DISPARATE EFFECTS OF ADENOSINE-A(1)-RECEPTOR AND A(2)-RECEPTOR AGONISTS ON INTRARENAL BLOOD-FLOW
DISPARATE EFFECTS OF ADENOSINE-A(1)-RECEPTOR AND A(2)-RECEPTOR AGONISTS ON INTRARENAL BLOOD-FLOW
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DOI：
10.1152/ajprenal.1993.265.6.f802
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发表时间：
1993-12-01
影响因子：
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通讯作者：
BREZIS, M
中科院分区：
文献类型：
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作者：
AGMON, Y;DINOUR, D;BREZIS, M
内源性腺苷，在组织缺氧时由肾脏局部分泌，诱导异质性肾血流动力学反应。我们研究了皮质和外髓血流反应肾上腺注射腺苷和腺苷A1和A2受体激动剂在麻醉大鼠。这些药物通过长期植入的胶囊注入肾动脉，并通过激光多普勒探头测量血流量。短时间（1分钟，0.05 ml）肾内输注腺苷（0.5 μ mol）使皮质血流量降低至基线的27 ± 10%（n = 7，P < 0.0005）。延髓血流反应是双相的，即，血流量短暂下降至基线的52 +/- 8%（n = 17，P < 0.0001），随后血流量持续增加至135 +/- 6%（n = 17，P < 0.0001）。腺苷A1受体激动剂N6-环戊基腺苷使皮质和髓质血流量分别减少至基线的59 +/- 4%（n = 10，P < 0.0001）和38 +/- 5%（n = 11，P < 0.0001）。相比之下，腺苷A2受体激动剂2-[p（carboxyethyl）phenethylamino]-5 '-N-ethylcarboxamidoadenosine（CGS-21680 C）使髓质血流量显著增加至基线的184 +/-15%（n = 12，P < 0.0005），而皮质血流量无重大变化。我们的结论是，肾内腺苷减少皮质血流量，主要是通过A1和A2受体分别增加髓质流量。这些血流动力学反应可能在保护外髓免受缺氧中起作用。
Endogenous adenosine, secreted locally by the kidney during tissue hypoxia, induces heterogeneous renal hemodynamic responses. We investigated the cortical and outer medullary blood flow responses to intrarenal infusions of adenosine and adenosine A1- and A2-receptor agonists in anesthetized rats. These agents were infused into the renal interstitium through chronically implanted capsules, and blood flow was measured by laser-Doppler probes. Short (1 min, 0.05 ml) intrarenal infusions of adenosine (0.5 mumol) lowered cortical blood flow to 27 +/- 10% of baseline (n = 7, P < 0.0005). Medullary blood flow response was biphasic, i.e., a transient decrease in flow to 52 +/- 8% of baseline (n = 17, P < 0.0001) followed by a more-sustained increase in flow to 135 +/- 6% (n = 17, P < 0.0001). N6-cyclopentyladenosine, an adenosine receptor A1 agonist, reduced both cortical and medullary blood flow to 59 +/- 4% (n = 10, P < 0.0001) and 38 +/- 5% (n = 11, P < 0.0001) of baseline, respectively. By contrast, 2-[p(carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS-21680C), an adenosine receptor A2 agonist, increased dramatically the medullary blood flow to 184 +/- 15% of baseline (n = 12, P < 0.0005), without major changes in cortical flow. We conclude that intrarenal adenosine reduces cortical blood flow and predominantly increases medullary flow via A1 and A2 receptors, respectively. These hemodynamic responses could play a role in protection of the outer medulla from hypoxia.