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At least 811 records · Page 45Linked to original sources
PubMed1976

The influence of beta-adrenergic antagonists on the adrenergic responses of the rat vas deferens.

The influence of beta-adrenergic antagonists (propranolol, pronethalol, alprenolol, isopropylmethoxamine, H 35/25, sotalol and practolol) on isotonic contractile responses to norepinephrine (NE) was studies. All drugs caused an increase in the maximum responses while depressant effects were seen only with high doses of propranolol, pronethalol and alprenolol. The enhancement of responses to NE was considerably greater at low concentrations of calcium (0.5-1.0 mM) than at high (8 mM) concentrations. The inhibitory effects of propranolol, pronethalol and alprenolol were diminished but not completely overcome by increasing calcium concentrations form 1.8 to 8 mM. Cumulative dose-response curves of calcium showed no increase in maximum responses although responses to low concentrations of calcium were augmented by sotalol and practolol. Evidence suggests that the enhancing effects of these drugs may be due to their facilitatory effect on calcium mobilization following alpha-adrenoceptor activation while their depressant properties probably reflect their membrane stabilizing properties.

Adrenergic beta-Antagonists↗
PubMed1982

Beta 2-mediated hypotension and myocardial injury.

This study was designed to investigate the importance of beta 2 receptor mediated hypotension in the pathogenesis of myocardial injury. The effect of isoproterenol and the putative beta 2 agonist albuterol on arterial blood pressure, heart rate, the myocardial content of ATP and cAMP, and the serum content of MB-CPK was examined in conscious rats. Isoproterenol (5.25 mg/kg, s.c.) and albuterol (45 mg/kg, s.c.) lowered blood pressure and elevated heart rate to the same extent. Also, both agonists increased the myocardial content of cAMP, decreased the myocardial content of ATP, and elevated serum MB-CPK. The beta 1 antagonist practolol, but not the ganglionic blocking agent chlorisondamine, attenuated the elevation in heart rate to albuterol without reducing its effect on blood pressure. Practolol, but not chlorisondamine, abolished the effects of albuterol on cAMP, ATP, and MB-CPK. These data suggest that the myocardial injury which is associated with an increased heart rate and changes in cAMP, ATP, and MB-CPK following the administration of albuterol is not the result of beta 2-mediated hypotension, but is due to stimulation of myocardial beta 1 receptors.

Albuterol↗
PubMedDate not supplied

Inhibition of angiotensin II potentiation of sympathetic nerve activity by beta-adrenergic antagonists.

Since beta-adrenergic blockers are effective in the therapy of hypertension by a mechanism related to the degree of activation of the renin-angiotensin system, the effect of eight beta blockers was examined on angiotensin II potentiation of nerve stimulation (NS) in isolated perfused rat mesenteric vessels. The vasoconstrictor response to periarterial NS was obtained by monitoring changes in perfusion pressure while a beta blocker or a beta blocker and angiotensin II (3 ng/ml) were added to the perfusate. Although each beta blocker tended to decrease responses to NS, in the concentrations used, only metoprolol significantly inhibited responses to NS. Angiotensin II, when infused alone, potentiated the responses to NS by 63% (p less than 0.01). These enhanced responses following angiotensin II were inhibited in a dose-related manner (10--300 ng/ml) by beta 1, beta 2, and mixed beta blockers. At the 100 ng/ml concentration, DL-propranolol, timolol, metoprolol, practolol, butoxamine, and H35/25 inhibited the angiotensin II potentiation of NS by 83%, 76%, 77%, 59%, 72%, and 41% respectively. The order of potency for this action was as follows: timolol = metoprolol = butoxamine greater than propranolol greater than practolol greater than H35/25. Administration of D- and L-propranolol also reduced the responses by 75%. The vasoconstrictor responses to injected norepinephrine (NE), in the presence and absence of angiotensin II, were not altered by DL-propranolol or timolol. In conclusion, beta-adrenergic blockers were found to interfere with the effect of angiotensin II on the sympathetic neuron, a property that could contribute to the antihypertensive action of these drugs.

Adrenergic beta-Antagonists↗
PubMed1972

Differences in direct effects of adrenergic stimuli on coronary, cutaneous, and muscular vessels.

