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PubMedDate not supplied

Effects of sympathomimetic agonists and antagonists on mucociliary activity.

The effect on the mucociliary (m.c.) wave frequency of sympathomimetic agonists and antagonists was studied in the maxillary sinus in anesthetized rabbits. The non-selective beta-adrenoceptor agonist isoprenaline (0.005-10 micrograms/kg i.a.) and the selective beta2-adrenoceptor agonist salbutamol (0.01-10 micrograms/kg, i.a.) induced a dose-dependent acceleration of the m.c. wave frequency, whereas the beta1-adrenoceptor agonist prenalterol (1-200 micrograms/kg, i.a.) did not influence the basal m.c. activity. The selective alpha1-adrenoceptor agonist phenylephrine (0.01-20 micrograms/kg, i.a.) and the selective alpha2-adrenoceptor agonist oxymetazoline (0.001-1 microgram/kg, i.a.) both induced a dose-dependent retardation of the m.c. wave frequency. The non-selective beta-adrenoceptor antagonist propranolol (2-200 micrograms/kg, i.a., and 1 mg/kg, i.v.) and the non-selective alpha-adrenoceptor antagonist phentolamine (0.1-1 000 micrograms/kg, i.a.) had no influence on the basal m.c. wave frequency. Propranolol (1-2 mg/kg, i.v.) reduced the effect of isoprenaline and salbutamol (both in the dose range of 0.01-10 micrograms/kg, i.a.) and similarly phentolamine (0.2 and 1 mg/kg, i.a.) reduced the effect of oxymetazoline (0.01-10 microgram/kg, i.a.). It was concluded that during basal conditions in the anesthetized rabbit the m.c. activity functions independently of sympathetic activity and that sympathomimetic agonists acting on beta2-adrenoceptors accelerate the wave frequency, whereas sympathomimetic agonists acting on alpha1 and alpha2-adrenoceptors have a retarding effect, all in a dose-dependent manner.

Albuterol↗
PubMed1991

Thymus-induced recovery of age-related decrease of brain cortex alpha- and beta-adrenoceptors.

It has previously been demonstrated that thymus exerts a regulatory influence on beta-adrenergic system during aging. In particular, it has been shown that thymus can correct the beta-adrenoceptor density decrease in old mice. In the present paper results of experiments are reported dealing with the influence of the thymus on alpha-adrenoceptors of mouse brain cortex. Both subtypes of alpha-adrenoceptors are studied separately, using different labelled ligands. Results show that alpha 1-adrenoceptor density decreases in old animals, while alpha 2-adrenoceptor density does not change significantly. A neonatal thymus grafted into old recipients is capable of correcting the alteration observed in old mice. The differential impairment of alpha-adrenoceptors resembles that one previously observed on beta-adrenoceptors, where beta 1-type decreases in number during aging with a parallel decrease of adenylyl-cyclase activity, while beta 2-type remains unchanged.

Adenylyl Cyclases↗
PubMed1983

Influence of beta blockade on gastric acid secretion and changes in gastric mucosal blood flow before and after parietal cell vagotomy in dogs and man.

The aim of the present study was, in paired experiments in dogs, to examine the effect of beta-receptor blockade on gastric acid secretion and mucosal blood flow before and after parietal cell vagotomy (PCV). The secretory response to pentagastrin was reduced after vagotomy. beta-Adrenergic blockade had no effect on pentagastrin-stimulated gastric acid secretion before PCV, but after PCV beta blockade caused a modest increase in acid secretion, mediated mainly by the beta 2 receptors. A similar trend was seen in man. A marked increase in mucosal blood flow occurred 30 min after propranolol and was followed by a late decrease. One may conclude that a modest beta-adrenergic tone, which reduces secretion, becomes manifest after vagal denervation and that an increase in the ratio between mucosal blood flow and acid secretion was induced by the PCV. This increase cannot be explained as a beta-receptor-mediated effect.

Adrenergic beta-Antagonists↗
PubMed1985

Rectosigmoid motility response to beta-adrenoceptor stimulation in patients with the irritable bowel syndrome.

