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At least 1,135 records · Page 63Linked to original sources
PubMed1989

Enhanced presynaptic beta 2-adrenoceptor-mediated facilitation of the pressor responses in the prehypertensive SHR.

The effects of beta-adrenoceptor agonists and antagonists on pressor responses of the isolated perfused mesenteric arteries to periarterial nerve stimulation (PNS) in the prehypertensive 4-week-old spontaneously hypertensive rat (SHR) and the age-matched Wistar Kyoto rats (WKY) were examined. The systolic arterial blood pressure (SBP) of SHR and WKY were not significantly different at this young age. The pressor responses of the mesenteric arteries to PNS at various stimulating frequencies, however, were significantly greater in SHR than WKY. Cocaine, isoproterenol (a nonselective beta-adrenoceptor agonist) and salbutamol (a selective beta 2-adrenoceptor agonist) significantly enhanced the pressor responses to PNS in SHR and WKY, with significantly greater increase in SHR than WKY. The nonselective beta-adrenoceptor antagonist (propranolol) and the selective beta 2-adrenoceptor antagonist (ICI 118,551) significantly inhibited the pressor response to PNS in SHR without affecting that in WKY. The selective beta 1-adrenoceptor antagonist (practolol) was without effect on the PNS-induced pressor responses in both SHR and WKY. These results demonstrate that the presynaptic beta 2-adrenoceptor-mediated facilitation of neurogenic pressor response in mesenteric arteries already are enhanced in 4-week-old SHR. In view of the higher concentration of circulating epinephrine (Epi) in prehypertensive SHR, the enhanced facilitatory modulation via presynaptic beta 2-adrenoceptors in prehypertensive SHR may be involved in development of hypertension.

Animals↗
PubMed1979

Labetalol-induced Peyronie's disease? A case report.

Peyronie's disease (induratio penis plastica) has been observed in a 58-year-old man 8 months after initiation of treatment with the new combined alpha- and beta-blocking agent, labetalol. During the last 2 months before onset of symptoms he had received 2400 mg labetalol daily. He showed no other signs of abnormal fibrous tissue production and the ANF test was negative. Cessation of the drug revealed no improvement. Peyronie's disease has also been observed in relation to treatment with propranolol, practolol and metoprolol and might be due to an impaired balance between alpha- and beta-receptors in connective tissue, but there may also be an immunological basis for the fibrosis. A possible coincidence is stressed, as the ages of the reported cases are within the range where this disease most often develops.

Ethanolamines↗
PubMed1975

Isoprenaline antagonism of cardioselective beta-adrenergic receptor blocking agents on human and rat adipocytes.

1. The beta-adrenergic blocking potencies of practolol, ICI 66082, tolamolol, acebutolol, H 93/26, H 87/07, pindolol and Ro 3-4787 were compared with that of propranolol, on human and rat adipocytes. 2. A good correlation was found between the potencies on adipocytes of the two species but not between our results and literature data on antagonism of isopernaline tachycardia in the anaesthetized cat. 3. The results indicate that differences between adrenergic beta-receptors in heart and adipose tissue may be detected using cardioselective beta-adrenergic receptor blocking agents.

Adipose Tissue↗
PubMed1981

Influence of environmental temperature and humidity on bronchial responses during assessment of selectivity of beta-adrenoceptor antagonists in man.

1 The effects of beta-adrenoceptor antagonists given intravenously in single doses were examined in a double-blind, placebo controlled study performed in six healthy volunteers. Heart rate and peak expiratory flow rate (PEFR) were measured at rest and during standardised exercise. 2 Atenolol 0.2 mg/kg, betaxolol 0.15 mg/kg, practolol 1 mg/kg and propranolol 0.2 mg/kg all reduced heart rate to a similar extent during exercise at 2 and 4 h after administration; betaxolol 0.6 mg/kg had a significantly greater effect than the other treatments at all times. Only betaxolol 0.15 and 0.6 mg/kg significantly inhibited exercise tachycardia at 24 h. 3 None of the treatments studied had any effect on PEFR at rest or during exercise. 4 A second study was performed to determine whether this lack of effect of propranolol on exercise PEFR could have been due to the warm and humid conditions prevailing during the experiment. Eight healthy men underwent a standardised exercise test under alternately 'warm and humid' and 'cool and dry' conditions before and after propranolol 0.2 mg/kg or saline placebo intravenously. 5 Propranolol treatment did not influence resting or exercise PEFR in either environment, but did reduce FEV1 immediately after exercise under the cool and dry conditions but not under the warm and humid conditions. 6 Comparison of the effects of beta-adrenoceptor antagonists on exercise heart rate and PEFR is not a reliable or sensitive method of measuring the cardioselectivity of these drugs. 7 Environmental temperature and humidity should ideally be controlled when the action of any drug on airflow resistance is being studied.

