The accumulation and metabolism of dopamine by the human platelet

Solomon, Harvey M.; Spirt, Nena; Abrams, William B.

doi:10.1002/cpt1970116838

Cited by 59 publications

(32 citation statements)

References 6 publications

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“…In addition, it has been reported that the DA transport system is distributed not only in neurons but also in lymphocytes 16) and platelets. 17) These results supported our hypothesis that Trp-P-1 would be taken up into splenocytes and thymocytes through the DA transport system. On the other hand, this raises the question of whether Trp-P-1 was transported into cells or bound to the plasma membrane.…”

Section: Discussionsupporting

confidence: 85%

3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) Is Incorporated into Rat Splenocytes, Thymocytes, and Hepatocytes Through Monoamine Transporters and Induces Apoptosis

Hashimoto

Furuyashiki

Sano

et al. 2002

Bioscience, Biotechnology, and Biochemistry

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Section: Discussionsupporting

confidence: 85%

3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) Is Incorporated into Rat Splenocytes, Thymocytes, and Hepatocytes Through Monoamine Transporters and Induces Apoptosis

Hashimoto

Furuyashiki

Sano

et al. 2002

Bioscience, Biotechnology, and Biochemistry

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“…From his findings that washed platelets accumulated less quinidine that those suspended in their own plasma, and that platelet ghosts do not bind immunologically detectable amounts of drug he concluded that quinidine does not attach directly to the platelet membrane. Solomon & Zieve (1967) found, however, by measuring quinidine directly, that it bound avidly to human blood platelets. We confirm this and show that uptake occurs in Krebs solution, indicating that formation of an antibody complex is not a prerequisite for binding.…”

Section: Discussionmentioning

confidence: 95%

“…Therefore we cannot dismiss the possibility that different results might be obtained if calcium were present. However, this does not seem likely because the extensive accumulation of many other substances by platelets, including chlorpromazine, imipramine and reserpine (Ahtee & Paasonen, 1966;Boullin & O'Brien, 1968;Solomon & Zieve, 1967) has been studied in calcium free conditions; also the uptake of catecholamines is dependent on sodium, but not calcium (Iversen & Kravitz, 1966;Tissari, Sch6nhofer, Bogdanski & Brodie, 1969).…”

Section: Discussionmentioning

confidence: 99%

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Accumulation of quinidine by human blood platelets: effects on platelet ultrastructure and 5‐hydroxytryptamine

Boullin

O'Brien

1971

British J Pharmacology

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Summary1. We have studied the mechanism of quinidine uptake by normal human blood platelets. 2. Platelets in plasma or Krebs solution took up quinidine extremely rapidly, the maximal drug concentration ratio of platelet to medium being 24 to 1 after 1 minute. 3. The effects of metabolic inhibitors on uptake were equivocal. Ouabain had no effect but iodoacetate and dinitrophenol were effective. However, as accumulation was not inhibited by low temperature, it was probably not energy dependent. 4. Interactions between quinidine and 5-HT were also investigated. 5. Quinidine blocked 5-HT uptake, but conversely, neither 5-HT itself nor 5-HT uptake inhibitors, such as cocaine, dexamphetamine, and desipramine interfered with quinidine accumulation. 6. Electronmicrographs of platelets incubated with 10-5, 10-4 or 2 x 10-3M quinidine in Krebs solution for 2 h showed no changes at the lower concentrations, but gross ultastructural damage, including disintegration of the plasma membrane, at 2 x 10-3M.7. Further evidence for intracellular penetration was obtained because quinidine released endogenous 5-HT and ATP, and also 14C-5-HT from loaded cells. 8. We conclude that quinidine is taken up by the platelet by a passive process, unrelated to the 5-HT transport mechanism. It is probably accumulated largely in the plasma membrane and outer protein layer, but intracellular penetration and ultrastructural damage may occur.9. Although the effects on 5-HT and ATP were not due to platelet damage, this may occur in vivo and be the cause of quinidine induced thrombocytopenic purpura.

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“…The platelet CA are likely to be of plasma origin since it is known that platelets lack CA synthesizing enzymes (Lahovaara, Paasonen & Airaksinen, 1968;Solomon, Spirt & Abrams, 1970;Boullin & Green, 1972).…”

Section: Catecholamines In Plateletsmentioning

confidence: 99%

Content and Subcellular Localization of Catecholamines and 5‐hydroxytryptamine in Human and Animal Blood Platelets: Monoamine Distribution Between Platelets and Plasma

Prada

Picotti

1979

British J Pharmacology

151

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The content of adrenaline (Ad), noradrenaline (NA) and dopamine was measured in human, guinea‐pig, cat, rabbit and rat blood platelets by a highly sensitive and specific radioenzymatic method. In all platelet specimens analyzed, the content of the three catecholamines (CA) was several thousand times lower than that of 5‐hydroxytryptamine (5‐HT). In basal conditions, the NA concentration in platelets and plasma always exceeded that of Ad and dopamine. In rat and rabbit platelets, Ad, NA and dopamine were present only in the free (unconjugated) form. Platelets of rats with storage pool deficiency (Fawn‐hooded) contained much less 5‐HT and CA than normal rat platelets. Following restraint stress, platelets of Fawn‐hooded rats, in contrast to normal rat platelets, did not accumulate CA in spite of a dramatic rise in plasma CA. Reserpine, a monoamine depletor, released CA as well as 5‐HT from rabbit platelets in vivo. Subcellular fractionation experiments with rabbit platelets indicate that both CA and 5‐HT are most concentrated in the fraction consisting of pure 5‐HT organelles. Both in humans and rabbits the concentration gradient between platelets and plasma was much lower for CA than for 5‐HT, indicating that a high affinity transport mechanism operates in vivo for 5‐HT but not for CA. In conclusion, the present data show that both human and animal platelets contain Ad, NA and dopamine. The bulk of the CA seems to be stored as unconjugated amines together with 5‐HT, histamine and p‐octopamine in a multitransmitter storage site, namely the 5‐HT organelle.

show abstract

The accumulation and metabolism of dopamine by the human platelet

Cited by 59 publications

References 6 publications

3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) Is Incorporated into Rat Splenocytes, Thymocytes, and Hepatocytes Through Monoamine Transporters and Induces Apoptosis

3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) Is Incorporated into Rat Splenocytes, Thymocytes, and Hepatocytes Through Monoamine Transporters and Induces Apoptosis

Accumulation of quinidine by human blood platelets: effects on platelet ultrastructure and 5‐hydroxytryptamine

Content and Subcellular Localization of Catecholamines and 5‐hydroxytryptamine in Human and Animal Blood Platelets: Monoamine Distribution Between Platelets and Plasma

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