Direct effects of adrenergic stimuli on coronary vessels in dogs were compared with effects on vessels to skin (hind paw) and skeletal muscle (gracilis muscle) after intravenous administration of practolol (2 mg/kg), a selective myocardial beta receptor blocker which minimized indirect effects of myocardial stimulation on coronary vascular resistance. The left circumflex coronary, cranial tibial, and gracilis arteries were perfused separately but simultaneously at constant flow. Perfusion pressures, left ventricular pressure and dP/dt. and heart rate were recorded. Changes in perfusion pressure to each bed reflected changes in vascular resistance. The direct constrictor effects of sympathetic nerve stimulation, norepinephrine and phenylephrine on coronary vessels were minimal compared with effects on cutaneous and muscular vessels. Subsequent blockade of vascular beta receptors did not augment the constrictor responses. Angiotensin, a nonadrenergic stimulus, produced striking coronary vasoconstriction which exceeded that in skin and approximated that in muscle. These results suggests that there is a paucity of alpha adrenergic receptors in coronary vessels compared to cutaneous and muscular vessels. Direct dilator responses to isoproterenol were similar in coronary and cutaneous vessels, but were greater in muscular vessels. Responses to glyceryl trinitrate, a nonadrenergic dilator, also were greater in skeletal muscle. Therefore, differences in effects of isoproterenol on the three beds may reflect differences in reactivity to dilator stimuli rather than differences in the density of beta receptors. In contrast to norepinephrine, the predominant direct effect of epinephrine on coronary vessels was dilatation mediated through activation of vascular beta receptors. A constrictor effect caused by stimulation of alpha receptors was unmasked by propranolol.Finally, the order of potency of agonists in stimulating coronary vascular beta receptors and the demonstration of selective beta receptor blockade with practolol suggest that beta receptors in coronary vessels resemble those in peripheral vessels more than those in myocardium.

Adrenergic beta-Antagonists↗
PubMed1975

Effect of beta and beta2 adrenoreceptor stimulants infused intrapancreatically on glucagon and insulin secretion.

L-Isoproterenol was infused at a dose of 20 pmol/kg/min for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. Arterial plasma glucose, blood flow, and plasma concentrations of both glucagon and insulin in the cranial pancreaticoduodenal vein were significantly enhanced during the infusion, resulting in a greater increase of bihormonal output. Intrapancreatic pretreatment with propranolol abolished all of the isoproterenol-induced increases except for glucagon secretion which was suppressed only in part. Pretreatment with practolol, a specific receptor blocker of the beta1 type, did not exert any discernible inhibiting effect upon the isoproterenol-induced enhancement. Intrapancreatic infusion of trimetoquinol, a selective receptor stimulant of the beta2 type in some mammals, at an equimolar dose caused similar increases in plasma glucose, pancreatic venous blood flow, and bihormonal output when compared to those induced by isoproterenol. Pretreatment with a larger dose of propranolol totally abolished the trimetoquinol-induced enhancement of both glucagon and insulin secretion. Pretreatment with an isomolar dose of practolol, in contrast, did not show any suppressive effect on the parameters investigated. There was a dose-dependency in the bihormonal responses to trimetoquinol. Another beta2 receptor agonist, salbutamol, also significantly raised plasma glucose, pancreatic venous blood flothough to a lesser extent than did trimetoquinol. These results indicate that the adrenergic control over the function of the endocrine pancreas through beta adrenoreceptors may be mediated mainly via those of the beta2 type.

Adrenergic beta-Agonists↗
PubMed1976

Clinical pharmacokinetics of beta-adrenoreceptor blocking drugs.

