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Biomedical subjects

M Bek

Publications and source records attributed to M Bek.

10 recordsLinked to original sources
PubMed2001

Adrenergic and endothelin B receptor-dependent hypertension in dopamine receptor type-2 knockout mice.

Polymorphism of the dopamine receptor type-2 (D(2)) gene is associated with essential hypertension. To assess whether D(2) receptors participate in regulation of blood pressure (BP), we studied mice in which the D(2) receptor was disrupted. In anesthetized mice, systolic and diastolic BPs (in millimeters of mercury) were higher in D(2) homozygous and heterozygous mutant mice than in D(2)+/+ littermates. BP after alpha-adrenergic blockade decreased to a greater extent in D(2)-/- mice than in D(2)+/+ mice. Epinephrine excretion was greater in D(2)-/- mice than in D(2)+/+ mice, and acute adrenalectomy decreased BP to a similar level in D(2)-/- and D(2)+/+ mice. An endothelin B (ET[B]) receptor blocker for both ET(B1) and ET(B2) receptors decreased, whereas a selective ET(B1) blocker increased, BP in D(2)-/- mice but not D(2)+/+ mice. ET(B) receptor expression was greater in D(2)-/- mice than in D(2)+/+ mice. In contrast, blockade of ET(A) and V(1) vasopressin receptors had no effect on BP in either D(2)-/- or D(2)+/+ mice. The hypotensive effect of an AT(1) antagonist was also similar in D(2)-/- and D(2)+/+ mice. Basal Na(+),K(+)-ATPase activities in renal cortex and medulla were higher in D(2)+/+ mice than in D(2)-/- mice. Urine flow and sodium excretion were higher in D(2)-/- mice than in D(2)+/+ mice before and after acute saline loading. Thus, complete loss of the D(2) receptor results in hypertension that is not due to impairment of sodium excretion. Instead, enhanced vascular reactivity in the D(2) mutant mice may be caused by increased sympathetic and ET(B) receptor activities.

Adrenergic alpha-Antagonists↗
PubMed2000

Ultrafiltration profiling and measurement of relative blood volume as strategies to reduce hemodialysis-related side effects.

Hemodialysis (HD) side effects, such as hypotension and muscle cramps, may be related to excessive ultrafiltration (UF) in relation to refilling of fluids from the extravascular space, resulting in hemoconcentration and reduction of relative blood volume (RBV). This study examines the suitability of RBV measurements and UF modeling to reduce the incidence of dialysis side effects. We followed up 188 dialysis sessions in 53 patients. RBV and incidence of side effects were evaluated. Six treatment regimens were examined: UF profile 0, with a constant UF rate; UF profile 1, with a linear decreasing UF rate; UF profile 2, with a stepwise decreasing UF rate; and UF profiles 3 through 5, with intermittent high UF rates interrupted by UF pauses. During dialyses with a constant UF rate (UF profile 0), 10.6% of the treatments were associated with symptomatic hypotension. UF profiles 2 through 5, intermittently using high UF rates, caused a marked increase in hypotensive episodes (18.4%). In contrast, UF profile 1, providing a continuously decreasing UF rate, showed a reduced incidence of hypotension at only 5.7%. Symptomatic hypotension occurred in 13 of 53 patients during one or more dialysis sessions. With the help of RBV measurements, a subgroup of 8 patients with hypovolemia-induced hypotension could be identified. In these patients, an individual threshold of RBV could be defined, below which 92.3% of all hypotensive episodes occurred. In the remaining 5 hypotension-prone patients, there was no correlation between the occurrence of symptomatic hypotension and low RBV during HD treatments. In conclusion, UF profiles intermittently using high UF pulses cannot be recommended. RBV measurements help define a subgroup of patients at risk for hypovolemia-induced hypotension. Only these patients may benefit from blood volume-controlled UF. The incidence of symptomatic hypotension can likely be reduced if an individual threshold of RBV is avoided during HD treatments, eg, using lower UF rates in these patients.

Blood Volume↗
PubMed1999

Dopamine depolarizes podocytes via a D1-like receptor.

BACKGROUND: Dopamine influences glomerular haemodynamics and dopamine receptors have been demonstrated in the glomerulus, but little is known about the cellular effects of dopamine in glomerular cells. The aim of this study was to investigate the influence of dopamine on the cellular functions of podocytes. METHODS: The effect of dopamine on membrane voltage was investigated in differentiated mouse podocytes. The membrane voltage was measured using the patch clamp technique. Reverse transcribed-polymerase chain reaction (RT-PCR) studies were performed to investigate the expression of dopamine receptor mRNA in mouse glomeruli and podocytes. RESULTS: The addition of dopamine (100 nM-1000 microM) caused a concentration-dependent depolarization of podocytes (EC50 is approximate to 10 microM). Like dopamine, the selective agonist of the D1-like receptor, SKF 82958, depolarized podocytes in a concentration-dependent manner. (EC50 is approximate to 50 microM). SKF 82958 stimulated a time-and concentration-dependent accumulation of cyclic adenosine 3',5'-monophosphate (cAMP) in podocytes (EC50 is approximate to microM). RT-PCR studies with primers derived from mouse sequences amplified mouse mRNA for the D1-like and the D2-like receptor in glomeruli, which were obtained by the sieve technique, whereas only mRNA for the D1-like receptor was detected in cultured mouse podocytes. CONCLUSION: The data indicate that dopamine induces a cAMP-dependent depolarization via a D1-like receptor in podocytes.

Animals↗
PubMed1999

Characterization of prostanoid receptors in podocytes.

Prostaglandins participate in the regulation of important glomerular functions and are involved in the pathogenesis of glomerular diseases. This study investigates the influence of prostaglandins on membrane voltage, ion conductances, cAMP accumulation, and cytosolic calcium activity ([Ca2+]i) in differentiated podocytes. Prostaglandin E2 (PGE2) caused a concentration-dependent depolarization and an increase of the whole cell conductance in podocytes (EC50 approximately 50 nM). Compared with PGE2, the EP2/EP3/EP4 receptor agonist 11-deoxy-PGE1 caused an equipotent depolarization, whereas the DP receptor agonist BW 245 C, the EP1/EP3 receptor agonist sulprostone, and the IP receptor agonist iloprost were at least 100 to 1000 times less potent than PGE2. The EP2 receptor agonist butaprost did not change membrane voltage of podocytes. The depolarizing effect of PGE2 was increased in an extracellular solution with a reduced Cl- concentration (from 145 to 32 mM). PGE2 and the prostaglandin agonists, but not the IP receptor agonist iloprost and the EP2 receptor agonist butaprost, induced a time- and concentration-dependent cAMP accumulation in podocytes. In fura-2 fluorescence experiments, PGE2, sulprostone, PGF2alpha, fluprostenol (a potent FP agonist), and U-46619 (a selective thromboxane A2 agonist) induced a biphasic increase of [Ca2+]i in 60 to 80% of podocytes. In reverse transcription-PCR studies, podocyte mRNA for the EP1, EP4, FP, and TP receptor could be amplified. These data indicate that in podocytes, PGE2 regulates distinct cellular functions via the EP1 and EP4 receptor, thereby increasing [Ca2+]i and cAMP, respectively. Furthermore, PGF1alpha and U-46619 increase [Ca2+]i via their specific receptors.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Infection control and contaminated waste disposal practices in Southern Sydney Area Health Service Dental Clinics.

The sterilization and contaminated waste disposal practices in all 14 dental clinics operated by the Southern Sydney Area Health Service were surveyed. All of the clinics used autoclaves for sterilization. All hand instruments, handpieces and triplex syringes were autoclaved between patients. Chemical disinfection solutions were used in 12 of the 14 dental clinics, mainly for surface decontamination. Five dental clinics had separate storage areas for contaminated waste which compiled with contaminated waste separation and disposal guidelines. The practice of recapping needles with fingers and some inadequate washing facilities are areas that require particular attention.

Catchment Area, Health↗
PubMed1996

[Weil's disease and necrotizing herpes pneumonia as the cause of death of a 39-year-old sewage drain worker].

