Search Results
You are looking at 1 - 3 of 3 items for
- Author: J. J. STERN x
- Refine by access: All content x
Search for other papers by J. J. STERN in
Google Scholar
PubMed
Search for other papers by M. MURPHY in
Google Scholar
PubMed
SUMMARY
The wheel-running activity of 19 male rats was examined before and after castration. Castration significantly reduced spontaneous activity. Testosterone propionate (TP) administration increased activity to levels before castration. Cyproterone acetate given with TP did not inhibit the increase in activity but inhibited the growth of seminal vesicles.
Search for other papers by JEFFREY J. STERN in
Google Scholar
PubMed
Search for other papers by RICHARD JANKOWIAK in
Google Scholar
PubMed
Oestrogen stimulation increases spontaneous activity in laboratory rats and this effect appears to be mediated by the anterior hypothalamic—preoptic region (AH—POA) of the diencephalon (Kennedy, 1964). The present study sought to determine whether the antioestrogenic agent actinomycin-D (Act-D) implanted bilaterally in the AH—POA would antagonize the increase in running produced by exogenous oestrogen.
Thirteen virgin Sprague—Dawley rats (260–355 g) aged 85–125 days were housed in individual, metal activity wheels with attached living cages described elsewhere (Stern & Zwick, 1972). Food and water were available ad libitum. The laboratory was on an artificial 12 h light: 12 h dark cycle. Activity (number of revolutions) was recorded daily. The animals were ovariectomized under methoxyfluorane (Metofane) anaesthesia 14 days before implantation under the same anaesthetic. Records of activity were started 7 days after ovariectomy. Double-walled cannulae were implanted bilaterally in the AH—-POA (anterior 7·5; lateral 1·0; vertical — 1·2; deGroot, 1959). The
Search for other papers by F. R. Bringhurst in
Google Scholar
PubMed
Search for other papers by A. M. Stern in
Google Scholar
PubMed
Search for other papers by M. Yotts in
Google Scholar
PubMed
Search for other papers by N. Mizrahi in
Google Scholar
PubMed
Search for other papers by G. V. Segre in
Google Scholar
PubMed
Search for other papers by J. T. Potts Jr in
Google Scholar
PubMed
ABSTRACT
Parathyroid hormone (PTH) is rapidly metabolized, mainly by liver and kidney, to smaller fragments that are believed to be biologically inactive. The significance of this peripheral metabolism in the overall actions of PTH is unclear. Generation of circulating biologically active amino-terminal PTH fragments during metabolism in vivo has been suggested by certain observations in vitro, and what are believed to be amino-terminal fragments may be detectable in blood under pathological circumstances in vivo (such as renal failure and coexistent hyperparathyroidism) when highly sensitive assays are employed. We recently reported, however, that administration to normal rats of [35S]bovine PTH ([35S]bPTH) directly labelled at amino-terminal methionines, followed by high-resolution chromatographic analysis of extracted [35S]peptides, does not result in appearance of radioactive amino-terminal fragments in blood, even when the tracer is continuously infused to near-physiological plasma concentrations. We have now employed these techniques to address a second question regarding hormonal metabolism: is hormonal metabolism modified during metabolic perturbations such as changing calcium availability or altered levels of calciotrophic hormones? Metabolism of [35S-Met]bPTH (900 Ci/mmol), either alone or together with [3H-Pro]bPTH, however, did riot lead to alterations in the rate of hormonal clearance nor to detectable circulating amino-terminal fragments, either in calcium-deprived or thyroparathyroidectomized rats or when animals were first rendered intoxicated with vitamin D or maintained on a high calcium intake. Likewise, tissue localization and specific cleavage patterns of intact hormone in liver or kidney were all unaltered by these various manoeuvres. We conclude that regulation of peripheral metabolism of PTH does not exert important physiological control over the concentration of circulating biologically active PTH and that active amino-terminal fragments of the hormone are not released into blood even under circumstances of calcium deprivation or hypocalcaemia.
Journal of Endocrinology (1989) 122, 237–245
