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J Cardiovasc Pharmacol. 2002 Jun;39(6):814-23.
Pulmonary vasodilatory action of testosterone: evidence of a calcium antagonistic action.

Jones RD, English KM, Pugh PJ, Morice AH, Jones TH, Channer KS.

Academic Unit of Endocrinology, Division of Genomic Medicine, The University of Sheffield, UK. R.D.Joneheffield.ac.uk

Recent evidence supports a beneficial effect of testosterone on the cardiovascular system. Testosterone acts as a coronary vasodilator and reduces myocardial ischemia in men with coronary heart disease. The aim of the current study was to determine whether testosterone has a similar vasodilatory action in the pulmonary circulation and to characterize the underlying mechanism of action. The vasodilatory action of testosterone was studied in pulmonary arteries (n = 132, mean internal diameter = 344 +/- 8 microm) isolated from male rats (n = 48, mass = 396 +/- 7 g) mounted in a small vessel wire myograph and loaded to a tension equivalent to 17.5 mm Hg. Micromolar concentrations of testosterone induced dilatation in pulmonary arteries preconstricted with prostaglandin F2alpha (100 microM) within seconds of application. Dilatation to testosterone was similar in vessels treated with N-gamma-nitro-l-arginine methyl ester (l-NAME) (10 microM) or vehicle (5 microl distilled water), -38.2 +/- 2.9%, and -38.1 +/- 3.4%, respectively, and in vessels treated with indomethacin (10 microM), flutamide (10 microM), or vehicle (5 microl ethanol), -35.5 +/- 2.8%, -43.2 +/- 3.6%, and -35.7 +/- 4.6%, respectively (all p > 0.05). Maximal dilatation to testosterone occurred following preconstriction with agents that activated voltage-gated calcium channels such as prostaglandin F2alpha (-34.6 +/- 5.0%), BAY K8644 (-32.9 +/- 8.7), or potassium chloride (-26.7 +/- 1.5%), compared with calcium-independent protein kinase C activation by phorbol dibutyrate (-14.7 +/- 1.6%) or capacitative calcium entry via thapsigargin (-5.1 +/- 0.9%). This study demonstrates that testosterone induces pulmonary dilatation via a mechanism that is independent of the classic androgen receptor and also of the release of nitric oxide or dilator prostaglandins. The data support a calcium antagonistic action for testosterone in the pulmonary circulation, primarily against voltage-gated calcium channels.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12021575&dopt=Abstract

J Gerontol A Biol Sci Med Sci. 2002 Jun;57(6):M385-91.
Bone density and bone-related biochemical variables in normal men: a longitudinal study.

Scopacasa F, Wishart JM, Need AG, Horowitz M, Morris HA, Nordin BE.

Department of Medicine, University of Adelaide, South Australia, Australia. franca.scopacasdelaide.edu.au

BACKGROUND: The objective of this study was to determine the pattern of forearm bone loss and its relationship to markers of bone turnover and sex steroids in normal men. This was a longitudinal study over a median interval of 41 months. The study was conducted in Adelaide, Australia. Study participants were 123 healthy male subjects, between the ages of 20 and 83 years. METHODS: Fat-corrected forearm bone mineral content (fcBMC), markers of bone formation (alkaline phosphatase, osteocalcin, procollagen type 1 C-terminal extension peptide) and bone resorption (collagen type I cross-linked telopeptide, hydroxyproline/creatinine, pyridinoline/creatinine, and deoxypyridinoline/creatinine), calculated serum bioavailable testosterone, and serum estradiol were measured. RESULTS: The mean time-weighted rate of change in forearm fcBMC was -0.33% +/- 0.72 (SD) per year. Bone loss commenced after 30 years of age and increased with age (p <.001), particularly after age 70 years. There was no relationship between the rate of change in fcBMC and either markers of bone turnover or serum sex steroids. CONCLUSIONS: In normal men, bone loss increases with age; there does not appear to be any relationship between this loss and either markers of bone turnover or levels of free androgen or estrogen.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12023268&dopt=Abstract

Eksp Klin Farmakol. 2002 Jan-Feb;65(1):53-5.
[Hormone level and metabolism of xenobiotics in rats with various phenotype of resistance to hypoxia]

[Article in Russian]

Grek OR, Efremov AV, Grek OO.

Pharmacology Department, Novosibirsk State Medical Academy, Krasnyi pr. 52, Novosibirsk, 630091 Russia.

The blood of rats with initially low (LR) and high (HR) resistance to hypoxia was characterized with respect to the levels of testosterone, corticosterone, insulin and the activity of liver monooxygenase system enzymes. In response to the acute hypoxia model induction, the level of corticosterone in LR rats was significantly greater than that in HP rats (179 and 24%, respectively). The increase in the blood corticosterone level was accompanied by an increase in the activity of enzymes involved in the metabolism of xenobiotics. Animals with the high corticosterone level were also characterized by more intensive metabolism of testosterone and erythromycine. The metabolism of these substrates depends on the activity of isoforms of the cytochrome P-450 3A family. The high corticosterone concentrations in the plasma of LR rats, appearing in response to the acute hypoxia, exhibit a pronounced stimulating action upon the enzyme 11 beta-hydroxysteroiddehydrogenase, which is accompanied by a more pronounced increase in the corticosterone concentration in liver tissues as compared to that in HR animals. The higher content of corticosterone in LR rats leads to an increase in the concentration of cytochrome P-450 and stimulates the enzymatic activity of 3A isoforms in the liver tissues.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12025787&dopt=Abstract

Asian J Androl. 2002 Dec;4(4):273-9.
Effect of adrenalectomy on rat epididymidis.

Nair N, Bedwal RS, Mathur RS.

Cell Biology Laboratory, Department of Zoology, University of Rajasthan, Jaipur - 302 004, India. fasileth.net

AIM: To investigate the effect of adrenalectomy (ADX) on the epididymidis of Sprague-Dawley rats. METHODS: The histological, biochemical (cholesterol protein, zinc, copper, alkaline and acid phosphatase aryl sulphatase, lactic dehydrogenase and leucine amino peptidase) and hormonal (FSH, LH and testosterone) changes of caput and cauda epididymis in ADX rats were observed. RESULTS: Organ wet weight, histological studies and morphometric measurements indicated a cellular degeneration in caput and cauda epididymis of ADX rats. Serum testosterone level was significantly lower in ADX than in sham-operated rats, while the serum FSH and LH were below the detection limit of 1 mIU/mL. The enzymatic activity was higher in ADX than in sham-operated rats. Epididymal zinc level increased whereas copper level decreased in ADX rats compared to the sham-operated. CONCLUSION: Adrenalectomy leads to degeneration of caput and cauda epididymidis epithelial cells as a result of decreased supply of testosterone.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12508128&dopt=Abstract

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