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A Kurtz

Publications and source records attributed to A Kurtz.

At least 235 records · Page 13Linked to original sources
PubMed1987

Mechanism of NaCl transport-stimulated prostaglandin formation in MDCK cells.

Recently we have found that stimulation of NaCl transport in high-resistance MDCK cells enhances their prostaglandin formation. In the present study, we investigated the mechanisms by which prostaglandin formation could be linked to the ion transport in these cells. We found that stimulation of transport caused a transient stimulation of prostaglandin formation lasting 5-10 min. The rise in prostaglandin formation was paralleled by a rise of free intracellular arachidonic acid. Analysis of membrane lipids revealed that the rise of free arachidonic acid was paralleled by a loss of arachidonic acid from polyphosphoinositides. We failed to obtain indications for the stimulation of calcium-dependent phospholipase A2. However, we did obtain evidence that the incorporation of arachidonic acid into phospholipids was diminished during stimulation of ion transport, indicating a decreased rate of reesterification. Despite the fact that there was no significant fall in total cellular ATP on stimulation of ion transport, we found a high and transient rise of lactate production of the cells on stimulation of the ion transport indicating an alteration of the ADP/ATP ratio. Moreover, prostaglandin formation and lactate formation were linearly correlated in this situation. When glucose utilization was inhibited by mannoheptulose, the rise in lactate formation was abolished, whereas that of PG formation was unaltered, indicating that lactate formation and prostaglandin formation were not causally linked on stimulation of ion transport. Our results suggest that an increase in the rate of sodium chloride transport by MDCK cells stimulates formation by an inhibition of reesterification of free arachidonic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1987

Control of diabetes through a subcutaneous peritoneal access device (SPAD) in patients with resistance to subcutaneously injected insulin.

In 2 patients with insulin dependent diabetes and resistance to subcutaneously injected insulin, adequate glucose homeostasis was achieved following the administration of insulin through a subcutaneous peritoneal access device (SPAD). Fasting and post-prandial plasma glucose concentrations fell to near normal levels and HbA1 fell from 17.8% to 9% and from 15.4% to 8% respectively. Insulin requirements fell from 3,000 and 8,000 units to 160 and 100 units per day, respectively. Measurements of sequential free insulin concentrations in serum following subcutaneous and intraperitoneal insulin injection (100 i.u.) showed a significant increase in serum free insulin following intraperitoneal injection, but none after subcutaneous injection. Glucose concentrations fell after intraperitoneal injection of insulin, but not after subcutaneous injection. It is concluded that: intraperitoneal insulin administration is an effective alternative to subcutaneous injections of insulin in patients with this form of insulin resistance; and in patients with this form of insulin resistance, subcutaneous injections of insulin are not followed by an increase in serum free insulin.

Adult↗
PubMed1987

Multicenter validation study of real-time (B-mode) ultrasound, arteriography, and pathologic examination.

The ability of high-resolution ultrasound, angiography, and pathologic examination of endarterectomy specimens to identify and quantitate atherosclerosis was compared in a five-center study. The carotid bifurcation in 900 patients was evaluated by angiography and ultrasound. In 216 cases, high-quality endarterectomy specimens were available for comparison with the preoperative images. All comparisons were made in a blinded fashion. Results indicate that ultrasound is able to differentiate angiographically normal from abnormal arteries with a sensitivity of 88% (1077 of 1233 arteries) and accuracy of 79% (1251 of 1578 arteries). Angiographic stenoses equal to or greater than 50% diameter were accurately identified by ultrasound imaging in 72% (1133 of 1578 arteries) of cases, and this was improved by the addition of other functional data (i.e., Doppler spectral analysis and oculoplethysmography). There was only modest correlation of absolute measurements of lesion width, minimal lumen, and standard lumen by the two imaging techniques (r = 0.28 to 0.55). Ultrasound measurements of lesion width were on the average 2 mm greater than those of angiography. The lumen averaged 1.5 mm larger when measured by ultrasound techniques. In the subset in which data were available from endarterectomy specimens, ultrasound showed the best correlation with lesion width (mean difference -1.1 mm) and angiography correlated best with minimal lumen (mean difference -0.1 mm). Neither examination consistently identified ulcerated plaques. Although ultrasound imaging alone has limited usefulness in quantitating luminal stenosis, this can be improved by the use of Doppler spectral analysis and oculoplethysmography. Ultrasound is superior to angiography for quantifying atherosclerotic plaque (lesion width) and will be an important tool for further study of atherosclerotic lesions.

