The effect of saponins from Ampelozizyphus amazonicus Ducke on the renal Na+ pumps' activities and urinary excretion of natriuretic peptides.

Background: In a previous study, we showed that a saponin mixture isolated from the roots of Ampelozizyphus amazonicus Ducke (SAPAaD) reduces urine excretion in rats that were given an oral loading of 0.9 % NaCl (4 ml/100 g body weight). In the present study, we investigated whether atrial natriuretic peptides (ANP) and renal ATPases play a role in the SAPAaD- induced antidiuresis in rats.

The stimulatory effect of angiotensin II on Na(+)-ATPase activity involves sequential activation of phospholipases and sustained PKC activity.

Angiotensin II (Ang II) stimulates the proximal tubule Na(+)-ATPase through the AT(1) receptor/phosphoinositide phospholipase Cbeta (PI-PLCbeta)/protein kinase C (PKC) pathway. However, this pathway alone does not explain the sustained effect of Ang II on Na(+)-ATPase activity for 30 min. The aim of the present work was to elucidate the molecular mechanisms involved in the sustained effect of Ang II on Na(+)-ATPase activity.

Modulation of sodium pumps by steroidal saponins.

Costus spicatus, used in Brazilian traditional medicine to expel kidney stones, contains steroidal saponins with different chemical characteristics. In spite of its popular utilization as potent diuretic, no scientific reports correlate this activity with the chemical constituents of the extract. Therefore, two steroidal saponins (3 beta,22 alpha,25R)-26-(beta-D-glucopyranosyloxy)-2-methoxyfurost-5-en-3-yl O-D-apio-beta-D-furanosyl-(1-->2)-O-[6-deoxy-alpha-L-mannopyranosyl-(1-->4)]-beta-D-glucopyranoside (1) and (3 beta,22 alpha,25R)-spirostan-3-yl O-D-apio-beta-D-furanosyl-(1-->2)-O-[6-deoxy-alpha-L-mannopyranosyl-(1-->4)]-beta-D-glucopyranoside (1a), were isolated from the rhizomes of this plant and their effects on the Na+-ATPase and (Na+ + K+)-ATPase activities of the proximal tubule from pig kidney were evaluated.

Involvement of the Gi/o/cGMP/PKG pathway in the AT2-mediated inhibition of outer cortex proximal tubule Na+-ATPase by Ang-(1-7).

The molecular mechanisms involved in the Ang-(1-7) [angiotensin-(1-7)] effect on sodium renal excretion remain to be determined. In a previous study, we showed that Ang-(1-7) has a biphasic effect on the proximal tubule Na+-ATPase activity, with the stimulatory effect mediated by the AT1 receptor. In the present study, we investigated the molecular mechanisms involved in the inhibition of the Na+-ATPase by Ang-(1-7).