Effects of angiotensin II on renal dopamine metabolism: synthesis, release, catabolism and turnover.

Background/aims: Dopamine (DA) uptake inhibition in the renal cortex, elicited by angiotensin II (ANG II), is mediated by AT(1) receptors and signals through the phospholipase C pathway and activation of protein kinase C and CaM-kinase II. By this indirect way, ANG II stimulates renal Na(+),K(+)-ATPase activity through DA intracellular reduction. In the present work, we continued to study different aspects of renal DA metabolism in DA-ANG II interaction, such as DA synthesis, release, catabolism and turnover.

Sodium load combined with low doses of exogenous angiotensin II upregulate intrarenal angiotensin II.

Background/aims: The present study was designed to evaluate the effects of a salt load combined with exogenous low nonhypertensive angiotensin II (Ang II) doses on Ang II intrarenal regulation.

Methods: Sprague-Dawley rats were infused with Ang II nonhypertensive doses (0.1 microg.

Angiotensin II regulation of renal dopamine uptake and Na(+),K(+)-ATPase activity.

Background/aims: Angiotensin II (ANG II) decreases dopamine (DA) uptake in renal cortex activating AT(1) receptors. We investigated the signaling pathways that mediate this action and the incidence of DA-ANG II interaction on renal Na(+),K(+)-ATPase activity.

Methods: ANG II effects on [(3)H]-DA uptake and Na(+),K(+)-ATPase were measured in samples from the outer renal cortex of Sprague-Dawley rats.

Urodilatin and dopamine: a new interaction in the kidney.

Since renal natriuretic peptide urodilatin (URO) exerts similar natriuretic and diuretic actions to those of atrial natriuretic factor (ANF), we hypothesized that URO regulates renal dopamine (DA) availability, contributing to Na(+), K(+)-ATPase inhibition. URO (1-100 nM) increased (3)H-DA uptake in outer and juxtamedullar renal cortex and medulla slices from Sprague Dawley rats. Hydrocortisone blocked URO-stimulated DA uptake, demonstrating that DA uptake was extraneuronal.