Adolescent↗
PubMed1986

Role of phospholipase C and protein kinase C in vasoconstrictor-induced prostaglandin synthesis in cultured rat renal mesangial cells.

It was the aim of the present study to find out if a common mechanism exists by which the vasoconstrictive hormones angiotension II, noradrenaline and 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (AGEPC) increase prostaglandin E2 (PGE2) synthesis in cultures of rat renal mesangial cells. Angiotension II, noradrenaline and AGEPC stimulated PGE2 synthesis and uptake of 45Ca2+ in cultured mesangial cells. Both of these effects could be completely suppressed by the calcium channel blocker verapamil. Angiotensin II, noradrenaline and AGEPC caused a rapid breakdown of phosphatidylinositol 4,5-bisphosphate with a concomitant increase of 1,2-diacylglycerol and inositol trisphosphate, indicating an activation of phospholipase C by these hormones. Addition of verapamil had no effect on the hormone-induced stimulation of phospholipase C. The synthetic analogue of diacylglycerol, 1-oleoyl-2-acetylglycerol, and the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), both of which are known to stimulate protein kinase C, enhanced PGE2 synthesis. Chelation of extracellular calcium with EDTA or addition of verapamil abolished the effect of 1-oleoyl-2-acetylglycerol and phorbol ester on PGE2 synthesis. 1-Oleoyl-2-acetylglycerol and phorbol ester increased the uptake of 45Ca2+ by the cells in a dose-dependent manner and this effect could be blocked by verapamil. The entirety of these data leads us to suggest that vasoconstrictor-evoked synthesis of PGE2 in rat mesangial cells is mediated by the subsequent activation of phospholipase C and protein kinase C. The activation of protein kinase C by diacylglycerol is likely to be involved in the increase of the calcium permeability of the plasma membrane which is a prerequisite for PGE2 synthesis induced by vasoconstrictive hormones.

Animals↗
PubMed1986

The beta-glucanase gene from Bacillus amyloliquefaciens shows extensive homology with that of Bacillus subtilis.

The nucleotide sequence of a 1583-bp DNA fragment containing gene bg1A for endo-beta-1,3-1,4-glucanase (EC 3.2.1.73) of Bacillus amyloliquefaciens strain BE20/78, a high producer of secreted enzymes, has been determined. The gene bg1A comprises an open reading frame (ORF) of 717 bp (= 239 codons) starting with ATG at 469 up to the translation stop codon TAA at 1188. Upstream from the translation initiation codon ATG, the ribosome-binding sequence 5'-AAAAAAGGGGG-3' and two putative bglA promoters have been identified. A box of eleven AT out of twelve base pairs (bp) precedes the -35 region of promoter P1. Beyond the translation stop codon UAA, a sequence of 69 bp can be folded into a hook-like stem-loop structure which probably functions as a transcriptional terminator. The ORF region of the gene bglA reveals about 90% homology with another beta-glucanase gene, bglS of Bacillus subtilis C120 sequenced by Murphy et al. (1984). Three regions of frequent amino acid (aa) changes are indicated. However, the major difference between these is a set of deletions within the non-coding region separating the bglA gene from an unknown preceding ORF and by one deletion shortening the proposed signal peptide by three aa (Pro-Tyr-Leu-). The putative transcription terminator of gene bglA completely lacks homology with a B. subtilis bglS gene. The signification of deletions erasing the 'sacR-homology region' in B. amyloliquefaciens, which have been detected in proximity of the beta-glucanase gene of B. subtilis by Steinmetz and Aymerich (1986), is discussed.

Bacillus↗
PubMed1986

Atrial natriuretic peptide inhibits renin release from juxtaglomerular cells by a cGMP-mediated process.

We have examined the effect of a synthetic analogue of human alpha-atrial natriuretic peptide (ANP), APII, on renin release in cultured renal juxtaglomerular cells (JGA cells). Using cell cultures containing 80-90% renal juxtaglomerular cells, we found that ANP (10(-13)-10(-9) M) strongly inhibited renin release from the cells in a dose-dependent fashion (ki, 10 pM) to about 10% of control. Inhibition of renin release by ANP was paralleled by an increase in cellular cGMP levels; while in the presence of the cGMP-phosphodiesterase inhibitor M&B 22948 (1 mM), concentrations of ANP lower by a factor of 100 were required to obtain the same effects on renin release and cGMP levels. The guanylate cyclase inhibitor methylene blue (10 microM), on the other hand, shifted the dose-response curves for renin release and cGMP levels to 100-fold higher concentrations of ANP. Neither the influx of 45Ca into the cells nor the intracellular quin-2 signal, which is a measure for changes of intracellular Ca concentration, was in any way altered by ANP. Our results suggest that ANP inhibits renin release from juxtaglomerular cells by a cGMP-dependent process that does not involve changes in intracellular calcium.