Adrenergic beta-Antagonists↗
PubMed1982

Beta-adrenoceptor blockade and atrio-ventricular conduction in dogs. Role of intrinsic sympathomimetic activity.

1 Atrio-ventricular conduction and its modifications induced by six beta-adrenoceptor blocking agents and isoprenaline have been investigated in the anaesthetized dog using the extrastimulus technique and measuring atrial (AERP), nodal (NERP), global (GERP) effective refractory periods as well as global functional refractory period (GFRP). 2 When beta-adrenoceptor blockade was produced by (+/-)-propranolol (beta 1 + beta 2-adrenoceptor blockade) which is devoid of intrinsic sympathomimetic activity (ISA) but has membrane stabilizing effects (MSE), sotalol (beta 1 + beta 2-adrenoceptor blockade, no ISA, no MSE) and atenolol (beta 1-adrenoceptor blockade, no ISA, no MSE), all parameters were significantly increased. When beta-adrenoceptor blockade was achieved with pindolol (beta 1 + beta 2-adrenoceptor blockade) and practolol (beta 1-adrenoceptor blockade) which have ISA but no MSE, all parameters remained unchanged, as was also the case with (+)-propranolol, which has MSE but neither ISA nor beta-adrenolytic properties. 3 Isoprenaline at high doses significantly reduced the refractory periods but when infusion was stopped, marked but reversible conduction depression was observed. 4 It thus appears that beta-adrenoceptor blockade but not MSE is responsible for the onset of atrial and AV-conduction impairment and that ISA affords protection against this impairment.

Adrenergic beta-Antagonists↗
PubMed1977

Factor-VIII activity and antigen, platelet count and biochemical changes after adrenoceptor stimulation.

Adrenaline, isoprenaline and salbutamol were administered by intravenous infusion to human subjects. Isoprenaline was covered with practolol in an attempt to reduce the unpleasantness of the circulatory effects. Changes were recorded in pulse rate and blood pressure, and in blood levels of factors V, VIII, X, XI, and XII, platelet count, lactate, pyruvate, potassium and free fatty acids. Factor VIII was studied by clotting assays, by reactions with two rabbit antisera and two human antibodies, and by desulphated agarose chromatography. At the rate at which they were adiminstered, all three drugs increased the pulse rate by 20-40 beats/min. Factor VIII rose c. 2.5 X with adrenaline but only c. 1.5 X with isoprenaline and salbutamol; but other clotting factors did not alter. Chromatography provided no evidence of a change in the size of the molecule carrying factor-VIII clotting activity. The rate of clearance of the heightened plasma activity could not be shown to differ from that of "ordinary" factor VIII infused into haemophiliacs. The platelet count rose after adrenaline, fell after salbutamol and did not change significantly after isoprenaline. Among the biochemical responses, the only significant difference between the drugs was that lactate rose after adrenaline and salbutamol but did not change after isoprenaline. The rise in factor-VIII clotting activity after adrenaline is considered to represent a real increase in blood concentration, presumably by release of additional factor VIII from stores. The evidence suggests that this could be classified as a beta2 effect; and that the quantity which can be released is unrelated to the current plasma level. The rise in platelet count produced by adrenaline may be the resultant of an alpha-mediated rise due to contraction of the exchangeable splenic pool and a beta2-mediated fall, the alpha effect predominating.

Adult↗
PubMed1984

Beta-adrenergic regulation of cyclic adenosine 3',5' monophosphate accumulation in human gastric epithelial glands. Inhibitory effect of somatostatin.

