Absence of ß-endorphin causes an increase in systolic blood pressure and sympathetic activity during sodium overload.

CAEIRO, X.; HANSEN, C.; PIETRANI, L.; RUBINSTEIN, M.; GARCÍA, N.; VIVAS, L

Pinamar, Buenos Aires.

Congreso; XX Reunión Anual de la SAN, X Congreso de la PABMB y XLI Reunión Anual de SAIB; 2005

SAN, PABMB y SAIB

ABSENCE OF ß-ENDORPHIN CAUSES AN INCREASE IN SYSTOLIC BLOOD PRESSURE AND SYMPATHETIC ACTIVITY DURING SODIUM OVERLOAD. Ximena Caeiro1, Cristian Hansen2, Lorena Pietrani2,  Marcelo Rubinstein3, Nestor García4, Laura Vivas1. 1INIMEC-CONICET, 2LACE, Cba, Arg. 3INGEBI, Bs.As., Arg. 4IPEM, Cba, Arg.  xcaeiro@immf.uncor.edu.  The objective of this study was to test the hypothesis that low levels of ß Endorphins are involved in the development of salt sensitivity hypertension probably due to an enhance in sympathetic activity.   ß-Endorphin KO (ßend-/-), HT (ßend+/-) and WT (ßend+/+) mice were submitted for two weeks with either low- or high-sodium diet (HSD) and systolic blood pressure (SBP), urinary catecholamines and brain pattern of Fos immunoreactivity (Fos-ir) were evaluated in each group. HSD caused a significant increase in SBP in ßend-/- mice (P < 0.01) but non-changes were observed in βend+/+ and βend+/- mice when kept on the same experimental conditions. With regard to brain activity, ßend-/- mice maintained on a HSD showed a significant increase in Fos-ir neurons in the median preoptic nucleus (p< 0.01) when compared to ßend+/- and ßend+/+ animals. Additionally, βend-/- mice had higher levels of urinary epinephrine excretion (p < 0.05 ) when placed on a HSD in comparison to ßend+/+ and ßend+/- animals. Thus, these results suggest that the ß-endorphinergic system may participate in blood pressure regulation during sodium overload probably inhibiting sympathethic activity.