All beta-adrenoreceptor blocking drugs seem to be fairly rapidly and completely absorbed from the gastro-intestinal tract. The rate of absorption, however, appears to be lower in elderly patients and possibly also in patients with renal failure than in younger patients. The extent of bioavailability varies considerably between different beta-blockers. Some of these drugs(e.g. alprenolol and propranolol) have a low extent of bioavailability due to a high first-pass elimination effect, while pindolol and practolol for example are in influenced very little by this effect. However, as some beta-blockers from active metabolites, the bioavailability calculated as the ratio between the area under the plasma concentration time curve of unchanged drug after oral and intravenous administration does not give an accurate estimation of the fraction of the biologically active dose reaching the systemic circulation. The beta-blockers so far studied are rapidly distributed in the body. The t1/2 of distribution ranges between 5 to 30 minutes. The apparent volume of distribution varies 3- to 4-fold between the compounds but in all cases the apparent volume of distribution exceeds the physiological body space. In patients with impaired liver function an increase of the volume of distrubution of propranolol has been found. The beta-blockers are relatively rapidly eliminated from the body and most of them have an elimination half-life between 2 to 4 hours. For atenolol, practolol and sotalol higher values have been reported. The most lipophilic beta-blockers are almost completely metabolised in the liver, wheras those of lower lipophilicity are mainly excreted via the kidneys. Impraired liver and kidney function have been found to significantly influence the rate of elimination of those beta-blockers eliminated via the insufficient organ of elimination. Numerous investigators have shown that the beta-blocking effect is linearly related to the logarithm of the plasma concentration. In spite of this relationship, it is difficult from mean data to predict the individual plasma concentration which is necessary for a certain degree of beta-blockade. This might be due to variations in the quantitative formation of active metablolites, individual differences in the plasma protein binding and rather flat plasma level-response curves. Also with respect to the therapeutic effect, the plasma levels vary considerably between individuals. This limits the value of determination of plasma concentrations in order to adjust the therapeutic dose. Our recommendation is that these facilities should be utilised in selected patient groups, eg. those who have a poor therapeutic response to a beta-blocker although the dose is high, and those patient with impaired renal or liver function. The duration of beta-blockade is dose-dependent since the pharmacological effect declines with a constant rate (zero-order kinetics) within relatively wide dosage intervals...

Adrenergic beta-Antagonists↗
PubMed1993

Sclerosing peritonitis associated with keratoconjunctivitis sicca, pleurisy, and secretory otitis media.

A male case of sclerosing peritonitis of unknown cause, associated with keratoconjunctivitis sicca, pleurisy, and secretory otitis media, is presented. These unusual complications are very similar to the adverse reactions to the beta-adrenergic blocking agent, practolol, which is known to cause sclerosing peritonitis. This similarity suggests an etiological association between the sclerosing peritonitis of this case and that caused by practolol. The sclerosing peritonitis of this case may be considered to occur as part of some systemic disorder, and thus casts doubt on the hitherto accepted hypothesis that sclerosing peritonitis results from infectious peritonitis.

Humans↗
PubMed1981

Effect of a beta2-sympathomimetic on urecholine-stimulated gastric acid secretion in dogs.

The effect of a selective beta2-adrenoceptor agonist on urecholine-stimulated gastric acid secretion was studied in conscious gastric fistula dogs. A dose-dependent inhibition was found, most pronounced for the highest doses of urecholine. The inhibition was primarily on volume, whereas the acidity showed a decreasing tendency only. The pulse rate was increased by the beta2-agonist and by urecholine in high doses. Propranolol prevented both the inhibition of acid secretion and the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion and the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with five doses of urecholine and two doses of the beta2-agonist showed a decrease in maximal response, and transformation of the curve suggested an unchanged D50. It is concluded that the beta2-agonist inhibits urecholine-stimulated acid secretion in the dog to the same degree as pentagastrin-induced acid secretion, and much stronger than found for histamine-induced acid secretion in earlier experiments. The inhibition seems to follow a noncompetitive kinetic, and beta2-receptors are probable involved.

Adrenergic beta-Agonists↗
PubMed1982

Effect of isoprenaline on bethanechol-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of isoprenaline on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility for both frequency and strength. Isoprenaline, a beta 1- and beta 2-agonist, was used alone and in conjunction with selective blockade of beta 1 and beta 2 receptors. The stimulated antral motility was dose-dependently inhibited by isoprenaline. The effect was significantly blocked by the beta 1 + beta 2-adrenoceptor blocker propranolol and by using in conjunction the beta 1-adrenoceptor blocker practolol and the beta 2-adrenoceptor blocker H 35/25. H 35/25 and particularly practolol reduced the effect of isoprenaline to some extent, but the reduction was not of statistical significance. This indicates that isoprenaline acts on antral motility through both beta 2 and beta 1 receptors. Dose-response experiments with five logarithmically increasing doses of bethanechol and one dose of isoprenaline showed inhibition of a non-competitive type.