The action of catecholamines and somatostatin on cyclic adenosine 3',5' monophosphate (cyclic AMP) formation in human isolated gastric glands is reported. We show that: (1) there is a beta 2 receptor-mediated stimulation of cyclic AMP production in fundus. Catecholamines act with the order of potencies isoproterenol (ED50 = 50 nmol 1(-1) greater than epinephrine (ED50 = 0.1 mumol 1(-1] greater than norepinephrine (ED50 = 5 mumol 1(-1]. Their action is completely reversed by propranolol at doses 10(3) times lower than practolol, while unaffected by phentolamine; (2) isoproterenol and Vasoactive Intestinal Peptide (VIP) have additive effects on cyclic AMP in fundic glands whereas no additivity is observed between histamine and isoproterenol; this, together with the absence of catecholamine effect in antral glands, suggests that the beta 2 receptor is located on parietal cells; (3) somatostatin (1 mumol 1(-1] non-competitively inhibits the stimulation by catecholamines but does not affect VIP and histamine stimulations. These results suggest a physiological stimulatory effect of catecholamines on gastric acid secretion in man, through a beta 2 receptor coupled to the cyclic AMP system, regulated by somatostatin.

Catecholamines↗
PubMedDate not supplied

Beta-adrenoreceptors in denervated skeletal muscles of the cat.

1. A number of sympathomimetic amines have been compared with (-)-isoprenaline for their ability to produce contractions in chronically denervated soleus and tibialis anterior muscles and to increase heart rate in bilaterally vagotomized anaesthetized cats. 2. The mean dose-ratios ((-)-isoprenaline equals 1) for adrenaline, orciprenaline and salbutamol were 2.9, 29.7 and 11.5 respectively in the tibialis anterior muscle and 3.5, 24.1 and 14.3 in the soleus muscle. The dose-ratios for noradrenaline were 21.1 in the tibialis anterior and 57.6 in the soleus muscle. 3. The dose-ratios ((-)-isoprenaline equals 1) obtained for the positive chronotropic effects of the drugs in bilaterally vagotomized cats were 14.5, 14.6, 29.6 and 24.2 for adrenaline, noradrenaline, orciprenaline and salbutamol respectively. 4. The beta2-receptor antagonists butoxamine and H35/25 antagonized the vasodepressor and skeletal muscle responses to (-)-isoprenaline to a greater extent than the cardiac responses, whereas the beta1-receptor selective antagonists practolol and H93/26 antagonized cardiac to a greater extent than vascular and skeletal muscle responses. 5. The results obtained suggest that the contractions of denervated skeletal muscle to sympathomimetic drugs result from stimulation of beta2-adrenoreceptors.

Adrenergic beta-Agonists↗
PubMedDate not supplied

The inhibitory response of the rabbit anococcygeus muscle.

1. Strips of rabbit anococcygeus muscle were submaximally contracted by the addition of phenylephrine to the bath fluid. 2. Acetylcholine, dimethylphenylpiperazinium and electrical field stimulation caused relaxation. Relaxation induced by acetylcholine and field stimulation was blocked by tetrodotoxin but only the acetylcholine-induced response was inhibited by lignocaine, tetraethylammonium and hexamethonium. The responses to both acetylcholine and field stimulation were resistant to atropine, practolol, and sotalol. 3. Relatively high concentrations of ATP caused relaxation. 4. Histological investigation did not show any cells resembling autonomic ganglion cells. 5. It is suggested that both acetylcholine and field stimulation release an inhibitory transmitter from nerve endings and that the release by acetylcholine is mediated through nicotinic receptor stimulation.

Acetylcholine↗
PubMedDate not supplied

Adrenergic factors influencing the mitotic rate in stratified squamous epithelium of the buccal mucosa of the rat.

1. An in vivo stathmokinetic technique was used to determine the immediate effect of various adrenoceptor agonists and antagonists on the mitotic rate in the stratified squamous epithelium of the rat buccal mucosa. 2. The mitotic rate increased significantly in rats treated with propranolol and with practolol, whereas the mitotic rate decreased significantly in rats treated with metaraminol. In animals treated with isoprenaline and phentolamine the mitotic rate did not differ significantly from the control value. 3. The nature of the involvement of adrenergic mechanisms with cell proliferation is still uncertain but both alpha- and beta-adrenergic mechanisms appear to be associated with the control of cell proliferation.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Peripheral muscle effects of levodopa in the anesthetized cat.

