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T Balla

Publications and source records attributed to T Balla.

85 records · Page 5Linked to original sources
PubMed1985

Pressor-type vasopressin receptors in the adrenal cortex: properties of binding, effects on phosphoinositide metabolism and aldosterone secretion.

Specific, high affinity sites that bound tritium-labeled arginine-vasopressin (3H-AVP) were detected in a crude membrane fraction of rat adrenal capsules (chiefly zona glomerulosa). Binding displacement experiments with peptide analogs of AVP suggested that the binding site is a pressor (V1) type receptor for AVP. When added to dispersed rat adrenal glomerulosa cells, vasopressin (10(-8)-10(-6)M) stimulated the incorporation of 32P-phosphate into phosphatidylinositol, and the effect was blocked by the AVP receptor antagonist peptide d(CH2)5Tyr(Me)AVP. Vasopressin also increased the breakdown of phosphatidylinositol-4,5-bisphosphate within 1 min after its addition to the incubation medium. Superfused zona glomerulosa cells responded to AVP (10(-8)-(-6)M) by increasing their aldosterone production. The response could be blocked by the antagonist peptide. These data show that functionally active V1 receptors are present in rat glomerulosa cells, and suggest that vasopressin may regulate the function of the adrenal glomerulosa.

Adrenal Cortex↗
PubMed1984

Effects of lithium on angiotensin-stimulated phosphatidylinositol turnover and aldosterone production in adrenal glomerulosa cells: a possible causal relationship.

Turnover of 32P-labelled phosphatidylinositol (PI) was examined in isolated adrenal glomerulosa cells. Increased incorporation of [32P]phosphate into PI in response to angiotensin II was completely prevented by Li+. A simultaneous accumulation of 32P activity in phosphatidic acid (PA) was also observed. Angiotensin II increased the breakdown of PI despite the presence of Li+. These results suggest that Li is a suitable tool to interrupt the accelerated PI cycle in angiotensin-stimulated cells. Aldosterone production of superfused cells was inhibited by Li+ when the cells were stimulated with angiotensin II. On the other hand, Li+ did not inhibit the aldosterone response of the cells to ACTH, a hormone which acts via cyclic AMP and does not enhance PI turnover in these cells. On the basis of these results, we assume that the inhibitory effect of Li+ on aldosterone production is related to its effect on PI turnover.

Adrenal Cortex↗
PubMed1983

Angiotensin II stimulates phosphatidylinositol turnover in adrenal glomerulosa cells by a calcium-independent mechanism.

Angiotensin II enhances phosphatidylinositol turnover in isolated adrenal glomerulosa cells. In the present experiments we examined whether this effect required the presence of extracellular Ca2+. It was found that neither the stimulation of phosphatidylinositol breakdown nor the stimulation of incorporation of [32P]phosphate into phosphatidic acid and phosphatidylinositol required the presence of extracellular Ca2+. These observations suggest that the enhancement of phosphatidylinositol turnover may precede, but does not depend on, angiotensin-induced Ca2+ influx.

Adrenal Cortex↗
PubMed1982

Control of phosphatidylinositol turnover in adrenal glomerulosa cells.

The purpose of the present experiments was to compare the effects on phosphatidylinositol metabolism of agents stimulating aldosterone secretion. Glomerulosa cells, isolated from rat adrenals, were incubated in the presence of one of the following stimuli: angiotensin II, elevated potassium concentration, corticotropin, dibutyryl cyclic AMP and prostaglandin E2. Of all these substances, only angiotensin II stimulated the incorporation of [32P]phosphate into phosphatidylinositol. The effect was already detected 2.5 min and was still maintained 60 min after the onset of stimulation. A slight enhancement of the incorporation into other phospholipids was observed in the first minutes of stimulation. Cycloheximide abolished the effect of angiotensin II on aldosterone production, but not on phosphatidylinositol synthesis. In cells prelabelled with [32P]phosphate, radioactivity in phosphatidylinositol relative to that in other phospholipids decreased in response to angiotensin II within 5 min. This indicates that angiotensin II induces a specific breakdown of phosphatidylinositol. Corticotropin failed to enhance the incorporation of [32P]phosphate into phosphatidylinositol and other phospholipids in isolated fasciculate-reticularis cells. The results suggests that although both angiotensin II and potassium are presumed to act through changes in calcium metabolism, angiotensin alone generates the calcium signal by increased phosphatidylinositol turnover.

Adrenal Glands↗
PubMed1982

Possible role of calcium uptake and calmodulin in adrenal glomerulosa cells: effects of verapamil and trifluoperazine.

The effects of verapamil and trifluoperazine were examined on isolated rat adrenal glomerulosa cells so as to assess the role of calcium ion influx and calmodulin in the function of this cell population. Verapamil (10(-5) and 10(-4) moles/1) slightly reduced the basal production rate of aldosterone and strongly inhibited the response to angiotensin II, potassium ions, corticotrophin (ACTH) and dibutyryl cyclic AMP (db-cAMP). The concentration of verapamil required to reduce the response to these agonists by 50% varied between 2 and 6 mumoles/1. Trifluoperazine (30 mumoles/1) slightly increased the basal production rate of aldosterone. The response to angiotensin and potassium was variably antagonized by 3 mumoles/1 trifluoperazine and completely inhibited by the drug at 30 mumoles/1. The antagonist at a concentration of 3 mumoles/1 exerted either a facilitatory or inhibitory effect on the response to ACTH and db-cAMP, depending on the concentration of the agonist. Trifluoperazine at a concentration of 30 mumoles/1 reduced the response to both agonists to a level which was 2-3 fold higher than that observed in appropriate control samples. The present results indicate that (1) calcium influx is an essential event in the aldosterone stimulating action of angiotensin II, potassium ions, ACTH and cyclic AMP; (2) stimulation by angiotensin II and potassium ions are completely dependent on calmodulin; (3) stimulation by ACTH and cyclic AMP is mediated by calmodulin-dependent and independent mechanisms.