Adrenergic beta-Antagonists↗
PubMed1976

The beta adrenergic receptors of chromatophores of the frog, Rana pipiens.

The isolated skin of Rana pipiens was found to be a suitable model for the quantitative study of chromatophore beta adrenergic receptors uninfluenced by prejunctional phenomena. Cumulative concentration-response curves for adrenergic agonists were obtained in preparations in which effective alpha adrenergic blockade had been produced with phenoxybenzamine. The beta adrenergic agonists darkened the preparation, as did melanocyte-stimulating hormone, but the maximum effects differed. The maximum of the l-isoproterenol cumulative concentration-response curve was approximately 50% less than that of melanocyte-stimulating hormone, while the maxima for l-epinephrine and l-norepinephrine were significantly less than that for isoproterenol. Microscopic examination revealed a qualitative difference: while maximal darkening produced by melanocyte-stimulating hormone was associated with maximal changes in both interspot melanophores and iridophores, maximal adrenergic-induced darkening was associated with maximal iridophore granule concentration only. No qualitative differences could be observed in the darkening caused by the three adrenergic agonists. The beta adrenergic potencies of l-norepinephrine and l-isoproterenol relative to l-epinephrine were determined by four-point bioassay. Isoproterenol was found to be 138 times as potent as epinephrine, while norepinephrine was 4 times as potent. Similarly, antagonism of isoproterenol-induced darkening of phenoxybenzamine-pretreated skin samples by the beta adrenergic blocking agents dl-propranolol, dl-sotalol, dl-practolol, l-butoxamine and d-butoxamine was studied, and their KB and pA2 values, respectively, were found to be: dl-propranolol (1.44 X 10(-8)M, 7.81); dl-sotalol (7.25 X 10(-8)M, 7.23); l-butoxamine (6.92 X 10(-6)M, 5.10); dl-practolol (1.91 X 10(-5)M, 4.96); d-butoxamine (no activity). Comparison of the potency ratios and pA2 values cited above with similar parameters obtained by other investigators in several mammalian tissues suggests that there is wide variation among beta adrenergic receptors.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Alpha- and beta-adrenoceptor cross-talk in the regulation of glycogenolysis in dog and guinea-pig liver.

The dog liver glycogenolytic response to isoprenaline (EC50 = 3 x 10(-9) M) was selectively blocked by 10(-5) M of practolol, but not by butoxamine. In contrast, the glycogenolytic response to isoprenaline (EC50 = 3 x 10(-7) M) was inhibited by 10(-6) M of butoxamine, but not by practolol, in the guinea-pig liver. This suggests that, in the dog, the isoprenaline response is dominated by beta 1-adrenoceptors, while in the guinea-pig beta 2-receptors control such response. Glucose release from dog and guinea-pig liver slices was also stimulated by amidephrine (EC50 = 10(-6) M in the dog and 4 x 10(-5) M in the guinea-pig). Both prazosin and yohimbine blocked this response. The effectiveness of clonidine as a glucose-mobilizing agent could only be established in the dog liver. Prazosin showed greater activity than yohimbine in antagonizing the response to both agonists. In the dog, low concentrations of alpha-adrenoceptor agonists (10(-9) M), that failed to modify the basal glucose release per se, selectively depressed the isoprenaline response. Prazosin, but not yohimbine, reversed this inhibitory effect. It is concluded that glucose release from the dog liver is regulated by two opposite mechanisms that seem to be associated to alpha 1-adrenoceptors (inhibitory) and to beta 1-adrenoceptors (stimulatory).

Adrenergic alpha-Agonists↗
PubMed1977

Differences in pulmonary and cardiovascular beta receptors in the guinea pig and rabbit.

