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首页> 外文期刊>American Journal of Physiology >Interactive modulation of renal myogenic autoregulation by nitric oxide and endothelin acting through ET-B receptors.
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Interactive modulation of renal myogenic autoregulation by nitric oxide and endothelin acting through ET-B receptors.

机译：一氧化氮和内皮素通过ET-B受体相互作用对肾脏肌原性自我调节的交互调节。

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In rats, nitric oxide modulates renal autoregulation in steady-state experiments and the myogenic mechanism in dynamic studies. Interactive modulation of autoregulation by nitric oxide and endothelin-1, predominantly involving endothelin B receptors, has been reported although it remains unclear whether the interaction is synergistic or obligatory or whether it affects the myogenic component of autoregulation. Nonselective inhibition of nitric oxide synthase (L(omega)-nitro-l-arginine methyl-ester; l-NAME) with endothelin A and B selective receptor antagonists BQ-123 and BQ-788, all infused into the renal artery, plus time series analysis were used to test the interactive actions of nitric oxide and endothelin on renal vascular conductance and on autoregulation. Nonselective endothelin receptor antagonism blunted the constrictor response to subsequent l-NAME but had no effect on previously established l-NAME-induced vasoconstriction. BQ-123 did not affect conductance and caused only minor reduction in myogenic autoregulatory efficiency. Responses to BQ-123 and l-NAME were additive and not interactive. BQ-788 and l-NAME each caused strong vasoconstriction alone and in the presence of the other, indicating that coupling between nitric oxide- and endothelin B-mediated events is not obligatory. l-NAME augmented myogenic autoregulation, and subsequent BQ-788 did not alter this response. However, BQ-788 infused alone also enhanced myogenic autoregulation but resulted in significant impairment of myogenic autoregulation by subsequent l-NAME. Thus the interaction between nitric oxide and endothelin is clearly nonadditive and, because it is asymmetrical, cannot be explained simply by convergence on a common signal pathway. Instead one must postulate some degree of hierarchical organization and that nitric oxide acts downstream to endothelin B activation.
机译：在大鼠中，一氧化氮调节稳态实验中的肾脏自调节，并在动态研究中调节肌发生机制。尽管尚不清楚相互作用是否是协同作用或强制性的，或者是否影响自调节的肌源性成分，但一氧化氮和内皮素-1主要参与内皮素B受体的交互调节已被报道。用内皮素A和B选择性受体拮抗剂BQ-123和BQ-788对肾动脉中的一氧化氮合酶（L（ω）-硝基-1-精氨酸甲酯; l-NAME）进行非选择性抑制系列分析用于检验一氧化氮和内皮素对肾血管电导和自调节的相互作用。非选择性内皮素受体拮抗作用减弱了对随后的l-NAME的收缩反应，但对先前建立的l-NAME诱导的血管收缩没有影响。 BQ-123不会影响电导，只会导致肌原性自动调节效率的轻微降低。对BQ-123和l-NAME的回复是加性的，而不是互动的。 BQ-788和l-NAME各自单独引起强烈的血管收缩，并且在另一个存在时引起强烈的血管收缩，表明一氧化氮和内皮素B介导的事件之间的耦合不是强制性的。 l-NAME增强了肌源性自动调节，随后的BQ-788并未改变这种反应。然而，单独注入的BQ-788也增强了肌原性自动调节，但随后的l-NAME导致了肌原性自动调节的显着损害。因此，一氧化氮与内皮素之间的相互作用显然是不可加的，并且由于它是不对称的，因此不能简单地通过共同信号路径上的收敛来解释。取而代之的是，必须假设某种程度的层次结构，并且一氧化氮在下游激活内皮素B。

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