髓质内缓激肽分别使MBF增加45%、65%和70%，但这与MAP的变化无关。在血压正常的大鼠中，可见髓质组织钠显著减少。髓质内缓激肽特异性增加了去甲肾上腺素处理大鼠的水、钠和总溶质的肾脏排泄，但在其他两组中未增加。如先前在大鼠高血压模型中所示，在血压正常的大鼠和急性轻度血压升高（类似于人类不稳定临界高血压）的大鼠中，4小时肾髓质过度灌注未能降低MAP。在模拟低肾素型人类高血压的DOCA - 盐模型中也未降低。显然，在4小时观察期内，髓质灌注不是血压正常和高血压大鼠MAP的关键决定因素。