An in vivo preparation, in which a body plethysmograph was incorporated, was useful in monitoring the cardiopulmonary effects of pharmacological agents in the guinea pig and rabbit. Isoproterenol, given 30 seconds prior to histamine challenge, reproducibly blocked histamine-induced dynamic compliance decreases and increased heart in the artificially ventilated guinea pig. These effects were used to separate the activity of beta adrenergic blockers on airway and heart muscle. Dose-response data were obtained and ED50 values for pulmonary and cardiovascular blockade were compared. Relative potencies and cardioselectivity ratios for dichloroisoproterenol, practolol, dl-propranolol and d-propranolol were determined. Both practolol and dichloroisoproterenol were cardioselective; dl-propranolol was found to be the most potent. When a similar protocol was tried in the rabbit, isorpoterenol failed to antagonize either histamine or methacholine-induced airway constriction. This finding was supported in subsequent in vitro tests. Isoproterenol and epinephrine were ineffective in blocking methacholine-induced tracheal chain contractions and epinephrine did not significantly enhance adenylate cyclase activity. Our observations suggest rabbit airway smooth muscle is insensitive to beta adrenergic stimulants.

Adenylyl Cyclases↗
PubMed1989

[Effect of Chinoin-103 on Na+, K+-activated adenosine triphosphatase of the rat heart].

Effect of a new beta-blocking agent, a cardioselective aryl oxybutanolamine derivative, the Chinoin-103 on basal and total ATP-aze activities has been studied in total homogenizatum of rat heart. The effect has been compared to previous results of propranolol and to effect of practolol, respectively. It has been established that DL-Chinoin-103-similarly to DL-propranolol but in a little higher concentration--has significantly impeted both basal and total ATP-aze activities. Since in the nase of practolol similar effect was not obsreved and furthermore the effect could not be suspended by isoproterenol, the authors suppose that impediment of sarcolemmal ATP-aze activities cannot primarily be attributed to beta-blocking effect of compounds. Study of effect of racemic Chinoin-103 on enzymatic kinetic parameters of basal and total ATP-aze acticities has shown that primarily the reaction rate had decreased, affinity to substratum had not changed in the case of total ATP-aze and it has moderately decreased in the case of basal ATP-aze. The results of this publication has drawn attention to the fact that some beta-receptor blocking compounds may have other specific membrane effects besides antagonism on beta-receptors.

Adenosine Triphosphatases↗
PubMed1978

Hypotensive action of beta-blocking drugs injected into the cerebral ventricle of the rat.

Pindolol, propranolol, practolol, N-isopropyl-p-nitrophenyl-ethanolamine (INPEA), d and l-alprenolol were injected into the lateral cerebral ventricle of the anaesthetized rat. Except for INPEA, which has no action at the doses used, these various beta-blocking agents produce a dose-related fall in blood pressure. D-alprenolol and practolol seem to be the least active of the hypotensive agents. Our results show some relationship between the beta-blocking potency of the drugs studied and the hypotension induced when they were injected in the lateral ventricle.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Enhancement of insulin hypoglycaemia by beta adrenoceptor antagonists.

Interaction of insulin with beta-adrenoceptor antagonists was studied in conscious rabbits. Propranolol and metoprolol did not modify the peak of insulin hypoglycaemia but delayed its recovery. Practolol, sotalol and 1-INPEA enhanced the peak effect and delayed the recovery of insulin-induced hypoglycaemia. H 35/25 and d-INPEA did not modify insulin hypoglycaemia. The beta-blockers did not produce significant hypoglycaemia per se. Since sotalol, 1-INPEA (specific beta-adrenoceptor antagonists devoid of local anaesthetic activity); practolol and metoprolol (selective cardiac beta-1 adrenoceptor antagonists) enhanced hypoglycaemic action of insulin and H 35/25 (a selective beta-2 adrenoceptor antagonist) failed to affect it, it seems that selective beta-adrenoceptor blockade (similar to cardiac beta-1 adrenoceptors) mediates enhancement of insulin hypoglycaemia. Caution should, therefore, be exercised in administering beta-adrenoceptor antagonists and insulin together. A reduction in the dose of insulin may be necessary.

Adrenergic beta-Antagonists↗
PubMed1987

Comparison of the effect of eleven beta-adrenoceptor blocking drugs in perturbing lipid membrane: an ESR spectroscopy study.