1. Levodopa, dopamine, noraderanaline and adrenaline (in increasing order of potency) depressed the tension and degree of fusion of incomplete tetanic contractions of the slow-contracting soleus muscle in chloralose-anaesthetized cats. 2. The effects of all compounds were antagonized by propranolol (50-20 microgram/kg), but not practolol (1.0-5.0 mg/kg). This indicates that effects are mediated by beta2-adrenoceptor stimulation. 3. The effect of levodopa, but not of the catecholamines, was antagonized by prior administration of the dopa decarboxylase inhibitior benserazide. This indicates that levodopa itself is inactive, whereas its decarbodylated metabolites are active. 4. The depressant action of beta-adrenoceptor agonists on incomplete tetanic contractions of the cat soleus muscle, which are exerted directly on the muscle fibres, is a model for effects exerted on slow-contracting units of human muscles; the latter effects probably underlie the tremor observed after beta-adrenoceptor agonist administration. 5. These results therefore suggest that levodopa, via its decarboxylated metabolites, dopamine, noradrenaline and adrenaline, may produce or exacerabate tremor in man. Thus in Parkinsonian patients any centrally induced relief of tremor that levodopa may produce may be masked by tremorogenic effects of such metabolites exerted in the periphery.

Animals↗
PubMed1984

Ocular toxicology update.

The National Registry of Drug-induced Ocular Side Effects has accumulated 13 cases of possible major haemopoietic responses from topical ocular chloramphenicol. Over 75 cases of major haemopoietic events from carbonic anhydrase inhibitors are also reviewed. While numerous reports of local ocular effects secondary to timolol have been received by the Registry, the more significant adverse effects are the same systemic side effects seen with any beta-receptor blocking agent. Data in the Registry have shown that allopurinol may be possibly associated with cataract formation. Severe cardiovascular effects with elevated blood pressure and stroke are uncommon systemic adverse reactions following topical ophthalmic 10% phenylephrine, but these systemic effects have also been seen secondary to concentrations of 2.5%. Other drugs, such as adrenaline (epinephrine), ecothiopate (echothiophate), practolol, thiabendazole, and penicillamine are suspected of causing ocular pseudopemphigoid.

Adult↗
PubMed1989

Regulation of cyclic AMP formation in cultures of human foetal astrocytes by beta 2-adrenergic and adenosine receptors.

Two cell cultures, NEP2 and NEM2, isolated from human foetal brain have been maintained through several passages and found to express some properties of astrocytes. Both cell cultures contain adenylate cyclase stimulated by catecholamines with a potency order of isoprenaline greater than adrenaline greater than salbutamol much greater than noradrenaline, which is consistent with the presence of beta 2-adrenergic receptors. This study reports that the beta 2-adrenergic-selective antagonist ICI 118,551 is approximately 1,000 times more potent at inhibiting isoprenaline stimulation of cyclic AMP (cAMP) formation in both NEP2 and NEM2 than the beta 1-adrenergic-selective antagonist practolol. This observation confirms the presence of beta 2-adrenergic receptors in these cell cultures. The formation of cAMP in NEP2 is also stimulated by 5'-(N-ethylcarboxamido)adenosine (NECA) more potently than by either adenosine or N6-(L-phenylisopropyl)adenosine (L-PIA), which suggests that this foetal astrocyte expresses adenosine A2 receptors. Furthermore, L-PIA and NECA inhibit isoprenaline stimulation of cAMP formation, a result suggesting the presence of adenosine A1 receptors on NEP2. The presence of A1 receptors is confirmed by the observation that the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine reverses the inhibition of isoprenaline stimulation of cAMP formation by L-PIA and NECA. Additional evidence that NEP2 expresses adenosine receptors linked to the adenylate cyclase-inhibitory GTP-binding protein is provided by the finding that pretreatment of these cells with pertussis toxin reverses the adenosine inhibition of cAMP formation stimulated by either isoprenaline or forskolin.

Adenosine↗
PubMed1981

Adrenoreceptors in the human penis.

