INVESTIGADORES
CHOI Marcelo Roberto
artículos
Título:
Angiotensin II regulates extraneuronal dopamine uptake in the kidney
Autor/es:
CHOI MR; CORREA AH; DEL VALLE TURCO V; GARCÍA FA; FERNÁNDEZ BE
Revista:
NEPHRON PHYSIOLOGY
Editorial:
KARGER
Referencias:
Lugar: Basel; Año: 2006 vol. 104 p. 136 - 143
ISSN:
1660-2137
Resumen:
Backgroung/Aims: Angiotensin II (ANG II) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Previous studies demonstrate that atrial natriuretic factor (ANF) can regulate renal DA uptake and thereby Na+, K+-ATPase activity in external renal cortex. As ANG II counteracts most of ANF biological effects, the aim of the present study was to evaluate ANG II effects on renal DA metabolism and identify the receptor involved. Methods: To determine ANG II effects on renal DA metabolism, we evaluated 3H-DA uptake in vitro in kidney tissues samples from Sprague Dawley rats. Results: The results indicate that ANG II decreased DA uptake at 30 minutes, in a concentration-response fashion, in external and juxtamedullar cortex. DA uptake was characterized as an extraneuronal uptake and decreased at 0°C and in sodium free medium. The biological receptor type involved was the AT1, since losartan reversed ANG II effects on DA uptake while AT2 receptors were not involved since PD 123319 did not affect ANG II effects. The absence of sodium did not alter ANG II response. Conclusion: ANG II inhibits DA uptake by kidney tubular cells. These effects implicate AT1 receptors without participation of AT2 receptors. This mechanism could be related to DA effects on sodium reabsorption and linked to ANG II antinatriuretic effects in the kidney. Angiotensin II (ANG II) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Previous studies demonstrate that atrial natriuretic factor (ANF) can regulate renal DA uptake and thereby Na+, K+-ATPase activity in external renal cortex. As ANG II counteracts most of ANF biological effects, the aim of the present study was to evaluate ANG II effects on renal DA metabolism and identify the receptor involved. Methods: To determine ANG II effects on renal DA metabolism, we evaluated 3H-DA uptake in vitro in kidney tissues samples from Sprague Dawley rats. Results: The results indicate that ANG II decreased DA uptake at 30 minutes, in a concentration-response fashion, in external and juxtamedullar cortex. DA uptake was characterized as an extraneuronal uptake and decreased at 0°C and in sodium free medium. The biological receptor type involved was the AT1, since losartan reversed ANG II effects on DA uptake while AT2 receptors were not involved since PD 123319 did not affect ANG II effects. The absence of sodium did not alter ANG II response. Conclusion: ANG II inhibits DA uptake by kidney tubular cells. These effects implicate AT1 receptors without participation of AT2 receptors. This mechanism could be related to DA effects on sodium reabsorption and linked to ANG II antinatriuretic effects in the kidney.