Dopamine increases glomerular filtration rate by interacting with both DA1 and DA2 receptors, with DA2 receptor interaction increasing glomerular ultra-filtration pressure.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for DA2 effects on glomerular hemodynamics; leaves open translation to human renal therapeutics.
The effects of the interaction of dopamine (DA) and the DA2 receptors on glomerular filtration rate (GFR) has been studied by means of micropuncture technique in adult greater than or equal to 60-day-old and young 24-day-old rats. Most of the studies were performed in rats with intact adrenergic nervous systems to allow for evaluation of the presynaptic DA2 receptors. In adult and young rats, DA and LY-171555 (LY), a selective DA2 receptor agonist, induced prompt and significant increases in the single nephron (SN) GFR. Further studies were performed only in adult rats. The LY-induced increase in SNGFR was completely abolished during DA2 receptor blockade with S-sulpiride (S-SP), while the DA-induced increase in SNGFR was attenuated but still significant during S-SP treatment. Both DA and LY significantly increased the glomerular ultra-filtration pressure (PUFAA). In rats with ganglionic blockade, the LY-induced increase of SNGFR was attenuated but still significant, whereas the DA-induced increase was less affected. The results imply that DA significantly increases GFR by interacting with the DA2 as well as with the DA1 receptors. Interaction between DA and the DA2 receptors increases PUFAA. The results do not rule out the existence of both pre- and postsynaptic renal DA2 receptors.
No takes yet. Share an insight, caveat, or question.
Seri et al. (1988) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: