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Biomedical subjects

A Daul

Publications and source records attributed to A Daul.

36 records · Page 2Linked to original sources
PubMed1989

[Rapidly progressing glomerulonephritis. Spontaneous course and differential therapy with special reference to the infection-associated form].

Since 1971 we observed 31 patients with histologically proven rapidly progressive (crescentic) glomerulonephritis. At the onset of therapy 16 patients presented with end stage renal failure, the others with impaired renal function. 21 patients received combined immunosuppressive therapy, consisting of prednisone, cyclophosphamide and azathioprine. 8 patients were treated with membrane plasmapheresis, additionally. 10 patients received no specific therapy. After 5 years 13 patients were on hemodialysis, 4 had impaired renal function and 10 patients were dead. Two patients died due to the progression of underlying diseases, the others were lost following infectious diseases. There was no additional positive effect in the group treated with membrane plasma separation compared with patients treated only immunosuppressive. Only in 4 patients without specific therapy normalization of renal function occurred. In these patients RPGN appeared after an infectious disease. We conclude that an infectious disease associated RPGN is an own entity of glomerulonephritis that has a very good prognosis and needs only antibiotic therapy.

Adult↗
PubMed1988

Are alpha- and beta-adrenoceptor changes in patients with essential hypertension genetically determined?

In order to find out whether adrenoceptor changes in essential hypertension might be genetically determined, we measured platelet alpha 2- and lymphocyte beta 2-adrenoceptor density in 48 normotensive children with normotensive parents, and 41 normotensive children who had one essential hypertensive parent and thus should have had a genetic predisposition for the development of hypertension. The groups did not differ with regard to blood pressure and heart rate, age, body weight and height, plasma renin activity and catecholamines, and serum electrolytes and creatinine. Lymphocyte beta 2-adrenoceptor density (assessed by 125I-iodocyanopindolol binding) and responsiveness (assessed as 10 mumol/l isoprenaline-induced cyclic AMP increases) did not differ between the groups. Platelet alpha 2-adrenoceptor density (assessed by 3H-yohimbine binding) was significantly higher in children with one essential hypertensive parent. We conclude that platelet alpha 2- but not lymphocyte beta 2-adrenoceptor changes in essential hypertension are genetically determined.

Blood Platelets↗
PubMed1988

Differentiation of beta 1- and beta 2-adrenoceptor-mediated effects in humans.

To differentiate beta 1- and beta 2-adrenoceptor-mediated effects in humans, we studied the effects of a 2-wk treatment of 12 male volunteers with the selective beta 1-adrenoceptor antagonist bisoprolol (1 x 10 mg/day) and the beta 2-selective antagonist ICI 118,551 (3 x 25 mg/day) on lymphocyte beta 2-adrenoceptor density and responsiveness [10 microM l-isoproterenol (IPN) evoked adenosine 3',5'-cyclic monophosphate (cAMP) increase] as well as on exercise- and IPN-induced changes in lymphocyte beta 2-adrenoceptor density, blood pressure, heart rate, and plasma norepinephrine levels. ICI 118,551 administration increased lymphocyte beta 2-adrenoceptor density and responsiveness by approximately 50%, whereas bisoprolol had no effect. Dynamic exercise on a bicycle and infusion of graded doses of IPN led to an approximately 100% increase in lymphocyte beta 2-adrenoceptor density; this was abolished by ICI 118,551 but not affected by bisoprolol. ICI 118,551 markedly attenuated IPN-induced decrease in diastolic blood pressure but did not affect increase in systolic blood pressure, whereas bisoprolol had opposite effects. The IPN-induced increase in heart rate, however, was antagonized by both bisoprolol and (to a greater extent) ICI 118,551. Finally, ICI 118,551 completely abolished the IPN-induced increase in plasma norepinephrine levels, whereas bisoprolol had no effect. These results indicate that bisoprolol and ICI 118,551 are suitable tools to differentiate in humans beta 1- and beta 2-adrenoceptor-mediated effects.

Adult↗
PubMed1988

Plasma exchange and immunosuppression in rapidly progressive glomerulonephritis: a controlled, multi-center study.

In a randomized study of 26 patients with histologically confirmed rapidly progressive crescentic glomerulonephritis, 12 patients were treated with immunosuppressants alone (corticosteroids, cyclophosphamide and azathioprine) while the other 14 patients received not only the identical immunosuppressive treatment but also plasma exchange therapy for four weeks. No statistically significant difference was found between the two groups. After 8 weeks, 73% and 69% of the patients in each respective group showed recompensation of renal function; serum creatinine fell from initially 7.0 and 6.2 mg/dl mean to 2.7 and 2.3 mg/dl mean, and under continued immunosuppression did not rise in the following months. Thus, in non-autoantibody induced rapidly progressive glomerulonephritis, kidney function could be improved substantially by immunosuppressive therapy, but an advantage of supplementary plasma exchange could not be shown.