Acute leptospirosis in Europe (Weil's disease) is a rare and in more than 90% of the cases undiagnosed febrile, self-limited disease. We report the case of a 39-year-old sewerage worker, who was admitted to our hospital with fever, jaundice, pain in his calves and acute renal failure. Serology revealed elevated antibody titers against Leptospira canicola, L. icterhaemorrhagica and L. sejroe. The patient developed disseminated intravascular coagulation (DIC) with diffuse gastrointestinal bleeding due to thrombocytopenia. The ECG showed atrial fibrillation with irregularly irregular rhythm. Cardiac arrest developed, most likely due to hypoxia, with a drop in the blood pressure. Despite immediate resuscitation efforts the patient developed severe hypoxic brain damage and died a few days later. Autopsy disclosed histologic signs of a generalized leptospiral infection, signs of shock and within the lungs a necrotizing herpes simplex virus pneumonia causing the death of the patient. The virus pneumonia most probably was caused by retrograde canalicular dissemination of oral secretions since herpetic tracheitis and esophagitis were found and herpetic lesions were readily identified on the lips and tongue. A medical opinion asked for by the professional association having liability for occupational safety and insurance was given, the disease being recognized as an occupational disease.

Adult↗
PubMed1996

"On the spot' vaccination: does it work?

OBJECTIVE: To trial and evaluate a system of "on the spot' vaccination for children up to the age of 15 years in the Early Childhood Centres of the Central Sydney Area Health Service, at the Royal Alexandra Hospital for Children and in a number of general practices in the area. METHODOLOGY: A brief questionnaire was used to collect data from parents and health care professionals about the child's vaccination status and vaccines given "on the spot'. RESULTS: Over an 8 week period in August-September 1993, 5162 questionnaires were completed; 71% of children were up to date with their vaccination. If Haemophilus influenzae type b vaccine, which had been introduced only 2 months before commencement of the study, was excluded, 84% of the children were up to date. A total of 441 children were given 663 vaccinations "on the spot'. Very few children were too ill to be vaccinated (6%). However, only 30% of those who needed vaccination "on the spot' actually received it (441 of 1480), and only 41% (24 of 58) of a subset of those who were not vaccinated were known to have complied 1 month later. Children attending Early Childhood Centres were younger than children attending general practices or the hospital. CONCLUSIONS: A high proportion of children who attended for routine or acute health care had vaccinations overdue (30%). If this scheme could be continued and expanded it would have an important impact on vaccination coverage, and hence on the incidence of vaccine-preventable diseases.

Child↗
PubMed1995

Inhibition of nicotinic acetylcholine receptor channels in bovine adrenal chromaffin cells by Y3-type neuropeptide Y receptors via the adenylate cyclase/protein kinase A system.

The effect of neuropeptide Y [NPY(1-36)] and related peptides on the voltage-dependent currents and the nicotinic acetylcholine receptor (nAChR) currents (IACh) of bovine adrenal chromaffin cells was investigated using the whole-cell patch clamp technique. Catecholamine release from single chromaffin cells was measured by means of fast cyclic voltammetry. The potency order of these peptides in inhibiting IACh evoked by nicotine was NPY(1-36), NPY (16-36) > peptide YY(PYY) > [Leu31, Pro34]NPY. NPY(16-36) produced a similar degree of inhibition, irrespective of whether nicotine or an equipotent concentration of acetylcholine was used to evoke IACh. NPY(16-36) failed to alter voltage-dependent inward or outward currents. Intracellular cAMP, and extracellular dibutyryl-cAMP, produced a slowly developing increase in IACh. Intracellular cAMP, extracellular 8-Br-cAMP or dibutyryl-cAMP, and an inhibitor of cyclic nucleotide phosphodiesterases 3-isobutyl-1-methyl-xanthine (IBMX), decreased the inhibitory effect of NPY(16-36) on IACh. Although the intracellular application of the cAMP-dependent protein kinase A inhibitor [PKI(14-24)amide] alone did not alter IACh, it potentiated the effect of NPY(16-36) in interaction experiments. While the NPY(16-36)-induced inhibition of IACh was reversed on washout of the peptide, the slightly shorter C-terminal fragment NPY(18-36) caused a long-lasting depression of both IACh and catecholamine secretion evoked by nicotine. This depression was smaller in the presence of extracellular 8-Br-cAMP than in its absence. NPY(18-36) did not alter the secretory activity induced by a high concentration of potassium. It appears that, by activating Y3-receptors, NPY inhibits nAChR-current and the resulting secretion of catecholamines from bovine chromaffin cells. This process may involve a G protein-mediated decrease in intracellular cAMP with a subsequent decrease in the degree of phosphorylation of the nAChR-channel.

Acetylcholine↗