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At least 1,297 records · Page 72Linked to original sources
PubMed1984

The effects in myometrial preparations of D2343, a beta 2-adrenoceptor agonist possessing alpha 1-receptor blocking qualities.

D2343 is a compound with about the same beta 2-adrenoceptor-agonist effect as terbutaline and exhibiting in addition an alpha 1-receptor inhibitory activity. D2343 has been compared to the beta 2-agonist terbutaline on oestrogenized uterine preparations from rat and rabbit (in vitro and in vivo) and in myometrial strips from homo. Generally, D2343 has shown an ability to relax the uterine muscles to the same degree as terbutaline or even more, especially when the two drugs were compared in vitro in preparations from rabbit and rat.

Adrenergic alpha-Antagonists↗
PubMed1985

The effect of D2343 in transmurally stimulated rabbit isthmus muscle.

In in vitro experiments spirally cut isthmic preparations from oestrogenized rabbits have been contracted by transmural stimulation. The beta 2-agonistic and alpha 1-antagonistic drug D2343 (for chemical structure, see fig. 1 in Olsson et al. 1984) inhibits the evoked contractions in a concentration related fashion with 50% effect at 9.6 X 10(-6) mol/l. The alpha 1-antagonist prazosin has an inhibiting action in the same concentration range (EC50 = 14.0 X 10(-6) mol/l). To inhibit the contractile response to the same degree by the beta 2-agonist terbutaline the concentration has to be greater than 10(-3) mol/l. From received results the beta (beta 2)-adrenoceptor mediated effects seem to be of minor importance compared to the alpha (alpha 1)-receptor dominance in the isthmus muscle during oestrus.

Adrenergic alpha-Antagonists↗
PubMed1975

How does angiotensin II increase cardiac dopamine-beta-hydroxylation?

The potent accelerating effect of angiotensin II (Ang II) on caridac dopamine beta-hydroxylation was studied on slices of rat heart. Ang II did not affect the kinetics of beta-hydroxylation but it increased the axonal uptake of dopamine, and, concomitant with the acceleration of biosynthesis, it enhanced the accumulation of dopamine into tissue. Puromycin, in contrast to actinomycin D, antagonized the stimulation of dopamine beta-hydroxylation by Ang II, but did not suppress the rise in cardiac dopamine. Therefore, to promote the acceleration of dopamine beta-hydroxylation, (i) the rise in tissue dopamine available for conversion appeared to be insufficient, (ii) the formation of new proteins by activation of traduction seemed to constitute the basic mechanism of Ang II action.

Angiotensin II↗
PubMed2002

In vivo alpha(1)-adrenergic lipolytic activity in subcutaneous adipose tissue of obese subjects.

The role of alpha(1)-adrenoceptors in lipid mobilization and blood flow was investigated in situ using microdialysis of subcutaneous adipose tissue in severely obese subjects. The lipolysis rate was assessed by determination of interstitial glycerol concentration. The alpha(1)-adrenoceptor agonist norfenefrine caused an increase in glycerol level in adipose tissue that was similar to that observed with the physiologic alpha(1,2)-beta(1)-adrenoceptor agonist norepinephrine, whereas the alpha(1)-adrenoceptor antagonist urapidil showed no effect on basal lipolysis rate. However, the enhanced glycerol concentration due to norfenefrine and norepinephrine was suppressed in the presence of urapidil. The beta-adrenoceptor antagonist propranolol showed no effect on norfenefrine-stimulated glycerol outflow. Blood flow was assessed using the ethanol escape technique. Perfusion with norfenefrine decreased blood flow, whereas urapidil enhanced blood flow significantly. Despite the increase in blood flow, the basal interstitial glycerol concentration remained unchanged. Although norfenefrine at high concentrations could inhibit the urapidil-induced increase in blood flow, the norfenefrine-induced glycerol output was not affected. These results demonstrate that alpha(1)-adrenoceptors are involved in regulation of lipolysis rate and microcirculation of adipose tissue. However, the observed changes in local blood flow were not related to glycerol output.

Adipose Tissue↗
PubMed1970

Indole metabolism in the pineal gland: a circadian rhythm in N-acetyltransferase.

The activity of N-acetyltransferase in the rat pineal gland is more than 15 times higher at night than during the day. This circadian rhythm persists in complete darkness, or in blinded animals, and is suppressed in constant lighting. The N-acetyltransferase rhythm is 180 degrees out of phase with the serotonin rhythm and is similar to the norepinephrine and melatonin rhythms. Experiments in vitro indicate that norepinephrine, not serotonin, regulates the activity of N-acetyl-transferase through a highly specific receptor.

Aniline Compounds↗
PubMed1973

Methyltetrahydrofolic acid mediates N- and O-methylation of biogenic amines.

A variety of mammalian and avian tissues N- and O-methylate indoleamines and phenylethylamines, with methyltetrahydrofolic acid as the methyl donor. Because it is considerably more efficient than S-adenosylmethionine, methyltetrahydrofolic acid may be the natural methyl donor in this reaction. With methyltetrahydrofolic acid, serotonin is O-methylated to 5-methoxytryptamine, a novel indoleamine in mammalian brain.

Animals↗
PubMed1979

Embryonic development of identified neurons: temporal pattern of morphological and biochemical differentiation.

Individually identified neurons can be recognized in grasshopper embryos, and are accessible to examination by morphological, physiological, and biochemical techniques from their birth to their maturation. Only after the axon of an identified neuron reaches its postsynaptic target does the neurotransmitter accumulate, the soma rapidly enlarge, and the central arborizations greatly expand.

Animals↗