Adult↗
PubMed1986

Beta-adrenoceptor antagonists (non-selective as well as beta 1-selective) with partial agonistic activity decrease beta 2-adrenoceptor density in human lymphocytes. Evidence for a beta 2-agonistic component of the partial agonistic activity.

In the present study the effects of pindolol [non-selective beta-adrenoceptor antagonist with strong partial agonistic activity (PAA)] on beta 2-adrenoceptor density in lymphocytes (assessed by (-)-[125I]iodocyanopindolol (ICYP) binding) were compared with those of the beta 1-selective antagonists celiprolol (with PAA) and bisoprolol (no PAA) in normotensive young volunteers to get further insights into the nature of PAA. Administration of pindolol (2 X 5 mg/day) caused an about 25% decrease in lymphocyte beta 2-adrenoceptor density after 2 days; during treatment beta 2-adrenoceptor density declined further (maximum decrease after 7 days: 50%). After withdrawal of pindolol lymphocyte beta 2-adrenoceptor density recovered very slowly being still after 4 days significantly reduced, although no pindolol was detectable in plasma after 36 h. The KD-values for ICYP, however, did not change during or after pindolol treatment. The decrease in lymphocyte beta 2-adrenoceptor density induced by pindolol could be completely prevented by simultaneous administration of propranolol (3 X 40 mg/day) indicating that the PAA of pindolol is the cause of its beta-adrenoceptor decreasing effect. Administration of the non-selective beta-adrenoceptor antagonist bopindolol (1 X 2 mg/day) with PAA caused decreases in lymphocyte beta 2-adrenoceptor density (maximum decrease after 7 days: 40%); concomitantly the 10 mumol/l (-)-isoprenaline evoked increases in the intracellular level of lymphocyte cyclic AMP were attenuated to a similar extent indicating that the beta-adrenoceptor antagonist-induced decrease in beta-adrenoceptor density is accompanied by a loss in beta-adrenoceptor function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1986

Effect of propranolol, alprenolol, pindolol, and bopindolol on beta 2-adrenoceptor density in human lymphocytes.

Abrupt withdrawal of beta-adrenoceptor antagonists may lead to "rebound effects." To investigate the position of the new nonselective beta-adrenoceptor antagonist bopindolol [with moderate intrinsic sympathomimetic activity (ISA)], this drug was compared with propranolol (no ISA), alprenolol (weak ISA), and pindolol (marked ISA). The effects on lymphocyte beta 2-adrenoceptor density--assessed by (+/-)-[125I]iodocyanopindolol (ICYP) binding--were investigated in healthy volunteers aged 23-35 years. None of the test drugs changed the affinity of ICYP for beta 2 adrenoceptors. Propranolol treatment (4 X 40 mg/day) increased the density of beta 2-adrenoceptors by 25% after 2 days; during treatment beta 2-adrenoceptor density remained elevated. After withdrawal of propranolol, beta 2-adrenoceptor density declined slowly, being still significantly increased after 3 days, although propranolol was not detectable in plasma after 24 h, though heart rate was significantly increased. Alprenolol treatment (4 X 100 mg/day) did not significantly affect beta 2-adrenoceptor density. Pindolol treatment (2 X 5 mg/day) caused a 50% decrease of beta 2-adrenoceptor density after 2 days, which remained reduced during treatment. After withdrawal, beta 2-adrenoceptor density was still significantly diminished after 4 days. During and after treatment heart rate was not affected. Bopindolol treatment (2 mg/day) caused a 40% decrease of beta 2-adrenoceptor density after 2 days, which remained reduced during treatment. After withdrawal, beta 2-adrenoceptor density was still significantly diminished after 4 days. During and after treatment heart rate was not affected. It is concluded that the ISA may play an important role in modulating beta 2-adrenoceptor density and hence tissue responsiveness to beta-adrenoceptor stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Differential changes in lymphocyte beta 2-adrenoceptor density by beta-blocker administration: role of intrinsic sympathomimetic activity.

