sn-1,2 dioctanoylglycerol mimics the effects of angiotensin II on aldosterone production and potassium permeability in isolated bovine glomerulosa cells.

In order to elucidate the possible role in glomerulosa cells of diacylglycerol released by angiotensin II we have studied the action of a synthetic diacylglycerol, sn-1,2-dioctanoylglycerol (DiC8), on aldosterone production and potassium permeability in bovine adrenal cells. DiC8 elicited an increase in 86Rb efflux from cells previously equilibrated with the isotope. The action of DiC8 on the rate coefficient for 86Rb efflux was similar to that previously described for angiotensin II (Am. J. Physiol. 254 (1988) E144-149), i.e. DiC8 induced an immediate increase in 86Rb efflux followed by a sustained decrease in potassium permeability. This DiC8 induced inhibition was observed even in the presence of depolarizing concentrations of potassium. The effect of DiC8 on aldosterone secretion from adrenal glomerulosa cells was measured using a perifusion system. DiC8 (300 microM) caused a significant increase of aldosterone production, comparable to that seen with angiotensin II (100 nM). These results indicate that DiC8 has similar effects to angiotensin II on both potassium permeability and steroidogenesis, which suggests that activation of protein kinase C is involved in the changes of ionic permeability induced by this hormone in bovine adrenal glomerulosa cells.

[Effect of endotracheal instillation of hydrochloric acid on the contents of alveolar surfactant in rats]. / Efecto de la instilación endotraqueal de ácido clorhídrico sobre el contenido de surfactante alveolar en la rata.

Aspiration of gastric contents to the lung is a cause of Adult Respiration Distress syndrome. We studied the effects of endotracheal instillation of hydrochloric acid (2 ml/kg, 0.1 N solution) in anesthetized rats who were sacrificed 4 or 48 hr later. A control group received 0.9% saline solution instead. Total protein, phospholipids, disaturated phosphatidylcholine (DSPC) and number of cells were determined in the bronchoalveolar lavage fluid. Histologic studies were performed in one rat in each group. HCl caused edema and inflammatory reaction characterized by a rise in protein and cells in the bronchoalveolar fluid 48 hr after endotracheal instillation. This was associated with an increase in total phospholipid and in DSPC. Therefore, the inflammatory response to HCl is associated to an increase in alveolar surfactant 48 hr after instillation.