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Biomedical subjects

A Olivera

Publications and source records attributed to A Olivera.

45 records · Page 3Linked to original sources
PubMed1991

Glomerular binding and contractile response to angiotensin II in rats with chronic experimental cirrhosis of the liver.

1. The effects of angiotensin II on glomerular filtration rate and renal plasma flow were studied in surgically instrumented conscious control and cirrhotic rats. In addition, angiotensin II binding and the contractile response to angiotensin II were studied in glomeruli isolated from cirrhotic and control rats. 2. Cirrhotic rats had a higher glomerular filtration rate and a higher renal plasma flow than control animals. A non-pressor dose of angiotensin II induced small but significant decreases in glomerular filtration rate and renal plasma flow in both control and cirrhotic rats, the effect on renal plasma flow being the most pronounced. 3. Plasma renin and aldosterone concentrations were similar in control and cirrhotic rats. 4. The cross-sectional area of glomeruli from cirrhotic rats was 42% greater than that of glomeruli from control animals. Angiotensin II (10(-9) mol/l) decreased the cross-sectional area of glomeruli from control animals by 6.4 +/- 0.9% and of glomeruli from cirrhotic rats by 6.6 +/- 0.8% (P = not significant for comparison between control and cirrhotic animals). 5. There were no differences between control and cirrhotic rats in the affinity of angiotensin II for its glomerular receptors. However, the angiotensin II receptor density was higher in cirrhotic than in control rats, thereby producing an increased total angiotensin II binding in cirrhotic rats. 6. Since no functional differences between control and cirrhotic animals were present in the response to angiotensin II, even though angiotensin II binding was increased, a post-receptor blockade of the angiotensin II signal could be present in cirrhotic rats.

Angiotensin II↗
PubMed1991

Sphingosine-1-phosphate, a novel lipid, involved in cellular proliferation.

Sphingosine, a metabolite of membrane sphingolipids, regulates proliferation of quiescent Swiss 3T3 fibroblasts (Zhang, H., N. E. Buckley, K. Gibson. and S. Spiegel. 1990. J. Biol. Chem. 265:76-81). The present study provides new insights into the formation and function of a unique phospholipid, a metabolite of sphingosine, which was unequivocally identified as sphingosine-1-phosphate. The rapid increase in 32P-labeled sphingosine-1-phosphate levels induced by sphingosine was concentration dependent and correlated with its effect on DNA synthesis. Similar to the mitogenic effects of sphingosine, low concentrations of sphingosine-1-phosphate stimulated DNA synthesis and induced pronounced morphological alterations. Both sphingosine and sphingosine-1-phosphate stimulated DNA synthesis in cells made protein kinase C deficient by prolonged treatment with phorbol ester and sphingosine still elicited similar increases in sphingosine-1-phosphate levels in these cells. Although both sphingosine and sphingosine-1-phosphate acted synergistically with a wide variety of growth factors, there was no additive or synergistic effect in response to a combination of sphingosine and sphingosine-1-phosphate. Using a digital imaging system for measurement of calcium changes, we observed that both sphingosine and sphingosine-1-phosphate are potent calcium-mobilizing agonists in viable 3T3 fibroblasts. The rapid rise in cytosolic free calcium was independent of the presence of calcium in the external medium, indicating that the response is due to the mobilization of calcium from internal store. Our results suggest that sphingosine-1-phosphate may be a component of the intracellular second messenger system that is involved in calcium release and the regulation of cell growth induced by sphingosine.

Animals↗
PubMed1989

Adenosine induces mesangial cell contraction by an A1-type receptor.

Adenosine is known to decrease renal blood flow and glomerular filtration rate. We have tested the hypothesis that adenosine exerts contractile effects on mesangial cells. Furthermore, we have studied, using selective agonists and antagonists for adenosine, which kind of adenosine receptor, A1 or A2, is mainly implicated in this response. We also investigated whether calcium is involved in adenosine-induced mesangial cell contraction. Rat cultured mesangial cells were exposed to adenosine (10(-7) to 10(-3) M) and the contraction was measured as changes in planar cell surface area (PCSA). Adenosine induced a time- and dose-dependent reduction of PCSA. This reduction in PCSA was prevented by incubation with the A1 blocker PD116,948 but not with the A2 blocker PD115,199. Adenosine-5'-ethylcarboxamide (NECA), an A2 agonist, did not induce significant changes in PCSA whereas N6-S-1-methyl-2-phenylethyl adenosine (S-PIA), an A1 agonist, induced a dose-dependent decrease in PCSA. Adenosine-induced mesangial contraction was prevented by verapamil or by incubation in a calcium-free medium. These results suggest that adenosine induces a specific contraction of cultured rat mesangial cells that seems to be mediated by its binding to the adenosine A1-type receptor. This contraction seems to be dependent on the influx of extracellular calcium.

