PubMed Health⌕ Search

Biomedical subjects

M L Maayan

Publications and source records attributed to M L Maayan.

At least 19 recordsLinked to original sources
PubMed1989

Norepinephrine and TSH: effects on thyroidal radioiodine and thyroxine release.

Norepinephrine (NE) failed to increase thyroid hormone release in mice when endogenous TSH secretion had been greatly reduced by a variety of means. This was demonstrated by radioiodine release in mice pretreated with 131I and with thyroxine (T4) or 3,5,3' triiodothyronine (T3). by radioimmunoassay (RIA) in mice pretreated with 131I and T3, and in mice which had been hypophysectomized, or where TSH secretion had been decreased by prolonged administration of exogenous TSH. T4 could not be measured by RIA in mice pretreated with T4.

Animals↗
PubMed1989

Incidental detection of adult polycystic kidney disease on routine bone scan.

A routine bone scan performed on a 36-y old male incidentally demonstrated enlarged kidneys with multifocal areas of radionuclide concentration suggestive of polycystic kidneys. Further evaluation using ultrasonography, CT scan, and a 99mTc-GHA renal scan confirmed the initial impression. The routine evaluation of the kidneys on a bone scan is emphasized as a simple method of identifying previously unsuspected renal structural abnormalities.

Adult↗
PubMed1987

Inhibition of cholesterol-induced atherosclerosis in rabbits by dimethyl sulfoxide.

The effect of dimethyl sulfoxide (DMSO) on cholesterol-induced atherosclerosis in the rabbit was investigated. Two groups of rabbits were studied: a Control group which received regular chow and an Experimental group which received an atherogenic diet containing 1% cholesterol. DMSO was either omitted or added to the drinking water of both groups in amounts of 2, 4, 5 and 6%. After 3 months all animals were autopsied; the thoracic aorta was examined for atheromatous lesions and the abdominal aorta assayed for total cholesterol content. As expected the thoracic aortas of all rabbits in the Control group were free of atheromatous lesions. With the exception of one rabbit in the Experimental group, all rabbits on the atherogenic diet which did not receive DMSO had extensive aortic lesions covering 82 +/- 5% of the surface area of the thoracic aorta. Aortic lesions were inhibited by about 50% in rabbits on 2% (dose, 1.5 g/kg) DMSO and virtually absent in the majority of rabbits on 4 (dose, 3.5 g/kg), 5 (dose, 5.5 g/kg) and 6% (dose, 9.1 g/kg) DMSO. The food intake of rabbits on the atherogenic diet was not suppressed by DMSO. Changes in the cholesterol content of the abdominal aortas paralleled the presence or absence of lesions in the thoracic aorta. Blood cholesterol levels were greatly elevated in all rabbits on the atherogenic diet and not lowered by DMSO. In conclusion, cholesterol induced atherosclerosis in the rabbit was inhibited by DMSO. This action of DMSO was independent of the hypercholesterolemia and not due to a suppression of food intake. DMSO may provide a useful probe for investigating the underlying mechanism(s) in the development of cholesterol induced atherosclerosis.

Animals↗
PubMed1986

Dopamine and L-dopa: inhibition of thyrotropin-stimulated thyroidal thyroxine release.

Previous studies had suggested that norepinephrine (NE) and its precursors dopamine (DA) and L-DOPA acted similarly on iodine metabolism of isolated thyroid cells. Present studies indicate that this similarity extends to the inhibition by catecholamines of TSH-stimulated T4 release by mouse thyroids incubated in vitro. DA (5 X 10(-4) M), like NE, shown previously, inhibits TSH-stimulated T4 release. This inhibition was reversed by the alpha-blockers phentolamine, prazosin, and yohimbine, but not by the beta-blocker L-propranolol. DU-18288 and diethyldithiocarbamate, inhibitors of DA beta-hydroxylase, did not reduce DA inhibition, suggesting that prior conversion to NE was not a condition for DA activity. Apomorphine, a dopaminergic agonist but not a NE precursor, acted like DA, and its inhibition was also reversed by alpha-blockers. Furthermore, sulpiride, a dopaminergic blocker, reversed DA and apomorphine inhibition of TSH stimulation. These results suggest that DA inhibits TSH-stimulated T4 release through both adrenergic and dopaminergic receptors. On the other hand, L-DOPA, exerting an inhibition like that of DA, was also reversed by alpha-blockers, but its activity was greatly diminished by carbidopa, an inhibitor of aromatic L-amino acid decarboxylase, the enzyme converting L-DOPA to DA. This indicated that L-DOPA had to be converted to DA for activity. Both DA and L-DOPA inhibited stimulation of T4 release induced by (Bu)2cAMP, suggesting that their effect was exerted at a locus distal to cAMP generation. Indirect confirmation of a cAMP-independent pathway was obtained when DA inhibited TSH-stimulated cAMP formation, but, contrary to T4 release, this inhibition was not reversed by dopaminergic or adrenergic blockers. Presumably, therefore, DA inhibition of TSH-stimulated cAMP production was not related to T4 release. We conclude that 1) DA inhibits TSH-stimulated T4 release in mouse thyroids via alpha-adrenergic and dopaminergic receptors; 2) L-DOPA has to be converted to DA to produce inhibition; and 3) cAMP is unlikely to be an intermediary in DA inhibition.