To study the role of intrinsic sympathomimetic activity (ISA) in beta-blocker-induced changes of beta-adrenoceptors, the effects of administration of several beta-blockers for 9 days on lymphocyte beta 2-adrenoceptor density--assessed by 125iodocyanopindolol binding--were investigated in 47 normotensive volunteers. Propranolol (unselective; no ISA; 4 X 40 mg/day) increased beta 2-adrenoceptor density by 25-40%; after withdrawal beta 2-adrenoceptor density declined slowly, being still elevated for 3 days. In contrast, the unselective beta-blockers pindolol (ISA (isoprenaline = 1.0) = 0.39; 2 X 5 mg/day) and mepindolol (ISA = 0.27; 2 X 5 mg/day) decreased beta 2-adrenoceptor density by 50% and 35%, respectively, while alprenolol with weak ISA (=0.066; 4 X 100 mg/day) had no effect. Among the beta 1-selective blockers studied, celiprolol with ISA (=0.32; 1 X 200 mg/day) decreased beta 2-adrenoceptor density by 30% whereas bisoprolol without ISA (1 X 10 mg/day) had no effect. It is concluded that the ISA determines the direction and amount of beta-adrenoceptor alterations induced by beta-blockers. Furthermore, changes in human lymphocyte beta-adrenoceptors reflect subtype-selective changes in beta 2-adrenoceptors, since the beta 1-selective blocker bisoprolol without ISA--in contrast to propranolol--did not affect lymphocyte beta 2-adrenoceptors. Accordingly, the fact that the beta 1-selective blocker celiprolol with ISA decreased lymphocyte beta 2-adrenoceptors, is consistent with the hypothesis that celiprolol possesses in addition to its beta 1-antagonistic activity a beta 2-agonistic activity.

Adrenergic beta-Antagonists↗
PubMed1986

Differential haemodynamic effects induced by beta 1-(bisoprolol) or beta 2-(ICI 118,551) adrenoceptor blockade in man.

To characterize beta 1- and beta 2-adrenoceptor mediated effects in man the influence of the selective beta 1-adrenoceptor antagonist bisoprolol and the selective beta 2-adrenoceptor antagonist ICI 118,551 on changes in blood pressure, heart rate and lymphocyte beta 2-adrenoceptor density evoked by dynamic exercise or isoprenaline infusion was studied in 12 male normotensive volunteers. Bisoprolol administration (1 X 10 mg/day) did not affect lymphocyte beta 2-adrenoceptor density, while ICI 118,551 (3 X 25 mg/day) increased it by about 40%. Exercise as well as isoprenaline infusion caused 100% increases in lymphocyte beta 2-adrenoceptor density; these increases were completely abolished by ICI 118,551, but not affected by bisoprolol. ICI 118,551 markedly attenuated isoprenaline-induced decrease in diastolic blood pressure, but did not affect increase in systolic blood pressure; on the contrary, bisoprolol inhibited the isoprenaline-evoked increase in systolic blood pressure, but did not affect the decrease in diastolic blood pressure. ICI 118,551 antagonized the isoprenaline-induced tachycardia much more potently than bisoprolol, while bisoprolol, but not ICI 118,551, suppressed exercise-induced tachycardia. It is concluded that exercise-induced tachycardia is mediated by cardiac beta 1-adrenoceptor stimulation, whereas isoprenaline-induced tachycardia is mediated by both beta 1- and beta 2-adrenoceptor stimulation.

Adrenergic beta-Antagonists↗
PubMed1985

Effects of beta-adrenoceptor antagonist administration on beta 2-adrenoceptor density in human lymphocytes. The role of the "intrinsic sympathomimetic activity".

Abrupt withdrawal of beta-adrenoceptor antagonists may lead to "rebound-effects". To study the mechanism underlying this phenomenon, the effects of the nonselective beta-adrenoceptor antagonists propranolol [no intrinsic sympathomimetic activity (ISA)], alprenolol (weak ISA) and mepindolol (strong ISA) on lymphocyte beta 2-adrenoceptor density--assessed by (+/-)-[125I]-iodocyanopindolol (ICYP) binding--and plasma renin activity (PRA) were investigated in male healthy volunteers aged 23-35 years. Propranolol treatment (4 X 40 mg/day) increased the density of beta 2-adrenoceptors by 25% after 2 days; concomitantly PRA and heart rate were reduced. During treatment beta 2-adrenoceptor density remained elevated. After withdrawal of propranolol PRA reached pre-drug levels rapidly, while heart rate was significantly enhanced. Beta 2-Adrenoceptor density, however, declined slowly being still significantly increased after 3 days, although propranolol was not detectable in plasma after 24 h. The affinity of ICYP to beta 2-adrenoceptors was not changed during or after treatment. Mepindolol treatment (2 X 5 mg/day) caused a 30% decrease of beta 2-adrenoceptor density and PRA after 2 days; both parameters remained reduced during treatment. After withdrawal, PRA reached rapidly pre-drug levels, whereas beta 2-adrenoceptor density was still after 4 days significantly diminished. The KD-values for ICYP, however, were not changed. During and after treatment heart rate was not affected. Alprenolol treatment (4 X 100 mg/day) led to a rapid fall in PRA, but did not significantly affect beta 2-adrenoceptor density. It is concluded, that the ISA may play an important role in modulating beta 2-adrenoceptor density and hence tissue responsiveness to beta-adrenoceptor stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1985

