Papel da angiotensina II no controle da excitabilidade dos neurônios do gânglio nodoso

Abstract

Angiotensin II at 100 nM increased the spike frequency generation in the adult rat nodose neurons. Since AT1 receptor antagonist prevented this effect we could suggest that the AT1 receptor is responsible for the increase in excitability. We investigated if this peptide was able to modulate isolated potassium and calcium currents. Angiotensin IIinhibited only the IA type potassium current (~50 %). The peptide also inhibited the high-voltage activated calcium current by 50%. This inhibition was not mediated by AT1 receptor activation. Angiotensin II was able to change the high-voltage calcium current voltage dependence for activation. It caused a shift towards the hyperpolarized membranepotentials by about 6 mV. Angiotensin II probably did not inhibit one specific type of voltage-dependent calcium channel. The L-type calcium current was inhibited by 30% and the N and/or P/Q type had an inhibition of 20%. Angiotensin II generated calcium transients in these neurons. The activation of AT1 receptor was responsible for the observed changes in the intracellular calcium levels. Surprisingly, the calcium transientevoked by the application of angiotensin II depends on the presence of calcium in the extracellular millieu. None of these described effects caused by angiotensin II were reproduced in spontaneously hypertensive rats (SHR).