INICSA   23916
INSTITUTO DE INVESTIGACIONES EN CIENCIAS DE LA SALUD
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
SHR Animals Have ADH Induced Over Stimulation On Sodium Transport
Autor/es:
GUILLERMO B. SILVA; LUIS I. JUNCOS; NESTOR H. GARCIA
Lugar:
San Francisco
Reunión:
Congreso; HBPR 2014; 2014
Institución organizadora:
Council of High Blood Pressure
Resumen:
During hypertension kidney fails to maintain Na balance, leading to increased blood volume and blood pressure. It has been suggested that humoral defects and in the last decade in Na transport disorders have been described in different tubular segments. Our aim was to investigate the interaction between antidiuretic hormone (ADH) and angiotensin II (Ang II) in oxygen consumption (QO2, as a marker of Na transport ) in the loop of Henle , in normotensive and hypertensive animals. To do that we used suspensions of thick ascending limbs of the loop of Henle and and measured QO2, cAMP and superoxide production. We found that In normotensive animals, the basal QO2 was 112 ± 5 nmol O2/min/mg protein. ADH (1 nM) increased QO2 227% compared to baseline values. In the presence of ADH and Ang II (1 nM) initially decreased QO2 with a subsequent recovery (279 ± 17 nmol O2/min/mg protein). ADH increased cAMP levels, whereas Ang II decreased it. In contratst, ADH caused no effect in superoxide levels in thick ascending limbs of normotensive and increased after 3.3 minutes incubation. In hypertensive rats, the QO2 was stimulated by 98% after ADH. In these rats, and Ang II + ADH produced an initial decrease QO2 and a subsequent over-stimulation by ADH (184 % increase , p <0.05 vs normotensive animals) . Unlike what was observed in normotensive animals, Ang II increased early superoxide levels before at 1.7 minutes incubation and reached significant values compared to basal. In addition Losartan blocked the Ang II -induced effects. The superoxide scavenger tempol blocked the increase in Ang II -induced QO2 in both animal models. Taken together these results indicate that in hypertensive animals there is an additive effect between ADH and Ang II in the thick ascending limb of the loop of Henle. Therefore, the abnormal mechanism observed in hypertensive animals could explain the Na positive balance in this model of arterial hypertension