Terbutaline-induced desensitization of human lymphocyte beta 2-adrenoceptors. Accelerated restoration of beta-adrenoceptor responsiveness by prednisone and ketotifen.

We investigated, in 36 healthy volunteers, the effects of prednisone and ketotifen on recovery of lymphocyte beta 2-adrenoceptor density (determined by (-)-125iodocyanopindolol binding) and responsiveness (assessed by lymphocyte cyclic AMP [cAMP] responses to 10 microM (-)-isoprenaline) after desensitization by the beta 2-agonist terbutaline. Terbutaline (3 X 5 mg/d) decreased lymphocyte beta 2-adrenoceptor density by approximately 40-50%; concomitantly, lymphocyte cAMP responses to 10 microM (-)-isoprenaline were significantly reduced. After withdrawal of terbutaline beta 2-adrenoceptor, density and responsiveness gradually increased, reaching predrug levels after 4 d. Prednisone (1 X 100 mg orally) accelerated beta 2-adrenoceptor recovery; only 8-10 h after administration of the steroid beta 2-adrenoceptor density and cAMP responses to (-)-isoprenaline had reached values not significantly different from pretreatment levels. Similar effects were obtained with ketotifen (2 mg; thereafter 2 X 1 mg/d for 4 d): 24 h after application of the drug beta 2-adrenoceptor density and cAMP responses to (-)-isoprenaline had reached pretreatment levels. Furthermore, ketotifen simultaneously applied with terbutaline completely prevented terbutaline-induced decrease in lymphocyte beta 2-adrenoceptor density and responsiveness. Prednisone (1 X 100 mg orally) or ketotifen (2 mg; thereafter 2 X 1 mg/d for 2 d) had no significant influence on lymphocyte beta 2-adrenoceptor density in healthy volunteers not pretreated with terbutaline, but shifted the ratio high-to-low affinity state of the lymphocyte beta 2-adrenoceptor toward high affinity state. We conclude that glucocorticoids as well as ketotifen can accelerate recovery of density and responsiveness of lymphocyte beta 2-adrenoceptors desensitized by long-term treatment with beta 2-agonists. Such an effect may have clinical implications for preventing tachyphylaxis of asthmatic patients against therapy with beta 2-agonists.

Adult↗
PubMed1985

Alpha- and beta-adrenoceptors in circulating blood cells of essential hypertensive patients: increased receptor density and responsiveness.

In 40 male patients with established essential hypertension (P diast greater than 95 mmHg) platelet alpha 2-adrenoceptor density (by 3H-yohimbine binding) and -responsiveness (by adrenaline-induced aggregation) as well as lymphocyte beta 2-adrenoceptor density (by (+/-)-125 iodocyanopindolol binding) and -responsiveness (by cyclic AMP responses to isoprenaline) were determined and compared with those in 40 male age-matched normotensives (P diast less than 90 mmHg). In essential hypertensive patients mean platelet alpha 2- and lymphocyte beta 2-adrenoceptor densities were significantly increased. When data from all 80 subjects were combined, significant positive correlations between mean arterial blood pressure and alpha 2- and beta 2-adrenoceptor densities, respectively, were found. The increases in alpha 2- and beta 2-adrenoceptor densities were accompanied by enhanced responsiveness to adrenergic stimulation: in platelets adrenaline-induced aggregation--via alpha 2-adrenoceptor stimulation--was exaggerated, and in lymphocytes isoprenaline produced significantly greater increases in the intracellular level of cyclic AMP. It is concluded that the increased density and responsiveness of alpha 2-and beta 2-adrenoceptors in circulating blood cells of essential hypertensive patients may reflect increased sympathetic activity, which might contribute to the elevation of blood pressure.

Adenylyl Cyclases↗
PubMed1984

Beta-adrenoceptor changes in human lymphocytes, induced by dynamic exercise.

