Are the renin-containing granules of juxtaglomerular epithelioid cells modified lysosomes? Phentermine self-administration in naive free-feeding and food-deprived rats: a dose response study. Role of the alveolar macrophage in the induction of pulmonary phospholipidosis by chlorphentermine. I. Drug and phospholipid levels. Ionamin online references

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Cell Tissue Res. 1985;239(3):575-87.
Are the renin-containing granules of juxtaglomerular epithelioid cells modified lysosomes?

Taugner R, Whalley A, Angermuller S, Buhrle CP, Hackenthal E.

Mature secretory granules of epithelioid cells--the so-called renin granules--exhibit certain properties, which in this particular combination are expressed only by lysosomes: Renin granules have autophagic capabilities; they react to the application of lipidosis-inducing, lysosomotropic substances by the gradual accumulation of polar lipids; all secretory granules of epithelioid cells contain acid phosphatase until maturity; and exogenous tracers reach renin granules without labeling the Golgi complex. Several functional implications can therefore be considered. Hydrolytic enzymes, constitutive elements of the granule matrix, might either cleave inactive prorenin to yield active renin within the granules or, by unspecific hydrolysis of renin, participate in the regulation of the overall quantity of secretory product. Autophagic phenomena, the involvement of renin granules in the traffic of exogenous tracers, and the build-up of polar lipids following experimental interference with lipid catabolism indicate a large turnover of membrane material in renin granules. They also suggest that cytoplasmic and extracellular fluid gains access to the granule content and may thus be involved there in the regulation of biochemical reactions by changing the intragranular milieu or via signal molecules. In addition to the lysosome-like properties of epithelioid cell secretory granules, the secretory product, renin, as a carboxyl protease, is structurally related to other acidic proteases. In the case of cathepsin D, even functional similarities exist.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3886148&dopt=Abstract

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Psychopharmacology (Berl). 1985;85(4):410-3.
Phentermine self-administration in naive free-feeding and food-deprived rats: a dose response study.

Papasava M, Singer G, Papasava CL.

In the present experiment graded doses of phentermine, an anorectic similar to amphetamine in structure and mechanism of action, were made available to naive free-feeding (FF) or 80% free-feeding weight (FFW) rats for IV self-administration. Findings showed that, in 80% FFW rats, the number of injections taken were an inverted U-shaped function of dose, whereas the amount of drug injected was a monotonically increasing function of dose. FF animals, however, failed to self-administer phentermine at rates that differed significantly from FF animals self-administering saline. These data suggest that the clinical use of anorectics which have a mechanism of action similar to amphetamine may increase the risk of drug dependence whenever weight loss is achieved.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3927335&dopt=Abstract

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J Pharmacol Exp Ther. 1986 Jan;236(1):55-9.
Role of the alveolar macrophage in the induction of pulmonary phospholipidosis by chlorphentermine. I. Drug and phospholipid levels.

Heyneman CA, Reasor MJ.

In this study we have shown that the alveolar macrophage (AM) plays a major role in the induction of phospholipidosis in rat lung by chlorphentermine (CP). Rats were administered CP (30 mg/kg i.p., 5 days/week) for 1, 4 and 8 weeks and the levels of CP and total phospholipid were measured in whole lungs and in the AM fraction recovered from the lungs by pulmonary lavage. Lungs accumulate CP to a much greater extent than liver or kidney and show a marked increase in phospholipid content by 8 weeks. Drug treatment is accompanied by the recovery of an elevated number of AMs at all time points. The CP and phospholipid levels in AMs reach a peak at 4 weeks with little change beyond that time. Initially the phospholipidosis is localized largely in the AMs with the disorder developing in other compartments of the lungs with increasing treatment time. The AMs contribute 3% of the total pulmonary phospholipid in control rats. After 1 week of CP, 34% of the pulmonary phospholipid is in the AM fraction with this value being 21% after 8 weeks. The CP to phospholipid molar ratio is higher in AMs than whole lung at all three time points.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3941400&dopt=Abstract

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