1. Adrenaline, noradrenaline and phenylephrine caused contraction of the corpus cavernosum muscle of the human penis. These sympathomimetic amines did not product inhibitory effects even in the presence of the alpha-adrenoreceptor blocker, phentolamine. The effect of dopamine was similar to that produced by these three sympathomimetic amines. Higher doses of isoprenaline and salbutamol also contracted this preparation. 2. Cocaine and guanethidine enhanced the motor response to adrenaline, noradrenaline and phenylephrine while the action of dopamine was blocked by these two drugs. 3. The motor response to adrenaline, noradrenaline and phenylephrine was antagonized by phentolamine and often potentiated by the beta-adrenoreceptors blocking drug, propranolol. The contractions produced by high doses of salbutamol and isoprenaline were also abolished by phentolamine. These findings indicate that the motor response to sympathomimetic amines is the result of activation of alpha-adrenoreceptors in the corpus cavernosum muscle. 4. At low doses, isoprenaline and salbutamol relaxed the corpus cavernosum muscle strip. The inhibitory action was blocked by low concentrations of the beta-adrenoreceptor antagonist, propranolol but not by practolol (beta 1-adrenoreceptor antagonist) and butoxamine (beta 2-adrenoreceptor antagonist). beta-adrenoreceptors are present in the corpus cavernosum muscle but these are unlikely to be either of the beta 1 or beta 2 type. The possible existence of a third type of beta-adrenoreceptor is suggested.

Catecholamines↗
PubMed1983

Nature of the beta-adrenoreceptors in the tracheal smooth muscle of the adult pig.

Relaxant responses to isoprenaline (ISO), adrenaline (ADR) and noradrenaline (NA) were investigated on carbachol-contracted, isolated tracheal smooth muscle preparations of the adult pig to determine the nature of the beta-adrenoreceptors present. The order of relaxant potencies of the catecholamines on this preparation was ISO greater than ADR greater than NA. The potency ratio at 37 degrees C was 1:0.06:0.005. This suggests that beta 2-adrenoreceptors predominate in isolated tracheal smooth muscle of the adult pig. Though the order of potency for the above catecholamines did not change, at the lower temperatures of 29 degrees and 33 degrees C, the potency ratios were slightly modified to 1:0.0.98:0.004 and 1:0.07:0.004 respectively. pA2 values on pig tracheal smooth muscle were 8.65 and 9.13 respectively, for the non-selective beta-blockers propranolol and alprenolol, and 5.63, 5.20 and 6.26 respectively, for the beta 1 selective blockers practolol, atenolol and metoprolol and 6.82 for the beta 2 selective beta-blocker, H 35/25. The results suggest the existence and predominance of beta 2-adrenoreceptors in tracheal smooth muscle of the adult pig.

Adrenergic beta-Agonists↗
PubMed1984

Mouse uterine muscle as a model for studying beta 2-adrenoreceptor mediated relaxation.

Effects of isoprenaline, adrenaline and noradrenaline on contractility were studied in longitudinal strips of mouse and rat uteri in vitro. In mouse uteri, isoprenaline produced an inhibitory effect on spontaneous contractions which was antagonized by propranolol, a nonselective beta-blocker, but not by practolol, a selective beta 1-blocker. Thus, the inhibitory effect of isoprenaline is mediated by beta 2-adrenoreceptor activation. Adrenaline and noradrenaline also inhibited the spontaneous contractions of mouse uteri. In rat uteri, isoprenaline produced only an inhibitory effect whereas adrenaline initially inhibited the force and frequency of contraction but also had a secondary excitatory effect on the frequency which could be antagonized by phentolamine. Noradrenaline had an inhibitory effect on force but had only a negligible effect on frequency of rat uteri. Phenylephrine also reduced the spontaneous contractility of mouse uteri by a beta 2-mediated effect. From results generated in this study, and from the literature, it is concluded that beta 2-adrenoreceptors are predominant in nonpregnant uteri of rodents, especially the mouse, while alpha-adrenoreceptors are predominant in nonpregnant uteri of rabbit, monkey and human.

Animals↗
PubMed1971

Antagonism by beta-adrenoceptor blocking agents of the antianaphylactic effect of isoprenaline.

1. beta-Adrenoceptor blocking agents antagonized the inhibitory (antianaphylactic) effect of isoprenaline on antigen-induced histamine release in isolated, passively sensitized, human lung and actively sensitized guinea-pig lung suggesting that the effect is exerted through beta-adrenoceptors. No antagonism was obtained with the human allergic leucocyte preparation.2. The antianaphylactic effect of isoprenaline was antagonized not only by propranolol but also by the ;selective' beta-adrenoceptor blocking agents, practolol and butoxamine.3. The classification of beta-adrenoceptors is discussed. Certain similarities between antianaphylactic and lipolytic beta-adrenoceptors are noted.

Acetanilides↗