Bertolino S, Julien C, Medeiros I A, Cuisinaud G, Vincent M, Barrès C
Département de Physiologie et Pharmacologie Clinique, Centre National de la Recherche Scientifique ESA 5014, Faculté de Pharmacie, Lyon, France.
Am J Physiol. 1996 Nov;271(5 Pt 2):R1199-204. doi: 10.1152/ajpregu.1996.271.5.R1199.
To characterize the renin secretory profile in Lyon hypertensive (LH) rats, renin responses to reductions of arterial pressure and beta-adrenoceptor stimulation were assessed in conscious unrestrained LH (n = 13) and Lyon normotensive (LN, n = 14) rats under normal-salt diet. Mean arterial pressure (MAP) in the infrarenal aorta was recorded beat to beat for 3 h. Then, plasma renin concentration (PRC) was measured 1) in basal conditions, 2) during 10-mmHg stepwise reductions of MAP down to 60 mmHg using a chronically implanted aortic inflatable cuff, and 3) during isoprenaline infusion (62.5, 125, and 250 ng.kg-1.min-1 iv). Compared with LN, LH rats had an elevated MAP (146 +/- 3 vs. 111 +/- 1 mmHg, P < 0.001) and decreased PRC [4.2 +/- 0.6 vs. 8.2 +/- 0.8 ng angiotensin (ANG) I.ml-1.h-1, P < 0.001] and kidney renin content (216 +/- 14 vs. 1,149 +/- 103 micrograms ANG I.h-1.g-1, P < 0.001). Pressure-dependent renin release occurred below 90 mmHg in LN rats and below 80 mmHg in LH rats, and its sensitivity in the low-pressure range did not differ between strains. Isoprenaline-induced increases in PRC were weaker (P < 0.01) in LH than in LN rats. In additional LH and LN rats (n = 6-8), acute ANG II AT1-receptor blockade with losartan (20 mg/kg, followed by 10 mg.kg-1.h-1 iv for 2 h) induced lesser (P < 0.001) PRC increases in LH than in LN rats. Renin responses to isoprenaline remained blunted (P < 0.01) during losartan infusion in LH rats. We conclude that, in LH rats, renin secretion is independent of MAP in the range of its spontaneous variations and is poorly responsive to beta-adrenoceptor stimulation, the alteration of which cannot be explained by an enhanced feedback inhibition by ANG II.
为了描述里昂高血压（LH）大鼠的肾素分泌特征，在正常盐饮食条件下，对清醒无束缚的LH大鼠（n = 13）和里昂正常血压（LN，n = 14）大鼠评估肾素对动脉压降低和β-肾上腺素能受体刺激的反应。连续3小时逐搏记录肾下腹主动脉的平均动脉压（MAP）。然后，在以下三种情况下测量血浆肾素浓度（PRC）：1）基础状态；2）使用慢性植入的主动脉可充气袖带使MAP逐步降低10 mmHg直至60 mmHg期间；3）异丙肾上腺素输注期间（静脉注射62.5、125和250 ng·kg-1·min-1）。与LN大鼠相比，LH大鼠的MAP升高（146±3 vs. 111±1 mmHg，P < 0.001），PRC降低[4.2±0.6 vs. 8.2±0.8 ng血管紧张素（ANG）I·ml-1·h-1，P < 0.001]，肾脏肾素含量降低（216±14 vs. 1149±103 μg ANG I·h-1·g-1，P < 0.001）。LN大鼠在MAP低于90 mmHg时出现压力依赖性肾素释放，LH大鼠在MAP低于80 mmHg时出现压力依赖性肾素释放，且两品系在低压范围内的敏感性无差异。LH大鼠中异丙肾上腺素诱导的PRC升高比LN大鼠弱（P < 0.01）。在另外的LH和LN大鼠（n = 6 - 8）中，用氯沙坦（20 mg/kg，随后以10 mg·kg-1·h-1静脉注射2小时）进行急性ANG II AT1受体阻断后，LH大鼠中PRC的升高比LN大鼠小（P < 0.001）。在LH大鼠氯沙坦输注期间，肾素对异丙肾上腺素的反应仍然减弱（P < 0.01）。我们得出结论，在LH大鼠中，肾素分泌在其自发变化范围内与MAP无关，并且对β-肾上腺素能受体刺激反应不佳，其改变不能用ANG II增强的反馈抑制来解释。
