Mizoguchi H, Dzau V J, Siwek L G, Barger A C
Am J Physiol. 1983 Jan;244(1):H39-45. doi: 10.1152/ajpheart.1983.244.1.H39.
We investigated the effect of intrarenal administration of dopamine on renin release in conscious dogs. Dopamine in doses ranging from 0.28 to 3.0 micrograms . kg(-1) . min(-1) produced a significant increase in systemic plasma renin activity (PRA) and renin secretion rate without altering systemic blood pressure. Dopamine also induced renal vasodilatation and natriuresis within this dose range. To determine if the dopamine-induced renin release is related to its vasodilatory action, two other vasodilators, papaverine and acetylcholine, were infused into the renal artery, but neither, in doses that produced a rise in renal blood flow similar to that of dopamine, had any effect on PRA. As dopamine can activate alpha- and beta-adrenergic receptors in addition to dopaminergic receptors, experiments were also performed to characterize the type of receptors involved in dopamine-induced renin release. Intrarenal infusion of sulpiride and haloperidol, dopamine antagonists, significantly inhibited dopamine-induced renin release and renal vasodilatation. In contrast, intrarenal infusion of propranolol failed to alter dopamine-induced rise in PRA or renal blood flow. Simultaneous infusion of phentolamine and dopamine, on the other hand, produced a significant potentiation of dopamine-induced renin release and renal vasodilatation. In conclusion, our studies demonstrate that dopamine is capable of inducing renin release and renal vasodilatation in conscious dogs. Moreover, such actions of dopamine are mediated through activation of specific dopamine receptors in the kidney. Finally, we present evidence for the existence of the intrarenal alpha-adrenergic mechanism that is inhibitory to renin release.
我们研究了肾内给予多巴胺对清醒犬肾素释放的影响。剂量范围为0.28至3.0微克·千克⁻¹·分钟⁻¹的多巴胺可使全身血浆肾素活性(PRA)和肾素分泌率显著增加,而不改变全身血压。在此剂量范围内,多巴胺还可诱导肾血管舒张和利钠作用。为了确定多巴胺诱导的肾素释放是否与其血管舒张作用有关,将另外两种血管舒张剂罂粟碱和乙酰胆碱注入肾动脉,但在产生与多巴胺相似的肾血流量增加的剂量下,两者均对PRA无影响。由于多巴胺除了能激活多巴胺能受体外,还能激活α和β肾上腺素能受体,因此还进行了实验以确定参与多巴胺诱导肾素释放的受体类型。肾内注入多巴胺拮抗剂舒必利和氟哌啶醇可显著抑制多巴胺诱导的肾素释放和肾血管舒张。相反,肾内注入普萘洛尔未能改变多巴胺诱导的PRA升高或肾血流量。另一方面,同时注入酚妥拉明和多巴胺可使多巴胺诱导的肾素释放和肾血管舒张显著增强。总之,我们的研究表明多巴胺能够在清醒犬中诱导肾素释放和肾血管舒张。此外,多巴胺的这种作用是通过激活肾脏中的特定多巴胺受体介导的。最后,我们提供了肾内α肾上腺素能机制抑制肾素释放的证据。