The perturbation effect of the beta-adrenoceptor blocking drugs atenolol, propranolol, practolol, oxprenolol, doberol, pronethanol, metipranolol, alprenolol, Kö-1124, pindolol, and exaprolol on rat brain lipid membrane was investigated by ESR spectroscopy using the spin probe method. Using stearic acids spin labeled at the 5th, 12th, and 16th positions, it was found that lipophilic drugs disorder the membrane and their effect is about 5-10 times higher at the 16th carbon membrane depth than at the 5th depth. Exaprolol induced nonlamellar phases in the bovine brain lipid membrane as detected by 31P NMR spectroscopy. The relative potencies of the drugs at 10 mmol/liter concentration to disorder the lipid membrane at the 16th carbon depth were in the order: exaprolol greater than alprenolol approximately equal to propranolol greater than metipranolol approximately equal to doberol greater than control sample greater than pindolol approximately equal to practolol approximately equal to atenolol. This order qualitatively corresponds with some of their nonspecific biological membrane activities but is not related to their beta-adrenoceptor blocking potencies. The inequality of the membrane perturbation propensities of the drugs indicates that they perturb the lipid membrane in a structure-dependent manner, i.e., that each induces a specific rather than a nonspecific membrane perturbation.

Adrenergic beta-Antagonists↗
PubMed1987

Circadian phase dependency of the effects of different beta-receptor blocking drugs on motor activity of rats. Importance of drug lipophilicity.

The effects of seven beta-receptor blocking drugs differing in lipophilicity by 3.5 orders of magnitude (propranolol, bupranolol, oxprenolol, metoprolol, sotalol, practolol, atenolol) were studied on the circadian rhythm in motor activity of light-dark-synchronized (light (L): 7-19 h, dark (D): 19-7 h) male rats. Motor activity after i.p. injection of saline or of the racemic mixtures of all drugs and the isomers of propranolol, bupranolol and practolol was measured in groups of 5 rats with a motimeter. Two doses of either drug were injected either at 7:30 a.m. in L or at 7:30 p.m. in D. In L the drugs did either not affect motor activity or even increased motility in comparison to saline. No dosage-dependency was observed in the drug effects in L. In contrast, during D a dosage-dependent decrease in motor activity was found for all compounds. ED50-values of decrease in motility during D were negatively correlated with lipophilicity (partition coefficient) of the compounds. No significant difference was found in the ED50-values of the isomers studied. The results clearly demonstrate a circadian phase dependency in the effects of beta-receptor blocking drugs on motor activity of rats. A dosage-dependent central depressant effect of the drugs could be observed only in D. It is concluded that the central depressant effects of beta-receptor blocking drugs are mainly due to the non-specific, lipophilic property of the drugs and not brought about by a specific blockade of central beta-adrenoceptors.

Adrenergic beta-Antagonists↗
PubMed1987

Beta-adrenergic regulation of secretion from Clara cell adenomas of the mouse lung.

Ethylnitrosourea-induced pulmonary adenomas of the mouse have been reported as being predominantly Clara cell in origin. The response of these tumor cells in vivo to the secretory agonist, isoproterenol (10 mg/kg) and the antagonist, propranolol (2.0 mg/kg) 1 hour after intraperitoneal injection into 120-day-old tumor-bearing mice was examined. Ultrastructural morphometry was used to quantitate the secretory response of tumor cells by measuring the volume density of the secretory granules. In the intact animal, isoproterenol stimulated secretion in the Clara cell adenomas (40% decrease in volume density with no change in surface to volume ratio of granules), while propranolol prevented this effect. In addition, beta-adrenergic receptors on isolated tumor cells were demonstrated by radioligand-binding assay by using [125I]iodocyanopindolol (ICYP). Scatchard analysis of data derived from whole cells indicates a maximum receptor-binding capacity of 27 fmoles/mg of protein and a KD of 0.029 nM. Isoproterenol displacement of ICYP binding yields an IC50 of 8 X 10(-7) M and a calculated KD of 3.36 X 10(-7) M. The beta 2 identity of these receptors was determined by utilizing the relatively specific beta 1 and beta 2 antagonists practolol and ICI-118,551, respectively. Practolol failed to displace more than 30% of ICYP binding even at 100 microM, while ICI-118,551 displacement of ICYP yielded a linear Hofstee plot (r = 0.93) and a KD of 5.04 X 10(-9) M. These findings suggest that the secretory activity of Clara cell-like pulmonary adenomas is under beta-adrenergic control similar to that of normal bronchiolar Clara cells.

Adenoma↗