Aminoquinolines↗
PubMed1986

Association between cheiroarthropathy and frozen shoulder in patients with insulin-dependent diabetes mellitus.

Twenty-nine patients with insulin-dependent diabetes mellitus (IDDM) were identified as having cheiroarthropathy. They were compared for the presence of shoulder problems with 28 controls with normal hands, matched for age, sex and duration of diabetes mellitus. Frozen shoulder was diagnosed in 13 of the 29 patients with cheiroarthropathy--10 with bilateral frozen shoulder, and in two of the 28 control patients--one bilateral (p = 0.0025). The increased incidence of frozen shoulder in patients with cheiroarthropathy has not been described previously. There was an increased frequency of microvascular complications in the diabetic patients with cheiroarthropathy compared with the controls. Advanced retinopathy was present in 18 of the 29 cheiroarthropathy patients, of whom six were blind, compared with seven of the 28 controls, of whom none was blind (p = 0.003). Peripheral neuropathy was found in 28 of the 29 cheiroarthropathy patients and in seven of the 28 controls (p = 0.001). There was no significant difference between the two groups in the frequency of nephropathy or in the degree of diabetic control.

Adult↗
PubMed1986

Pattern electroretinograms become abnormal when background diabetic retinopathy deteriorates to a preproliferative stage: possible use as a screening test.

The pattern electroretinogram (PERG) and other tests were given to a selected group of patients with diabetes, ranging from those who had no retinopathy or funduscopic changes to those in the preproliferative state. None had visual symptoms. The PERG was found to be normal in patients with microaneurysms and a few blot haemorrhages. However, when cotton-wool spots and angiographic evidence of areas of capillary non-perfusion were present, the PERG was reduced below the normal value. Similar changes occurred with the oscillatory potentials of the ERG evoked by an intense flash, but the results were more variable. So in the individual patient the test is not a reliable indicator of the progress of the retinopathy. The value of the PERG in screening is discussed.

Adult↗
PubMed1986

Role of protein kinase C in inhibition of renin release caused by vasoconstrictors.

It was the aim of the present study to get insight into some of the intracellular mechanisms by which the vasoconstrictor hormones angiotensin II (ANG II), arginine vasopressin (AVP), and norepinephrine (NE) inhibit renin release from renal juxtaglomerular cells. To this end a primary cell culture from rat renal cortex was established that consisted of 50% juxtaglomerular cells. The cultured juxtaglomerular cells contained prominent renin granules closely resembling those in the intact kidney and responded to a number of stimuli of renin release. By using these cultures, we found that ANG II (10(-7) M), AVP (10(-6) M), and NE (10(-5) M) inhibited renin release and increased the calcium permeability of the plasma membrane of the cultured cells. Both the effects on renin release and on calcium permeability could be diminished or even be abolished by the calcium channel blocker verapamil (Vp) (10(-5) M). ANG II, AVP, and NE led to an increased formation of diacylglycerol (DAG), a well-known stimulator of protein kinase C (PKC). Moreover, a direct stimulation of PKC by 12-O-tetradecanoylphorbol-13-acetate (TPA) (10(-8)-10(-6) M) also inhibited renin release and increased the calcium permeability of the cell membrane. Similar to ANG II, AVP, and NE, the effects of TPA on calcium permeability and renin release could be diminished by Vp. In conclusion, these results point toward a common mechanism by which vasoconstrictors inhibit renin release from renal juxtaglomerular cells: ANG II, AVP, and NE activate a phospholipase C, which generates DAG.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

NaCl transport stimulates prostaglandin release in cultured renal epithelial (MDCK) cells.

Prostaglandins (PGs) can modulate a variety of renal functions, including Na+ and Cl- reabsorption. However, it is not known if a direct interdependence exists between PG synthesis and transport activity. The present study was done to find out whether or not the rate of NaCl transport has an influence on PG synthesis in renal tubular cells. For our studies we used cultures of so-called high-resistance MDCK cells, which were originally derived from canine kidney. This cell type has a loop diuretic- and ouabain-sensitive NaCl transport that can be enhanced by activation of the adenylate cyclase (AC). In MDCK cell cultures we found that each state of increased NaCl transport during stimulation of AC by either epinephrine (10(-6) M), isoprenaline (10(-5) M), or forskolin (10(-5) M) was accompanied by a twofold increase in PG release. During inhibition of NaCl transport by furosemide (10(-4) M) or ouabain (2 X 10(-4) M), stimulation of AC failed to increase PGE2 release, whereas basal PG production was not inhibited by either furosemide or ouabain. Furthermore, PG formation during activation of AC was dependent on the concentration of extracellular Na+, whereas PG formation in the absence of activators of AC was independent of extracellular Na+. These results suggest that increased NaCl transport stimulates PG formation in cultures of high-resistance MDCK cells.

