Biomedical subjects

S W Wang

Publications and source records attributed to S W Wang.

At least 19 recordsLinked to original sources

PubMed1999

Inhibition of testosterone secretion by digitoxin in rat testicular interstitial cells.

Both in vivo and in vitro experiments were conducted to determined the effects of digitoxin on the secretion of testosterone, and its underlying mechanisms including testicular adenosine 3':5'-cyclic monophosphate (cAMP), and the activities of steroidogenic enzymes. Male rats were injected with digitoxin, human chorionic gonadotropin (hCG), or hCG plus digitoxin via a jugular catheter. Blood samples were collected immediately before and at 30 and 60 min after the challenge, and analyzed for testosterone by radioimmunoassay. In an in vitro study, rat testicular interstitial cells were isolated and incubated with digitoxin, hCG, 8-bromo-cAMP (8-Br-cAMP), digitoxin plus hCG, or digitoxin plus 8-Br-cAMP at 34 degrees C for 1 h. The media were collected and analyzed for testosterone. For studying cAMP accumulation, testicular interstitial cells were incubated for 1 h in the medium containing isobutyl-1-methylxanthine (IBMX) and different doses of digitoxin with the absence or presence of hCG. After incubation, cells were processed for determining cAMP content. Intravenous injection of digitoxin decreased hCG-stimulated, but not basal, plasma testosterone levels. Administration of digitoxin in vitro resulted in an inhibition of both basal and hCG- as well as 8-Br-cAMP-stimulated release of testosterone. In addition, digitoxin diminished hCG-stimulated cAMP accumulation in rat testicular interstitial cells. Furthermore, digitoxin inhibited the activity of cytochrome P450 side chain cleavage enzyme (P450scc) but failed to affect the activities of other steroidogenic enzymes. Taken together, these results suggest that the acute inhibitory effect of digitoxin on the testosterone production in testicular interstitial cells involves, at least partly, an inefficiency of post-cAMP events, and a decrease of P450scc activity.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1999

Regulation of testosterone secretion by prolactin in male rats.

The goal of this study was to characterize the mechanism by which hyperprolactinemia alters testosterone production in rat testicular interstitial cells (TICs). Hyperprolactinemia was induced by grafting 2 anterior pituitary (AP) glands under the subcapsular space of the kidney in experimental rats. Control rats were grafted with brain cortex (CX). Six weeks post-grafting, rats were challenged with human chorionic gonadotropin (hCG) then, the changes in either plasma testosterone or luteinizing hormone was measured. Additionally, TICs were isolated and challenged in vitro with hCG or prolactin, and the testosterone release measured by radioimmunoassay. Further investigation in signal transduction as intracellular 3':5' cyclic adenosine monophosphate (cAMP) production was observed under a regulation of forskolin or SQ22536. After the challenge of hCG or GnRH, the AP-grafted rats showed a suppressed response in testosterone release as compared to those in the CX-grafted group. The in vitro data from the AP-grafted rats compared to the CX-grafted animals showed a diminished response in testosterone release upon hCG stimulation. Administration of forskolin or SQ22536 disclosed dysfunction of adenylate cyclase in TICs from the AP-grafted rats. When 8-Br-cAMP was incubated with TICs, the testosterone production was lower in the AP-grafted compared to the CX-grafted group. These results suggest that in addition to adenylate cyclase dysfunction, inefficiency of post-cAMP pathways are also involved in the hypogonadism elicited by hyperprolactinemia in rats.

Animals↗

PubMed1999

POU domain factor Brn-3b is essential for retinal ganglion cell differentiation and survival but not for initial cell fate specification.

While the mammalian retina is well understood at the anatomical and physiological levels, little is known about the mechanisms that give rise to the retina's highly ordered pattern or its diverse neuronal cell types. Previous investigations have shown that gene disruption of the POU-IV class transcription factor Brn-3b (Brn-3.2) resulted in the loss of most retinal ganglion cells in retinas of postnatal mice. Here, we used lacZ and human placental alkaline phosphatase genes knocked into the brn-3b locus to follow the fate of brn-3b-mutant cells in the developing retina. We found that Brn-3b was not required for the initial commitment of retinal ganglion cell fate or for the migration of ganglion cells to the ganglion cell layer. However, Brn-3b was essential for the normal differentiation of retinal ganglion cells; without it, the cells underwent enhanced apoptosis. Retinal ganglion cells lacking brn-3b extended processes at the appropriate time in development, but these processes were disorganized, resulting in a thinner optic nerve. Explanted retinas from brn-3b-null embryos also extended processes when cultured in vitro, but the processes were shorter and less bundled than in wild-type retinas. Ultrastructural and marker analyses showed that the processes of mutant ganglion cells had dendritic rather than axonal features, suggesting that mutant cells formed dendrites in place of axons. These results suggest that Brn-3b regulates the activity of genes whose products play essential roles in the formation of retinal ganglion cell axons.

