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F M Perez

Publications and source records attributed to F M Perez.

25 records · Page 2Linked to original sources
PubMed1989

Possible participation of calcium in growth hormone release and in thyrotropin-releasing hormone and human pancreatic growth hormone-releasing factor synergy in a primary culture of chicken pituitary cells.

We previously reported that thyrotropin-releasing hormone (TRH) and human pancreatic growth hormone-releasing factor (hpGRF) exert synergistic (greater than additive) effects on growth hormone (GH) release from chicken pituitary cells in primary culture. In the present studies the possible participation of calcium in GH release and in TRH and hpGRF synergy was investigated. Following dispersion with collagenase, cells were cultured for 48 hr prior to exposure (2 hr) to test agents. Cultured cells were exposed to a range of calcium concentrations (0, 0.02, 0.2, and 2.0 mM) in the presence and absence of secretagogues. These results demonstrated that basal GH release was not altered by the concentration of calcium in the medium: however, secretagogue-induced GH release required calcium. Thus, TRH, hpGRF, 8 Br-cAMP, or forskolin stimulated GH release in the absence of calcium. Furthermore, synergistic GH release evoked by TRH and hpGRF, 8 Br-cAMP, or forskolin was observed only at the highest calcium concentration (2.0 mM). In other studies, ionomycin (10(-5) M), a calcium ionophore, stimulated GH release to a value about 125% over the basal (absence of test agent) value. Ionomycin-induced GH release was not affected by TRH (5.0 ng/ml); the combined effects of ionomycin (10(-7)-10(-5) M) and hpGRF (5.0 ng/ml) on GH release were less than additive. However, ionomycin (10(-5) M) further increased GH release over that resulting from the synergistic action of TRH and hpGRF (5.0 ng/ml each). Verapamil (a calcium channel blocker) did not affect GH release induced by either TRH or hpGRF (5.0 ng/ml each). However, this agent did inhibit synergistic GH release evoked by TRH and hpGRF, 8 Br-cAMP, forskolin, or isobutylmethylxanthine. These results suggest that calcium participates in secretagogue-induced GH release from chicken somatotrophs in vitro.

Animals↗
PubMed1987

Growth hormone secretion from chicken adenohypophyseal cells in primary culture: effects of human pancreatic growth hormone-releasing factor, thyrotropin-releasing hormone, and somatostatin on growth hormone release.

A primary culture of chicken adenohypophyseal cells has been developed to study the regulation of growth hormone (GH) secretion. Following collagenase dispersion, cells were exposed for 2 hr to vehicle (control) or test agents. Human pancreatic (tumor) growth hormone-releasing factor (hpGRF) and rat hypothalamic growth hormone-releasing factor stimulated GH release to similar levels. GH release was increased by the presence of dibutyryl cyclic AMP. Thyrotropin-releasing hormone (TRH) alone did not influence GH release; however, TRH plus hpGRF together exerted a synergistic (greater than additive) effect, increasing GH release by 100 to 300% over the sum of the values for each secretagogue acting alone. These relationships between TRH and hpGRF were further examined in cultured cells exposed to secretagogues for two consecutive 2-hr incubations. TRH pretreatment enhanced subsequent hpGRF-stimulated GH release by about 80% over that obtained if no secretagogue was present during the first incubation. In other experiments, somatostatin (SRIF) alone did not alter GH secretion. However, SRIF reduced hpGRF-stimulated GH release to levels found in controls. Furthermore, GH release stimulated by the presence of both TRH and hpGRF was lowered to control values by SRIF. The results of these studies demonstrate that a primary culture of chicken adenohypophyseal cells is a useful model for the study of GH secretion. Indeed, these results suggest that TRH and hpGRF regulate GH secretion by mechanisms which are not identical.

Animals↗
PubMed1986

Corticotropin-releasing factor stimulates the release of adrenocorticotropin from domestic fowl pituitary cells.

