Atropine (5 nM to 5 muM), but not D-tubocurarine or hexamethonium, enhanced the release of acetylcholine (ACh) from rat brain cortical slices exposed to high K+. The enhancement was dose-dependent, and it could be partially antagonized by oxotremorine (50-500 muM) or by dibutyryl or 8-bromo-cyclic GMP (1 mM), but not by tetrodotoxin (200 nM) or by dibutyryl cyclic AMP (1 mM). The effects of oxotremorine and the cyclic GMP derivatives were not due to diminished ACh synthesis, since these compounds did not influence the reduction of tissue ACh resulting from treatment with K+ and atropine. These results suggest that cyclic GMP may mediate the regulation of ACh release by presynaptic muscarinic receptors.

Acetylcholine↗

PubMed1980

Endocrine effects of cyproterone acetate in patients with prostatic cancer.

Cyproterone acetate was given to patients with stages C and D prostatic cancer and its effect on endocrine parameters was studied. At a daily oral dose of 100 mg. cyproterone acetate induced marked reduction in the size and consistency of tumor, while it caused moderate suppression of serum luteinizing hormone, follicle-stimulating hormone and testosterone levels. Elevation of serum prolactin levels was observed after treatment with cyproterone acetate but was to a lesser degree than that caused by estrogens.

Aged↗

PubMed1980

Polyamine and differentiation: induction of ornithine decarboxylase by parathyroid hormone is a good marker of differentiated chondrocytes.

The activity of ornithine decarboxylase (OD-Case:L-ornithine carboxy-lyase, EC 4.1.1.17) in rabbit costal chondrocytes in culture increased markedly after addition of parathyroid hormone (PTH), reaching a maximum 4 to 5 hr after PTH addition. The increase in ODCase activity was followed by increase in the intracellular concentrations of polyamines, especially putrescine, which increased in 6 hr to about 3-fold that of untreated cultures. The induction of ODCase by PTH was not observed in L, 3T3, HeLa, buffalo rat liver, or BHK cells. Retinyl acetate and retinoic acid both inhibited expression of the differentiated phenotype of chondrocytes by rabbit costal chondrocytes in culture within 3 days after their addition, as judged by morphological change and decrease in sulfate incorporation into glycosaminoglycans but did not inhibit cell proliferation. PTH could not induce an increase in ODCase in de-differentiated cells that had been pretreated with retinyl acetate or retinoic acid for 3 days. but 4 days after removal of the retinoids, these de-differentiated cells regained the ability to synthesize ODCase in response to PTH. These facts suggest that the induction of ODCase and the formation of putrescine by PTH are good markers of the differentiated phenotype of cultured chondrocytes.

Animals↗

PubMed1980

Secondary repair of the cleft-lip nose.

Secondary repair of the cleft-lip nose has to date concerned itself only with correction of the lip and external nasal deformity. However, intensive corrective surgery of the deformed nasal septum, which may cause functional and cosmetic handicaps, is also essential in reshaping the drooped nasal tip and alar wing. This paper presents the basic techniques for correcting the deformed nose and nasal floor including the oronasal fistula dn its supportive structures--deviated nasal septums, tilted columellas, and so on. Several patients are presented with cleft-lip nose deformities satisfactorily repaired using these techniques.

Adolescent↗

PubMed1980

Changes in alpha-adrenergic receptors in rat brain in vitro by preincubation with alpha-adrenergic ligands.

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Adrenergic alpha-Agonists↗

PubMed1980

Local anesthetic activity of beta-adrenergic blocking drugs in the Crayfish giant axon, with reference to calcium ion.

The actions of beta-adrenergic blocking drugs, propranolol, pindolol, timolol, carteolol, sotalol and practolol, were examined regarding effects on crayfish giant axon in an attempt to determine the relationship among chemical structure and local anesthetic activity, and the interaction of these drugs with Ca++. The activities of local anesthetics such as procaine and lidocaine served for comparisons. A conventional microelectrode technique was used to obtain the resting membrane and action potentials. All drugs except sotalol and practolol dose-dependently inhibited the dV/dt and amplitude of the action potential with a slight decrease (less than 6 mV) in the resting membrane potential. The relative potencies of these drugs in the reduction of the dV/dt were as follows: propranolol 13.3, pindolol 1.7, procaine 1.0, lidocaine 0.91, timolol 0.71 and carteolol 0.22. Sotalol and practolol had little activity. The chemical structure of the drugs for local anesthetic action was closely related to that of the lipophilic aromatic group; the most potent activity seen in the naphthyl group. Potentiation of the local anesthetic activity in low Ca++ solution was obtained with pindolol, timolol, carteolol, sotalol and practolol. Reduction of the activity in high Ca++ solution was observed with propranolol, pindolol, timolol, procaine and lidocaine. These results suggest that external Ca++ competes with the local anesthetic action of the beta-adrenergic blocking drugs, at the site of the action potential generating mechanism.

Action Potentials↗

PubMed1980

Dissociation of plasma renin activity and plasma aldosterone level during dexamethasone suppression test in non-salt-losers with congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

We have studied plasma renin activity, the plasma aldosterone level and urinary metabolites of glucocorticoid precursors before and during a dexamethasone suppression test in three non-salt-losers with congenital adrenal hyperplasia due to 21-hydroxylase deficiency, who had never been treated with glucocorticoid. Plasma renin activity, the plasma aldosterone level and urinary pregnanetriol excretion were found to be abnormally elevated before dexamethasone administration. After 7 days' dexamethasone administration, plasma renin activity still remained high above the normal level, while the plasma aldosterone level as well as urinary 17KS and pregnanetriol excretion were lowered to the normal ranges. Several possible mechanisms for this discordant suppression of plasma renin activity and aldosterone level were discussed and the presence of mineralocorticoid resistance, which is not related to ACTH dependent aldosterone antagonists, was suggested in the case of these patients.

17-Ketosteroids↗