Adenylyl Cyclases↗
PubMed1986

Erythropoietin production by fetal mouse liver cells in response to hypoxia and adenylate cyclase stimulation.

This study was done to investigate aspects of control of extrarenal erythropoietin (Ep) production. To this end we studied the effects of three stimuli of renal Ep production in the adult, i.e. hypoxia, cobalt, and activation of adenylate cyclase on Ep generation by cultured fetal mouse liver cells. The fetal liver was taken as a model for extrarenal Ep production because this organ is considered the predominant site of extrarenal Ep production. We found that Ep production by the cells increased as the oxygen concentration was decreased in the incubation atmosphere from 20% to 1%. Cobalt (10(-4)-10(-5) M) had no effect on Ep production. Activation of adenylate cyclase by forskolin (10(-5) M) or isoproterenol (10(-5) M) greatly enhanced Ep production. These findings indicate that the Ep-stimulating effect of cobalt is specific for the kidney. However, oxygen depletion and activation of adenylate cyclase seem to be more general stimuli in Ep-producing cells. Furthermore we found that Ep production in hypoxia correlated with lactate formation in the cultured liver cells. This finding suggests that Ep production in fetal livers under hypoxic conditions parallels the shift from aerobic to anaerobic cellular energy metabolism.

Adenylyl Cyclases↗
PubMed1986

Transmembrane signalling of atrial natriuretic peptide in rat renal juxtaglomerular cells.

Recently we have shown that atrial natriuretic peptide (ANP) inhibits renin release from isolated rat renal juxtaglomerular (JG) cells. ANP in general is thought to act on its target cells by the binding to specific membrane receptors. It is the objective of this contribution to summarize our present knowledge about the sequence of events by which the occupancy of ANP receptors could lead to an inhibition of renin release from juxtaglomerular (JG) cells. It was found that ANP did not affect the intracellular concentration of calcium. ANP led to a dose dependent increase in the intracellular concentration of cyclic GMP and to a dose dependent decrease of cAMPi. Inhibition of renin release from the JG-cells by ANP was clearly correlated to the level of cGMPi and not to the level of cAMPi. Concerning the mechanism by which ANP causes a rise in cGMPi in JG-cells it was found that the effect of ANP on cGMPi was potentiated by the cGMP phosphodiesterase specific inhibitor M & B 22,948. This finding suggests that ANP enhances cGMPi by the stimulation of a guanylate cyclase rather than by the inhibition of a cGMP phosphodiesterase. Moreover, evidence was obtained that the effect of ANP on cGMP, was markedly attenuated after pretreatment of the JG-cells with pertussis toxin. Since pertussis toxin is considered to inactivate guanine nucleotide binding proteins (G-proteins), this result could indicate that ANP receptors are coupled to a guanylate cyclase via a G-protein. Experimental evidence suggests that the G-protein in question might be the inhibitory unit (Ni) of the adenylate cyclase.

Animals↗
PubMed1986

Effect of synthetic atrial natriuretic peptide on rat renal juxtaglomerular cells.

We examined the effect of synthetic atrial natriuretic peptide (ANP) on unstimulated renin release from rat renal juxtaglomerular cells. Using renal cortical cell cultures containing 80-90% juxtaglomerular cells, we found that ANP strongly inhibited renin release from the cells in a dose-dependent fashion. Half-maximal inhibition was observed at 10(-11) mol/l ANP. Furthermore, ANP produced a rise in the intracellular concentration of cyclic guanosine monophosphate (cGMP) and a fall in the concentration of cyclic adenosine monophosphate (cAMP). Data indicated that the inhibition of renin release by ANP was related to the rise in cGMP and not to the fall of cAMP. Atrial natriuretic peptide (10(-10) mol/l) had no influence on the transmembrane calcium influx nor did it alter the intracellular calcium concentration of the juxtaglomerular cell. We found, however, that the inhibitory effect of ANP on renin release could be attenuated by the calcium channel blocker verapamil. Our results suggest that ANP inhibits renin release from juxtaglomerular cells by a mechanism that is mediated by cGMP; the mechanism is not linked to any alteration in intracellular calcium concentration but requires a normal level of calcium.

Animals↗