Adrenergic alpha-Antagonists↗
PubMed1979

Action of gold thioglucose on pericapillary structures in the ventromedial hypothalamus.

The administration of GTG to mice leads to death of all structures in a circumscribed area of the VMH as a result of loss of blood circulation. The loss of circulation is due to damage by GTG of neural processes adjacent to some of the capillaries in this area; damage to these processes leads to abnormal capillary permeability. Pericapillary damage occurs under conditions where capillary damage and consequent necrosis are prevented. Abnormal capillary permeability appears to follow release of a vasoactive substance from the damaged neural processes. Damage to the pericapillary neural processes by GTG is insulin-dependent and is counteracted by glucocorticoids.

Animals↗
PubMed1978

An in vitro procedure for the estimation of thyroid hormone releasing factors in sera of thyrotoxic patients.

LATS containing sera and a number of Graves' disease sera stimulated T4 release from mouse thyroids in vitro as determined by RIA, thus confirming the presence of a thyroid hormone releasing factor in sera of thyrotoxic patients. The pattern of stimulation was similar to that previously shown for TSH in terms of T4 release time sequence. cAMP increase and catecholamine inhibition via alpha-adrenergic receptors. In the same in vitro system, neutralization with a human thyroid homogenate showed presence of LATS-Protector (LPA) in LATS negative thyrotoxic sera. The present study describes a simpler procedure for estimating LATS or similar activity, as compared to the McKenzie assay, and suggests identical receptor sites for TSH and other thyroid stimulators.

Animals↗
PubMed1978

Inhibition by adenosine of thyroidal T4 release in vitro.

Adenosine, like catecholamines, inhibits the thyroidal T4 release in vitro, when stimulated by TSH,N,O'-dibutyryl cyclic AMP [(Bu) 2cAMP], and phosphodiesterase inhibitors. Unlike catecholamines, the adenosine-induced inhibition is independent of adrenergic receptors. It is postulated that TSH stimulates thyroidal T4 release through a cAMP activated, adenosine-sensitive, protein kinase.

Adenosine↗
PubMed1977

Catecholamine inhibition of thyrotropin-induced secretion of thyroxine: mediation by an alpha-adrenergic receptor.

Thyroxine secretion by mouse thyroid gland incubated in vitro was measured. Thyrotropin or dibutyryl cAMP increased thyroxine secretion several-fold. l-Epinephrine and l-norepinephrine strongly inhibited this stimulated release; l-isoproterenol was relatively ineffective. Phentolamine prevented the inhibition by catecholamines of thyroxine release; l-propranolol had no effect. These findings indicate that stimulation of alpha-adrenergic receptors opposes the action of thyrotropin in the regulation of thyroxine secretion.

Animals↗
PubMed1977

Inhibition of thyrotropin- and dibutyryl cyclic AMP-induced secretion of thyroxine and triiodothyronine by catecholamines.

Thyrotropin (TSH), 1 MU/ml and N6, O2'-dibutyryl adenosine 3',5-cyclic monophosphoric acid (dbcAMP) greatly enhanced the release of thyroxine (T4) and triiodothyronine (T3) from mouse thyroids incubated in vitro. L-Epinephrine (E) and L-norepinephrine (NE) strongly inhibited the TSH and dbcAMP-stimulated release of thyroid hormones; L-isoproterenol (IPNE) exerted a relatively weak inhibition. The inhibition by catecholamines was prevented by the alpha-adrenergic blocker, phentolamine; L-propranolol, a beta-adrenergic blocker, had no effect on the inhibition. The TSH-induced release of thyroid hormones was not affected by adrenergic blockers. Epinephrine did not affect the increase in thyroidal cAMP content induced by TSH. These results indicate that catecholamines act by way of an alpha-adrenergic receptor to suppress TSH-stimulated release of thyroid hormones at a point beyond cAMP formation.

Animals↗
PubMed1977

TSH and catecholamines: independent effects on active transport and iodine organification in isolated thyroid cells.

Catecholamines greatly stimulated iodine organification in thyroid cells isolated by trypsinization but failed to increase the cell-medium (C/M) ratio of 131I- or 99mTcO4- in the same cells preparation. Both TSH and catecholamines increased the concentration of organified iodine in thyroid cell despite the presence of active transport inhibitors, suggesting either the existence of a second thyroidal transport system or the possibility of an accelerated entry of anions into thyroid cells in the presence of stimulatory agents.

Animals↗
PubMed1977

Gold thioglucose obesity syndrome.

Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. The glucose moiety of gold thioglucose is essential for production of the lesion. Glucose analogues (2-deoxy-glucose, sodium thioglucose and phlorizin) prevent the gold thioglucose-induced lesion, and by themselves produce a transient hyperphagia. Insulin deficiency prevents the lesion. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Electron microscopic studies, in which general necrosis is avoided by administration of aspirin before gold thioglucose or by administration of subnecrotic doses of gold thioglucose, reveal that gold thioglucose primarily affects neural elements contiguous with capillaries in the ventromedial hypothalamus. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake.

Adrenalectomy↗