Adenosine↗
PubMed1989

Actions of cyclosporin A on cultured rat mesangial cells.

The effects of cyclosporin A (CsA) on planar surface area of cultured rat mesangial cells (PCSA) and cross-sectional area of isolated rat glomeruli (GCSA) were tested. The same experiments were performed after preincubation with platelet activating factor (PAF) antagonists (BN 52021, alprazolam) or calcium channel blockers (verapamil). Areas of cells or glomeruli were analyzed by a computer-assisted method. CsA reduced PCSA in a time-dependent (significant effects began at 15 min, about 12% of reduction with 10(-6) M CsA) and dose-dependent (no effect at 10(-9) M CsA, maximal reduction of about 30% at 60 min of incubation with 10(-7) M CsA) fashion. BN 52021 (5.10(-5) M) and alprazolam (10(-5) M) completely inhibited the reduction of mesangial cell area induced by CsA. Verapamil (10(-5) M) only partially inhibited this action. Glomerular cross-sectional area decreased after 30 minutes of incubation with 10(-6) M CsA (1.45 +/- 0.02 vs. 1.55 +/- 0.02 m2.10(-8), P less than 0.001), an effect that was inhibited by BN 52021 or verapamil. In addition, 10(-6) M CsA increased PAF production by isolated rat glomeruli (425 +/- 80 pg/mg vs. 198 +/- 13 pg/mg in control glomeruli, P less than 0.01), an effect which was not inhibited by verapamil. These results suggest that CsA could reduce GFR by decreasing the glomerular ultrafiltration coefficient, perhaps as a consequence of the contraction of mesangial cells. PAF seems to play a pivotal role in the genesis of this action.

Animals↗
PubMed1988

Atrial natriuretic peptide in rats with experimental cirrhosis of the liver without ascites.

Plasma levels of atrial natriuretic peptide (ANP) have been measured in eight sodium-retaining cirrhotic nonascitic rats and eight control animals before and after extracellular volume expansion by isotonic saline infusion (30 ml/kg BW, 20 min). In addition, disappearance of [125I]ANP was studied in six control and six cirrhotic rats. The effect of infusing synthetic rat ANP-(1-28) (1 microgram) on mean arterial pressure and renal function has been also studied. In basal conditions, cirrhotic rats showed higher ANP plasma levels than control animals (71.1 +/- 16.6 vs. 43.9 +/- 5.1 pg/ml; P less than 0.05). After extracellular volume expansion, ANP increased in both control and cirrhotic rats; the increase in cirrhotic was higher than that in control rats (88 +/- 27% vs. 33 +/- 8%; P less than 0.05). Disappearance of iodinated ANP from plasma was identical in control and cirrhotic rats. ANP infusion induced a larger decrease in mean arterial pressure in control (21 +/- 5%) than in cirrhotic rats (9 +/- 2.5%). ANP induced comparable increases in glomerular filtration rate and renal plasma flow in both groups of animals. However, diuretic and natriuretic effects were markedly impaired in cirrhotic animals. Thus, urinary flow increased by 91 +/- 18 microliters/min in control animals, but only by 37 +/- 7 microliters/min in cirrhotic animals. Fractional sodium excretion increased to 1.7 +/- 0.44% in controls and to 0.54 +/- 0.12% in cirrhotic rats (P less than 0.05). It is concluded that the defect in renal handling of sodium in cirrhotic rats is not due to a lack of ANP synthesis or release. In addition, these animals show an impaired renal response to ANP.

Animals↗
PubMed1988

Atrial natriuretic peptide inhibits angiotensin II-induced contraction of isolated glomeruli and cultured glomerular mesangial cells of rats: the role of calcium.

We examined the contractile effect of angiotensin II on isolated rat glomeruli and cultured glomerular mesangial cells, as well as the possible involvement of calcium in this contraction. In addition, the effect of rat atrial natriuretic peptide (ANP) on angiotensin II-induced contraction was studied. Computer-assisted image analysis was used to measure glomerular cross-sectional area and planar mesangial cell surface area in several experimental conditions. Angiotensin II induced a decrease in glomerular cross-sectional area and planar mesangial cell surface area that was both time and dose dependent. This effect was partially blocked by preincubation with verapamil or TMB-8, the latter compound being more effective. Incubation with ANP prevented angiotensin II-induced reduction of glomerular cross-sectional area and planar mesangial cell surface area and reversed contraction in mesangial cells. Incubation with TMB-8 impaired the effect of ANP. These data suggest that angiotensin II could exert part of its physiologic effects in the kidney through calcium-dependent mesangial and glomerular contraction. ANP inhibited this contraction, possibly explaining some of its renal effects.

Angiotensin II↗