In 10 healthy volunteers the effects of acute increases in concentrations of catecholamines in plasma induced by dynamic exercise (on a bicycle for 15 min at 80% of maximum heart rate) on lymphocyte beta 2-adrenoceptor density (determined by (+/-)-125iodocyanopindolol binding) and -responsiveness (determined by cyclic AMP responses to 10 mumol/l isoprenaline) were investigated. Immediately after exercise plasma catecholamines were increased about 4-fold; concomitantly receptor density and cyclic AMP production increased 55% and 65%, respectively. One hour after exercise beta-adrenoceptor density and plasma catecholamines had reached values, which were not significantly different from pre-exercise values, while cyclic AMP production was significantly diminished. It is concluded, that acute increases in concentrations of catecholamines in plasma may increase beta-adrenoceptor density and - responsiveness in human lymphocytes.

Adult↗
PubMed1984

Increased density and responsiveness of alpha 2 and beta-adrenoceptors in circulating blood cells of essential hypertensive patients.

In 40 male patients with established essential hypertension (P diastolic greater than mmHg) the density and responsiveness of platelet alpha 2-adrenoceptors and lymphocyte beta 2-adrenoceptors were measured and compared with those in 40 male age-matched normotensive subjects (P diastolic less than 90 mmHg). The mean densities of platelet alpha 2-adrenoceptors (assessed by 3H-yohimbine binding) and of lymphocyte beta 2-adrenoceptors (assessed by (+/-) 125 iodocyanopindolol binding) were significantly increased in essential hypertensive patients (P less than 0.01). If data from all 80 subjects were combined there were significant positive correlations between mean arterial blood pressure of the subjects and alpha 2-adrenoceptor density (r = 0.591, P less than 0.001) and beta 2-adrenoceptor density (r = 0.648, P less than 0.001), respectively. The increases in and beta-adrenoceptor densities in essential hypertension were accompanied by enhanced responsiveness alpha- of platelets to 10 microM adrenaline to adrenergic stimulation: the aggregatory response via alpha 2-adrenoceptor stimulation) was increased, and in lymphocytes isoprenaline (0.01 - 100 microM) produced (via adrenoceptor stimulation) greater increases in cyclic AMP at each concentration than in control. Furthermore, activation of platelet adenylate cyclase by prostaglandin E1 was exaggerated in essential hypertensive patients. It is concluded that the increased density and responsiveness of alpha- and beta-adrenoceptors in essential hypertension may reflect enhanced sympathetic activity, and may contribute to the elevation of blood pressure.

Adolescent↗
PubMed1983

Decreased number of alpha-adrenergic receptors in platelets of patients on maintenance haemodialysis.

In patients on maintenance haemodialysis the number of platelet alpha 2-adrenergic receptors, as assessed by 3H-yohimbine binding, was significantly lower than that in healthy volunteers. Responses to alpha 1-adrenergic receptor stimulation, determined by increases in systolic blood pressure produced by intravenous injections of phenylephrine, were also diminished in chronic haemodialysis patients. Thus, reduced sympathetic activity often observed during chronic haemodialysis treatment may be due to reduced number and/or sensitivity of alpha 1- and alpha 2-adrenergic receptors.

Adult↗
PubMedDate not supplied

Correlation between lymphocyte beta 2-adrenoceptor density and mean arterial blood pressure: elevated beta-adrenoceptors in essential hypertension.

In 41 normotensive volunteers (diastolic pressure, less than 90 mm Hg) the beta 2-adrenoceptor density in lymphocytes was determined by (+/-)-125 iodocyanopindolol (ICYP) binding and compared with that in nine patients with borderline hypertension (diastolic pressure, 90-95 mm Hg) and 45 patients with established essential hypertension (diastolic pressure, greater than 95 mm Hg). The mean number of beta 2-adrenoceptors for controls was 774 +/- 49 (range, 300-1,500) ICYP binding sites/cell. In borderline hypertension it was significantly higher, with 1,037 +/- 22 (range, 950-1,150) sites/cell, and increased further in patients with essential hypertension to 1,424 +/- 72 (range, 700-2,700) sites/cell. The KD values for ICYP, however, were nearly the same in all groups (approximately 50 pM). Calculation of the data of all 95 subjects resulted in a significant positive correlation between beta 2-adrenoceptor density and mean arterial blood pressure (r = 0.637; p less than 0.001). Since the properties of beta 2-adrenoceptors in human lymphocytes resemble those in other tissues, the hypothesis is presented that the increased density of beta 2-adrenoceptors may reflect sympathetic hyperactivity in essential hypertension, which might contribute (perhaps via enhanced release of endogenous noradrenaline through stimulation of presynaptic beta 2-adrenoceptors by adrenaline) to the elevation of blood pressure.

Adult↗