Effect of luminal angiotensin II on rabbit proximal convoluted tubule bicarbonate absorption

The present in vitro microperfusion study examined the effect of luminal angiotensin II on proximal convoluted tubule (PCT) volume absorption and bicarbonate transport. Neither 10−11 M, 10−10 M, nor 2 × 10−8 M luminal angiotensin II significantly affected PCT transport. When tubules were first perfused with enalaprilat to inhibit endogenous angiotensin II production, addition of 10−10 M luminal angiotensin II increased volume absorption (0.72 ± 0.08 vs. 0.86 ± 0.07 nl ⋅ mm−1 ⋅ min−1, P < 0.01) and bicarbonate transport (52.3 ± 3.7 vs. 67.9 ± 4.2 pmol ⋅ mm−1 ⋅ min−1, P < 0.01). Addition of 10−6 M losartan, an AT1 inhibitor, to the luminal perfusate inhibited volume absorption (0.95 ± 0.14 vs. 0.72 ± 0.11 nl ⋅ mm−1 ⋅ min−1, P < 0.05) and bicarbonate transport (65.0 ± 7.3 vs. 54.7 ± 9.2 pmol ⋅ mm−1 ⋅ min−1, P < 0.05). Addition of 10−4 M luminal PD-123319, an AT2 inhibitor, was without effect. In tubules perfused with 10−4 M luminal enalaprilat and 10−4 M luminal PD-123319, addition of 10−10M luminal angiotensin II in the experimental period resulted in a stimulation in volume absorption (0.61 ± 0.08 vs. 0.81 ± 0.10 nl ⋅ mm−1 ⋅ min−1, P < 0.01) and bicarbonate transport (49.9 ± 6.3 vs. 77.4 ± 14.3 pmol ⋅ mm−1 ⋅ min−1, P < 0.01). In tubules perfused with 10−6 M losartan and 10−4 M enalaprilat, addition of luminal 10−10 M angiotensin II resulted in no change in transport. These data are consistent with endogenous angiotensin II affecting PCT bicarbonate transport in vitro via luminal AT1receptors.

Prenatal glucocorticoids stimulate neonatal juxtamedullary proximal convoluted tubule acidification

The rate of neonatal proximal convoluted tubule (PCT) HCO3 absorption is lower than that of adult animals. The present in vitro microperfusion study examined whether prenatal dexamethasone (60 micrograms/kg daily to the doe for 3 days before delivery) would accelerate the maturation of neonatal juxtamedullary PCT acidification. Control neonates studied within 48 h of birth had a urine pH of 7.06 +/- 0.15 and a urine HCO3 concentration of 34.3 +/- 7.0 meq/l. Animals receiving dexamethasone had a urine pH of 6.47 +/- 0.11 and a urine HCO3 concentration of 10.1 +/- 4.0 meq/l, both of which were significantly lower than control (P less than 0.01). In juxtamedullary PCTs perfused in vitro, volume absorption was 0.27 +/- 0.03 nl.mm-1.min-1 in controls and 0.39 +/- 0.02 nl.mm-1.min-1 in dexamethasone-treated animals (P less than 0.05). HCO3 absorption was stimulated in the dexamethasone group (52.6 +/- 4.6 vs. 34.1 +/- 6.3 pmol.mm-1.min-1, P less than 0.05); however, glucose transport was not significantly affected (24.8 +/- 1.3 in dexamethasone vs. 21.5 +/- 3.5 pmol.mm-1.min-1 in controls). Intracellular pH was measured using 2',7'-bis(carboxyethyl)-5(6)-carboxyflourescin to examine whether prenatal dexamethasone stimulated the apical Na(+)-H+ antiporter and the basolateral Na(HCO3)3 symporter. Apical Na(+)-H+ antiporter proton flux was 108.5 +/- 14.2 pmol.mm-1.min-1 in the control group and 250.7 +/- 31.3 pmol.mm-1.min-1 in the dexamethasone group (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

The Ultrastructure of the Distal Tubule of Amphiuma: A Tem and Sem Study

Although the surface distal tubule of Amphiuma means has been used in transport and electrophysiology studies, a detailed description of its ultrastructure is lacking. In vitro microperfusion studies have identified three physiologically distinct segments. This study describes the morphology of the distal tubule of Amphiuma by transmission and scanning electron microscopy.Kidneys of ten animals were perfused via the aortic and portal vessels with amphibian ringers followed by fixative containing 1% paraformaldehyde, 1.25% glutaraldehyde, 0.05 M sucrose, 2% T40 Dextran, in 0.05 M Na cacodylate buffer, pH 7.2. For TEM, the kidneys were processed as described previously. For SEM, the tissue was osmicated, dehydrated and critical point dried using CO2