Patients with the irritable bowel syndrome were studied with regard to the effects of beta-adrenoceptor agonists on rectosigmoid motility. Pressure was recorded with a continuously inflated balloon in the upper rectum and recorded from a pressure catheter in the sigmoid colon. On different days the beta-2 agonist terbutaline, the beta-1 agonist prenalterol, and placebo, respectively, were administered intravenously after a control period. During each examination contractile activity was quantified for three consecutive periods of 25 min. Terbutaline in a total dose of 0.50 mg decreased sigmoid motility index significantly from 3.0 +/- 0.6 (SEM) to 1.1 +/- 0.3 kPa X min (p less than 0.01). After less than or equal to 5 mg prenalterol no significant changes of motility index were observed. After placebo an increase, although not significant, in contractile activity was seen compared with the initial control period. Rectal motility indices were low and not changed by the beta agonists. The serum concentrations of the drugs were within the therapeutic limits used in clinical practice and caused a dose-dependent increase of both systolic blood pressure and heart rate. It is concluded that beta-2 adrenoceptor stimulation significantly decreases sigmoid motility whereas the motility index seems to be unaffected by beta-1 adrenergic stimulation.

Adrenergic beta-Agonists↗
PubMed1985

Failure of beta-adrenergic stimulation to affect cholecystokinin-stimulated sigmoid motility in man.

Sigmoid motility, stimulated by the octapeptide of cholecystokinin (OP-CCK) and the effects of beta-adrenoceptor agonists, was studied in 12 healthy subjects in a randomized, double-blind fashion. Sigmoid pressure was recorded 18-20 cm from the anus, and contractile activity quantified as the area under pressure waves for three 25-min periods. OP-CCK (sincalide), 80 ng X kg-1 X h-1, was continuously infused throughout each session, resulting in a high sigmoid motility index. Preceded by a control period, terbutaline (beta-2 agonist), prenalterol (beta-1 agonist), or placebo was injected on 3 separate days. After 1 mg + 4 mg prenalterol or 0.25 mg + 0.25 mg terbutaline intravenously no significant changes in motility pattern were seen compared with the control period. Terbutaline and prenalterol infusions were followed by a dose-dependent increase of systolic blood pressure and heart rate. After placebo no effect on blood pressure or heart rate was seen. The study shows that CCK significantly enhances sigmoid motility in man and that selective beta-adrenergic agonists do not show any inhibitory influence on colonic motility stimulated with CCK. Since terbutaline inhibits sigmoid and rectal motility in man during rectal distention, it is suggested that the inhibitory effect of beta-2-adrenoceptor agonists may be dependent on the mode of background stimulation of the colon.

Adrenergic beta-Agonists↗
PubMed1985

Beta adrenergic influence on esophageal and colonic motility in man.

Gastrointestinal (GI) motility is centrally controlled through the sympathetic and parasympathetic nerves, sympathetic effects being partly mediated by beta adrenoceptors. Although beta adrenoceptor agonists and antagonists are widely used for different disorders, little is known about the influence of these agents on GI motility. The present study was initiated to investigate whether there is a physiological, beta adrenergic influence on human GI motility and to describe the effects of selective beta adrenoceptor stimulation on motility in the proximal and distal parts of the GI tract. Esophageal peristalsis was measured in healthy subjects using electronic catheters. Distal colonic motility was measured with an open-tipped, water-perfused catheter in the sigmoid colon and from an air-filled balloon in the rectum in healthy subjects and in patients with the irritable bowel syndrome (IBS). In one study, colonic motility was stimulated with continuous infusion of the octapeptide of cholecystokinin (CCK-OP). Esophagus: Peristaltic amplitude was increased in the distal smooth muscle part of the esophageal body after infusion of both the nonselective beta blocker propranolol and the beta-1 selective blocker metoprolol. After infusion of the beta-1 agonist prenalterol and the beta-2 selective agonist terbutaline, a profound decrease in esophageal peristaltic amplitude was seen. Pretreatment with metoprolol selectively blocked the response to a moderate dose of prenalterol but did not block the response to terbutaline. The latter response was blocked by propranolol. Peristaltic velocity in the proximal part of the esophagus was decreased by beta-1 stimulation and in the distal part by beta-2 stimulation. Distal colon: In healthy subjects the sigmoid motility index showed a dose-dependent increase after metoprolol and propranolol, respectively. The increase was more marked after propranolol infusion. Terbutaline decreased the sigmoid motility index both in healthy subjects and in patients with the IBS. Furthermore, the rectal motility index was decreased in the group of healthy subjects. The effects of prenalterol on rectal and sigmoid motility did not differ from those of placebo. The IBS patient group showed larger intraindividual variations in sigmoid motility from day to day and also lower rectal motility indices than the healthy subjects. Infusion of CCK-OP increased the sigmoid motility index compared to non-stimulated conditions. No effects on CCK-OP stimulated motility were seen after either terbutaline, prenalterol or placebo.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Agonists↗
PubMed1983

A method for dissecting two site receptor interactions in ligand binding studies.