The effect of synthetic ovine CRF on ACTH secretion of dispersed, domestic fowl pituitary cells was investigated. Cells preincubated for 2 h, 16 h, or after 48-h culture were incubated briefly with CRF (up to 4 h). ACTH was bioassayed using isolated rat adrenocortical cells; ACTH-(1-24) served as the standard for expressing the data. Results with 16-h preincubated cells were as follows: CRF induced ACTH secretion in a concentration-dependent manner: ED50 and maximal stimulatory concentrations were 1.0 nM and 5.0 nM, respectively. CRF (10 nM) induced significant ACTH secretion within 10 min of incubation; maximal secretion (370% over basal value) was attained at 2 h. Dexamethasone (DEX) inhibited basal and CRF-induced ACTH secretion in a concentration-dependent manner; half-maximal inhibitory and maximal inhibitory concentrations were approximately 10 nM and 1 microM, respectively. In addition, DEX (10 microM) acutely (within 2 h) inhibited maximal CRF-induced ACTH secretion by 46%. 8-Bromo-cAMP (1 mM) also induced ACTH secretion, and DEX inhibited this secretion with a potency equivalent to that for CRF-induced ACTH secretion. In contrast to the effect of CRF, high concentrations (100 nM) of ovine LHRH, TRH, and synthetic human pancreatic GH-releasing factor (1-32) failed to induce significant ACTH secretion, thus suggesting that the effect of CRF was peptide specific. Domestic fowl pituitary cells cultured for 48 h before treatment also responded to CRF but not to any greater extent than that of 16-h preincubated cells. In contrast to 16-h preincubated cells or 48-h cultured cells, 2-h preincubated cells had high basal values of ACTH secretion that may have partially diminished or masked the actions of CRF. These data suggest that 1) CRF is a potent and specific stimulator of ACTH secretion by domestic fowl pituitary cells and 2) 16-h preincubated cells or 48-h cultured cells are amenable for other in vitro investigations on the regulation of avian ACTH secretion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1977

Subcutaneous mastectomy data: a preliminary report.

This is a preliminary report on data accumulated in the first 12 months by the Subcutaneous Mastectomy Data Evaluation Center at Saint Francis Memorial Hospital in San Francisco, California. We present some statistics on 419 subcutaneous mastectomies performed by 105 plastic surgeons.

Adenocarcinoma↗
PubMedDate not supplied

Developmental changes in renin-containing cells from the ovine fetal kidney.

OBJECTIVE: To determine if the increase in intrarenal renin content that occurs in late gestation in the fetal lamb results from an increase in the proportion of cells containing renin, an increase in the amount of renin per renin-containing cell, or both. METHODS: Kidney cells with a density of 1.062 g/mL were isolated from ovine fetuses at 100-104 days gestation (n = 6, immature) and at 131-139 days gestation (n = 6, mature). This fraction was enriched with renin-containing cells. Total renin (TR) and active renin (AR) were measured by their ability to generate angiotensin I (AI). Renin mRNA was measured by RNase protection assay. The presence of renin in cells and the capacity to release it were identified by immunocytochemistry and cell immunoblot analyses. Data were analyzed by analyses of variance. RESULTS: The TR and AR in isolated cells increased from 3.7 +/- 0.3 and 2.5 +/- 0.2 micrograms AI/microgram protein . hr-1 in immature fetuses to 6.2 +/- 0.7 and 5.0 +/- 0.6 micrograms AI/microgram protein . hr-1 in mature fetuses (P < .01). The percentage of immunopositive renin cells (PC) was greater in mature (40.6 +/- 4.3) than in immature fetuses (15.2 +/- 1.2) (P < .01). The TR/PC and AR/PC were also higher in mature (8.2 +/- 0.6 and 6.6 +/- 0.4 ng AI/h . pc-1) than in immature animals (6.5 +/- 0.6 and 4.4 +/- 0.4 ng AI/h . pc-1) (P < .01). CONCLUSIONS: The data indicate that the increase in TR and AR occurring during development in fetal lamb kidney results from an increase in both the number of renin-containing cells and in the renin content per cell.

Animals↗