Scholz H, Kurtz A
Physiologisches Institut der Universität, Zürich, Switzerland.
Pflugers Arch. 1992 Jun;421(2-3):155-62. doi: 10.1007/BF00374822.
Using the model of isolated perfused rat kidneys this study was performed to investigate whether or not voltage-operated calcium channels are essentially involved in the pressure control of renin secretion from the kidneys. At a perfusion pressure of 100 mm Hg (13.3 kPa) renin secretory rates were 4.2 +/- 0.7 (ng angiotensin I h-1) min-1 g-1. Stepwise reduction of renal perfusion pressure to 80, 60, and 40 mm Hg (10.6, 8.0, 5.3 kPa) resulted in an increase of renin release yielding a 30-fold stimulation at 40 mm Hg vs 100 mm Hg. Increasing the perfusion pressure above 100 mm Hg did not further significantly decrease renin secretion. The perfusate flow rate was also pressure-dependent. Flow rates increased linearly with pressure and reached a plateau at 100 mm Hg, which was maintained up to 160 mm Hg (21.3 kPa). The averaged flow rate at the plateau was 15.5 ml min-1 g-1. In the presence of the three different calcium antagonists nifedipine (5 microM), nitrendipine (3 microM) and verapamil (5 microM), myogenic autoregulation of flow was abolished as indicated by the rise of the pressure/flow curve between 40 and 160 mm Hg. At the same time, however, these calcium channel blockers did not alter the relationship between perfusion pressure and renin secretion. Moreover, the calcium channel agonist Bay K 8644 (5 microM) caused a strong and long-lasting vasoconstriction, without changing renin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究采用离体灌注大鼠肾脏模型，旨在探究电压门控钙通道是否在肾脏肾素分泌的压力控制中起关键作用。在灌注压力为100 mmHg（13.3 kPa）时，肾素分泌率为4.2±0.7（ng血管紧张素I h⁻¹）min⁻¹ g⁻¹。将肾脏灌注压力逐步降至80、60和40 mmHg（10.6、8.0、5.3 kPa），导致肾素释放增加，在40 mmHg时与100 mmHg相比刺激增加了30倍。将灌注压力提高到100 mmHg以上并未进一步显著降低肾素分泌。灌注液流速也与压力相关。流速随压力呈线性增加，在100 mmHg时达到平台期，并维持至160 mmHg（21.3 kPa）。平台期的平均流速为15.5 ml min⁻¹ g⁻¹。在存在三种不同钙拮抗剂硝苯地平（5 μM）、尼群地平（3 μM）和维拉帕米（5 μM）的情况下，40至160 mmHg之间压力/流速曲线的上升表明，肌源性血流自动调节被消除。然而，与此同时，这些钙通道阻滞剂并未改变灌注压力与肾素分泌之间的关系。此外，钙通道激动剂Bay K 8644（5 μM）引起强烈且持久的血管收缩，但不改变肾素分泌。（摘要截短于250字）
