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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

González R, Fernández-Alfonso M S, Rodríguez-Martinez M A, Fuertes E, Angulo J, Sánchez-Ferrer C F, Marín J

Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.

Gen Pharmacol. 1994 Mar;25(2):333-9. doi: 10.1016/0306-3623(94)90063-9.

In the SHR juxtamedullary nephron preparation, the increase of the perfusion pressure from 80 to 160 mmHg increased the diameters of arcuate arteries but produced a pressure-dependent contraction of the afferent arterioles, a response that can account for renal autoregulation. 2. The pressure-induced contractions of the afferent arterioles were abolished by 1 microM nifedipine and by 10 microM furosemide, suggesting that the autoregulatory responses are mainly mediated by tubuloglomerular mechanisms and can be abolished by calcium antagonists.

在自发性高血压大鼠近髓肾单位标本中，灌注压力从80 mmHg升高至160 mmHg时，弓状动脉直径增大，但入球小动脉出现压力依赖性收缩，这一反应可解释肾的自身调节。2. 1 μM硝苯地平和10 μM呋塞米可消除压力诱导的入球小动脉收缩，提示自身调节反应主要由管球机制介导，且可被钙拮抗剂消除。

González R, Fernández-Alfonso M S, Rodríguez-Martinez M A, Fuertes E, Angulo J, Sánchez-Ferrer C F, Marín J

Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.

Gen Pharmacol. 1994 Mar;25(2):333-9. doi: 10.1016/0306-3623(94)90063-9.

In the SHR juxtamedullary nephron preparation, the increase of the perfusion pressure from 80 to 160 mmHg increased the diameters of arcuate arteries but produced a pressure-dependent contraction of the afferent arterioles, a response that can account for renal autoregulation. 2. The pressure-induced contractions of the afferent arterioles were abolished by 1 microM nifedipine and by 10 microM furosemide, suggesting that the autoregulatory responses are mainly mediated by tubuloglomerular mechanisms and can be abolished by calcium antagonists.

在自发性高血压大鼠近髓肾单位标本中，灌注压力从80 mmHg升高至160 mmHg时，弓状动脉直径增大，但入球小动脉出现压力依赖性收缩，这一反应可解释肾的自身调节。2. 1 μM硝苯地平和10 μM呋塞米可消除压力诱导的入球小动脉收缩，提示自身调节反应主要由管球机制介导，且可被钙拮抗剂消除。