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Biomedical subjects

C R Creveling

Publications and source records attributed to C R Creveling.

At least 91 records · Page 5Linked to original sources
PubMed1976

Cardiovascular toxicity of dihydroxytryptamines.

A comparison of the acute toxicity and a histological examination of the toxic effects in mouse of 4,7-; 5,6-; 5,7- and 6,7-dihydroxytryptamines and related compounds are present. A time and dose dependent induction of subepicardial lesions by 5,6-dihydroxytryptamine is demonstrated. The development of ischemic necrosis of the vaculature of the tail following 6,7-dihydroxytryptamine is described. The toxic effects of these tryptamines are discussed with regard to the phenomena of specific neurodegeneration induced by 5,6- and 5,7-dihydroxytryptamines.

5,6-Dihydroxytryptamine↗
PubMed1975

Norepinephrine uptake sites in cardiac tissue. Lack of affinity of 6-hydroxynorepinephrine and related compounds.

The effects of a series of phenethylamines and the corresponding phenethanolamines on (i) rate of uptake of radioactive norepinephrine into cardiac tissue in vivo and (ii) the rate of efflux of radioactive norepinephrine from prelabeled cardiac storage sites have been determined. The results indicate that m- and p-hydroxuphenethylamines and the corresponding phenethanolamines have high affinities for uptake into cytoplasm and storage vesicles of noradrenergic terminals in the heart. o-Hydroxyphenethylamines such as 2-hydroxyphenethylamine and 2,4,5-trihydroxyphenethylamine (6-hydroxydopamine) also have moderate to high activity as inhibitors of norepinephrine uptake and as releasing agents for norepinephrine, but o-hydroxyphenethanolamines such as 2-hydroxyphenethanolamine, 2,5-dihydroxyphenethanolamine, and 2,4,5-trihydroxyphenethanolamine (6-hyproxynorepinephrine) have little or no activity as inhibitors of uptake or as releasing agents. 2,6-Dihydroxyphenethylamines have little or no activity as inhibitors of uptake or as releasing agents. The results are consonant with significant binding of the gauche conformers of 2-hydroxyphenethylamines to uptake sites. Such conformers would be preferred because of stabilization by hydrogen bonding between nitrogen and phenolic oxygen. Apparently a hydrophobic region of the site prevents binding of such stabilized gauche conformers of 2-hydroxyphenethanolamines and 2,6-dihydroxyphenetylamines.

Animals↗
PubMed1975

Electron microscopic identification of adrenergic nerve endings on thyroid epithelial cells.

Electron microscopic observations were made of the microinnervation of the thyroids of normal mice and of mice given false adrenergic neurotransmitters, and the effects of the drugs on thyroidal norepinephrine uptake were measured. In addition to adrenergic nerve terminals on thyroid blood vessels, structures resembling nerve endings were seen in close apposition to the bases of thyroid epithelial cells. Because they take up false adrenergic neurotransmitters, and undergo degenerative change after administration of cytotoxic false neurotransmitters (6-hydroxydopamine and 5,7-dihydroxytryptamine), which also reduce thyroid norepinephrine uptake, they probably represent adrenergic nerve terminals on thyroid follicles. If so, they afford a morphological basis for the direct effects of catecholamines on thyroid function, which have been reported.

Animals↗
PubMed1970

Stimulated formation of adenosine 3',5'-cyclic phosphate in cerebral cortex: synergism between electrical activity and biogenic amines.

When cortical slices are incubated with adenine-(14)C, adenine nucleotides are labeled in a small and relatively stable pool. The ATP-(14)C of this pool is readily converted to cAMP-(14)C during incubations with depolarizing agents, such as K(+), ouabain, veratridine, or batrachotoxin. During incubations with these agents, release of acetylcholine and of adenosine into the medium is enhanced. The increase in release of adenosine parallels the enhanced formation of cAMP-(14)C elicited by depolarizing agents, providing further evidence that adenosine may serve to couple electrical activity in the central nervous system with formation of cAMP. When adenosine or a depolarizing agent are incubated, together with a biogenic amine, such as histamine, serotonin, or norepinephrine, the combined effect on cAMP-(14)C formation in cortical slices is much more than additive. Extracellular levels of biogenic amines could in this manner modulate cAMP formation and biochemical responses in nervous tissue during electrical activity.

Acetylcholine↗