Adrenal Cortex↗
PubMed1981

Effect of reduced extracellular sodium concentration on the function of adrenal zona glomerulosa: studies in conscious rats.

The present experiments were designed to study the effect extracellular hyponatraemia on aldosterone secretion. Hyperaldosteronism was induced by peritoneal dialysis with 5% glucose solution in dexamethasone-pretreated rats. In the narrow physiological range of 135-142 mmol/l, as well as in the whole range of the study (122-142 mmol/l), the plasma concentration of sodium showed a close negative correlation with the serum concentration of aldosterone (r = -0.71 and -0.83, respectively). Plasma renin activity increased after peritoneal dialysis; however, no close correlation was observed either between sodium concentration and plasma renin activity or plasma renin activity and serum aldosterone concentration within the dialysed group. The ratio of serum concentration of aldosterone to plasma renin activity showed no considerable change between 132 and 142 mmol/l but rose steeply below 132 mmol sodium/l suggesting that a factor(s) other than angiotensin may also contribute to the induction of hyperaldosteronism.U

Adrenal Glands↗
PubMed1980

Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat.

The purpose of the present study was to evaluate the role of the renin-angiotensin system in the secretion of aldosterone during restriction of dietary sodium intake. Rats were kept on control or low-sodium diet for one week. On the 7th morning of diet osmotic minipumps filled with the angiotensin converting enzyme inhibitor (CEI) SQ 20,881, or empty pumps, were implanted subcutaneously (sc). The rats were sacrificed 23 h later. Peripheral blood was analyzed for hormones and electrolytes. Adrenal capsular tissue (z. glomerulosa) was incubated for the determination of the conversion of [3H]corticosterone to [3H]aldosterone. Sodium depletion had no effect on plasma sodium, but it increased potassium concentration. Infusion of CEI had no significant effect on plasma electrolytes. Plasma renin activity was increased both by sodium depletion and CEI. The mean serum aldosterone level was twelve times higher in sodium depleted animals than in controls. Aldosterone level was reduced by about 60 per cent in CEI-infused animals both on control and low-sodium diet. The conversion of corticosterone to aldosterone was significantly stimulated by sodium deprivation. This effect was also inhibited by the CEI SQ 20,881.

Adaptation, Physiological↗
PubMed1979

Hyperaldosteronism in the sodium depleted rat: effect of a low sodium diet or diuretic treatment on steroid output by the superfused adrenal zona glomerulosa.

The effect of chronic and acute sodium depletion on the function of the adrenal zona glomerulosa was examined by means of superfusion of adrenal capsular glands. The glands were removed from rats kept on a low sodium diet for 7 days or from dexamethasone-pretreated rats 30 min after administration of the diuretic drug furosemide. Chronic sodium depletion brought about a high initial output of aldosterone followed by a rapid fall in output. The initial rate of corticosterone output did not differ significantly from that by control glands but exhibited a more rapid decline with time. Aldosterone: corticosterone ratio, an indicator of the rate of conversion of corticosterone to aldosterone, was much higher in the sodium depleted group throughout the whole superfusion period. Acute sodium depletion was followed by high initial and rapidly falling aldosterone and corticosterone output, without any significant change in the ratio of aldosterone to corticosterone output rate. The above dynamic patterns of steroid output indicate that a sodium deficient diet evokes hyperaldosteronism by increasing the formation of aldosterone from corticosterone (not excluding the possibility of increasing the formation of corticosterone as well) while diuretic treatment stimulates aldosterone secretion by acting on the formation of corticosterone only.

Adrenal Cortex↗
PubMedDate not supplied

Signaling events activated by angiotensin II receptors: what goes before and after the calcium signals.

Angiotensin II (Ang II) receptors of the AT1 subtype are coupled to heterotrimeric G nucleotide-binding proteins, G(q/11), to activate phospholipase C-beta isoforms with production of inositol 1,4,5-trisphosphate (InsP3) and diacylglycerol. The resultant release of intracellular Ca2+ and increased Ca2+ influx are major determinants of several acute cellular responses initiated by Ang II, including secretion of aldosterone from the adrenal cortex and smooth muscle contraction. However, cellular events related to more prolonged effects of Ang II, such as hypertrophic and hyperplastic responses, are triggered by intracellular signaling cascades that are less dependent on Ca2+ signals. The Ang II-induced activation of Raf-1 kinase, p42 MAP-kinase and c-fos expression in response to Ang II in adrenal glomerulosa cells does not require Ca2+ influx. Moreover, the dose-response relationships for Raf-1 activation, MAP-kinase activation and mitogenesis show significantly higher sensitivity to Ang II than the InsP3, Ca2+-release and aldosterone secretory responses. The sensitivities of both Raf-1 kinase and MAP-kinase stimulation by Ang II to the inhibitors of phosphoinositide kinases, wortmannin and LY 294002, suggest that inositol phospholipids may play a role in these activation events unrelated to their role in Ca2+ signaling. To investigate the changes of various inositides after stimulation at the single cell level, fluorescent probes were developed in which pleckstrin homology domains with distinct binding specificities to inositol phospholipids were fused to the green fluorescent protein and expressed in NIH 3T3 cells. The use of these probes revealed heterogeneity of the inositol lipid pools and their complex relationship to Ca2+ signals. The use of these tools will help to further clarify the complex role of these lipids in initiating Ca2+-dependent and -independent signaling responses.

3T3 Cells↗