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At least 19 recordsLinked to original sources
PubMed1979

Renal effects of propranolol, practolol and butoxamine in pentobarbital-anesthetized rats.

The renal effects of the beta-adrenergic blockers, propranolol, practolol and butoxamine, were examined in pentobarbital-anesthetized rats. All the beta-blockers, infused i.v., increased urine volume (V), urinary sodium excretion (UNaV) and p-aminohippuric acid clearance without change in inulin clearance. Indomethacin, an inhibitor of prostaglandin biosynthesis, did not affect the renal effects of these beta-blockers. Phentolamine abolished the renal effects of practolol, but not those of propranolol and butoxamine. Haloperidol abolished the renal effects of propranolol and butoxamine, but not those of practolol. A high correlation was found between the increased UNaV and the increased urinary phosphate excretion by butoxamine but not by propranolol and practolol. Therefore, it is suggested that alpha-adrenergic stimulation is involved in the mechanism of diuresis by practolol, a beta1-blocker, and that dopaminergic stimulation is involved in the diuresis caused by butoxamine, a beta2-blocker. Propranolol is similar to butoxamine, and partially similar to practolol.

Animals↗
PubMed1977

The effect of practolol and butoxamine on aortic arch malformation in beta adrenoreceptor stimulated chick embryos.

An equimolar dose of the beta-1 adrenoreceptor antagonist practolol administered to embryonic chicks prevents the induction of aortic arch malformations by isoproterenol. Whereas 3.75 X 10(-9) mole isoproterenol in 5 microliter saline solution induced aortic arch anomalies in 39% of embryos injected at Hamburger-Hamilton developmental stage 26, pretreatment with practolol one to two minutes before catecholamine administration reduced the anomaly rate to to 4%. Practolol when injected alone did not influence survival rate nor did it cause cardiovascular malformations. Probably the most significant result of this study involves the prevention by practolol of aortic hypoplasia and interrupted aortic arch complexes, anomalies frequently induced by isoproterenol when administered at this stage of embryonic chick development. Butoxamine, a beta-2 adrenoreceptor antagonist, did not block the overall effect of isoproterenol nearly as effectively as did practolol. Results from the present study suggest that aortic arch anomalies may be induced in embryonic chicks via beta-1 adrenoreceptor stimulation. Beta-2 receptor stimulation does not appear to be as significantly involved.

Abnormalities, Drug-Induced↗
PubMed1985

Modification of dobutamine- and terbutaline-induced calcium and fluid secretion from rat salivary glands by atenolol and butoxamine.

Saliva was elicited from rat salivary glands by terbutaline at i.p. doses of 1, 5, 10 and 25 mg/kg b.wt. but not by doses of 0.1 or 0.5 mg/kg b.wt. Dobutamine elicited no secretion at 1 or 2 mg/kg but did at 5, 10 and 25 mg/kg b.wt. At 5 mg/kg terbutaline evoked nearly maximal volumes but with dobutamine, volumes were small at this dosage. At dosages of 10 and 25 mg/kg volumes with the two agonists were similar for parotid, but with submandibular, the volumes evoked by dobutamine were nearly two times as high as those elicited by terbutaline. Mean [Ca] of parotid saliva was also similar at all dosages of dobutamine (approximately 12 mEq/liter) and generally similar at all dosages of terbutaline (11-15 mEq/liter). Mean [Ca] of dobutamine-elicited submandibular saliva was approximately 6, 7 and 8 mEq/liter at 5, 10 and 25 mg/kg b.wt, respectively. With parotid, [Ca] was approximately 10 mEq/liter at 1, 5 and 10 mg/kg b.wt. but increased to 16-18 mEq/liter at 25 mg/kg. The time course of calcium secretion is described for both agonists at each dosage. [Ca] of both glands was decreased 60 min after i.p. injection of 10 or 25 mg/kg doses of dobutamine or terbutaline but was not changed by 5 mg/kg doses. Administration of 10 mg/kg of atenolol, the selective beta 1 antagonist, 20 min prior to injection of a 10 mg/kg dose of either terbutaline (beta 2 agonist) or dobutamine (beta 1 agonist) blocked secretion from both glands, and prevented the usual agonist-induced reduction in glandular concentration of calcium. Butoxamine, on the other hand, did not modify effects of terbutaline on fluid secretion or depletion of glandular calcium; it did partially inhibit dobutamine-induced fluid and calcium secretion but not depletion of glandular calcium. The present data suggest that beta adrenoceptors of salivary glands are predominantly of the beta 1 subtype and that it is these that regulate calcium and fluid secretion. On the basis of the data with the antagonists, it is concluded that terbutaline activates beta 1 rather than beta 2 receptors since the beta 1 antagonist but not the beta 2 antagonist blocked secretory responses to terbutaline.

Animals↗
PubMed1980

Effects of salbutamol and butoxamine on the human fat cell adenylate cyclase.

In order to characterize the beta-adrenoceptors coupled to the human fat cell adenylate cyclase more extensively the effects of the beta 2-selective agonist salbutamol on basal and isoproterenol-stimulated rates of cAMP-accumulation were studied. Although exhibiting only low intrinsic activity salbutamol displayed only slightly lower affinity towards the beta-adrenoceptors linked to the human fat cell adenylate cyclase than isoproterenol. In addition, the beta 2-selective antagonist butoxamine was slightly more potent in inhibiting the isoproterenol-stimulated fat cell enzyme than the cardioselective beta-blocking agent practolol. These results further emphasize the difficulties in classifying the lipolytic response of adipose tissue to beta-adrenergic agonists and antagonists within a uniform beta-receptor theory.

Adenylyl Cyclases↗