A general model has been developed describing the relationship between the measured (IC50) and absolute affinities (KI), observed in radioligand binding studies when two ligands, one radioactive, interact with two receptors or binding sites. The model shows the dependence of the IC50's upon the concentration of radioligand for any combinations of the absolute affinities of the radioligand (Kd's) and the displacing ligand (KI's). By constraining the affinities of the two ligands for the sites, five special cases of the general model can be described that model all possible 'selectivities' the ligands may have for the sites. The properties of these five cases can be exploited experimentally to probe the nature of the ligand/site interactions by the simple expedient of constructing a number of displacement curves at different radioligand concentrations. The method has been tested experimentally in three situations where two ligand/two site interactions occur, and is shown to be a useful technique to qualitatively examine the underlying binding reactions.

Animals↗
PubMed1977

New approach of the cardio-vascular depressive mechanism during lateral hypothalamic stimulation.

Paraventricular nucleus stimulation acts directly on the alpha- and beta-adrenoreceptors in heart and arterioles, eliciting arterial hypotension and cardiac chronotropism and inotropism decrease. Efferent pathways follow sympathetic nervous fibres through the medulla and the thoraco-lumbar ganglionic chain. The role of the alpha- and beta-adrenoreceptors in these depressive reactions is discussed.

Adrenergic alpha-Antagonists↗
PubMed1975

Cardiovascular and platelet responses in the dog to the monoenoic prostaglandin precursor dihomo-gamma-linolenic acid.

The monoenoic prostaglandin precursor, dihomo-gamma-linolenic acid (DGLA), in a single dose intravenously (2.0 mg/kg) in dogs, produced a biphasic alteration in systemic arterial pressure (SAP) with a predominant and marked depressor effect. This SAP response is approximately equidepre-sor to the effect of PGE1 5 mug/kg. DGLA had a positive inotropic effect, causing a greater increase in myocardial contractility than PGE1 in an equidepressor dose. The effect of DGLA on MC was not altered by ganglion blockade or beta-adrenergic blockade. Aspirin blocked the sustained depressor response to DGLA but not an initial drop in SAP and increase of MC of very short duration. Aspirin had no effect on PGE1 or PGF1 alpha responses. DGLA caused no thrombocytopenia, but caused a decrease in sensitivity to platelet aggregation. Control fatty acid injections produced variable effects with no resemblances to DGLA responses. It is concluded that DGLA produces direct depressor and positive inotropic responses as well as responses which may be due to conversion to an endoperoxide formed in the biosynthesis of prostaglandins. In contrast, in equidepressor doses, arachidonic acid (AA), the bisenoic prostaglandin precursor, produces a delayed, single-phase depressor effect which may be due to endoperoxide formation alone. Further, the effect of AA on MC is reflex and is blocked by hexamethonium.

8,11,14-Eicosatrienoic Acid↗
PubMed1975

Effects of ganglionic and beta-adrenergic blockade on cardiovascular responses to the bisenoic prostaglandins and their precursor arachidonic acid.

Arachidonic acid (AA) 300 mug/kg, and PGE2, 5 mug/kg consistently produced a decrease in systemic arterial pressure in anesthetized dogs. PGF2alpha, 5 mug/kg, produced a pressor response. All three compounds increased myocardial contractile force, but the magnitude of the change following AA was less prominent. After ganglionic blockade, the depressor response to AA and PGE2 persisted and the pressor response to PGF2alpha was augmented. Myocardial contractile force did not increase following AA in ganglion-blocked animals indicating that the cardiac responses observed before hexamethonium were mediated by the baroreceptor reflexes. A much larger dose of AA (900 mug/kg) resulted in a small positive inotropic effect on the heart. This possibly represents a direct cardiac effect of AA, or may be indicative of increased biosynthesis of an intermediate endoperoxide, or PGE2 and PGF2alpha. Both PGE2 and PGF2alpha have a direct positive inotropic effect on the heart. The persist cardiac effects of PGE2 and PGF2 after beta-adrenergic blockade suggests that these compounds may not interact with the beta-receptors of the myocardium.

Adrenergic beta-Antagonists↗