Alkaline Phosphatase↗

PubMed1999

Wild-type p53 protein potentiates phototoxicity of 2-BA-2-DMHA in HT29 cells expressing endogenous mutant p53.

To better understand the effects of p53 on the process of photodynamic therapy (PDT)-induced cell death, we introduced a wild-type p53 gene into the HT29 colorectal carcinoma cell line, which bears an endogenous mutant p53, using a lipofectin system. The influence of p53 status on the sensitivity induced by 2-butylamino-2-demethoxy-hypocrellin A (2-BA-2-DMHA) photosensitization was then examined. The results indicate that infection with wild-type p53 induces a growth arrest but does not induce cell death, and sensitizes the cells to PDT. At a concentration of 5 microM 2-BA-2-DMHA with a red light of 18 J/cm2 (lambda = 600-700 nm), the survival is reduced from 58.72% in HT29 cells to 13.49% in wild-type p53-infected HT29 cells. Apoptosis following PDT appears earlier in HT29 cells infected with wild-type p53 than in parent HT29 cells and empty vector-infected HT29 cells. These findings suggest that although wild-type p53 is, by itself, insufficient to induce apoptosis in cells with p53 mutation, it enhances the photosensitivity of 2-BA-2-DMHA by strongly potentiating the induction of apoptosis.

Apoptosis↗

PubMed1999

Effects of estradiol on aldosterone secretion in ovariectomized rats.

The effects and action mechanisms of estradiol on aldosterone secretion in female rats were studied. Replacement of estradiol benzoate (EB) increased the levels of plasma estradiol and aldosterone in ovariectomized (Ovx) rats. The aldosterone release from zona glomerulosa (ZG) cells was higher in EB-treated rats than in oil-treated animals. EB treatment potentiated the responses of aldosterone release to adrenocorticotropic hormone (ACTH), forskolin (FSK), and 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP). Administration of EB in vivo did not alter cAMP production in response to ACTH or FSK. Although angiotensin II (Ang II) increased aldosterone secretion by rat ZG cells, the stimulatory effect of Ang II on the release of aldosterone was not altered by EB treatment. The conversions of [3H]-deoxycorticosterone to [3H]-corticosterone and [3H]-corticosterone to [3H]-aldosterone in EB-treated groups were greater than those in the oil-treated group. These results suggest that estradiol increases aldosterone secretion in part through the mechanisms involving the activation of the post-cAMP pathway, 11beta-hydroxylase and aldosterone synthase activity.

Adrenocorticotropic Hormone↗

PubMed1999

Stable sheared A.C pair in DNA hairpins.

Single-residue d(Pu1NPu2) (Pu1.Pu2=G.A, G.G or A.A) hairpin loops can be stably closed by sheared purine.purine pairs. These special motifs have been found in several important biological systems. We now extend these loop-closing base-pairs to a sheared purine. pyrimidine (A.C) pair at a neutral pH condition. High-resolution NMR spectroscopy, distance geometry, and molecular dynamics methods were used to study d(GTACANCGTAC) oligomers. Numerous idiosyncratic nuclear Overhauser enhancements, especially those across the A.C base-pair between C4NH2left and right arrow AH1', C4NH2left and right arrow AH2, and CH5left and right arrow AH2 proton pairs, clearly define the novel sheared nature of the closing A.C base-pair. This novel base-pair is possibly present in several biological systems and in two single-stranded DNA aptamers selected from oligonucleotide libraries.

Base Pairing↗

PubMed1999

Age-related differences in corticosterone secretion in female rats.

The effects of age on steroidogenesis in rat zona fasciculata-reticularis (ZFR) cells were studied. Young, adult, and middle-aged rats were ovariectomized (Ovx) and received replacement therapy with oil or estradiol benzoate ([EB] 25 microg/mL/kg). Rat ZFR cells were incubated with corticotropin (ACTH), prolactin (PRL), or forskolin at 37 degrees C for 1 hour. The effects of age on the activity of steroidogenic enzymes of ZFR cells were measured by the amount of intermediate steroidal products separated by thin-layer chromatography. Plasma levels were higher for PRL (54% to 254%) and corticosterone (179% to 257%) in middle-aged versus young rats. In oil-treated Ovx rats, basal and ACTH-stimulated corticosterone release by ZFR cells were also greater in middle-aged compared with young rats. Replacement with EB in Ovx rats increased the ACTH-stimulated release of corticosterone. Administration of ovine PRL in vitro resulted in a dose-dependent increase of corticosterone production. In oil-treated middle-aged rats, ovine PRL-stimulated corticosterone release was higher than in young rats. Forskolin-induced production of cyclic adenosine 3',5'-monophosphate (cAMP) was greater in middle-aged versus young rats and correlated with the increase of corticosterone production. The activity of steroidogenic enzymes in rat ZFR cells was unchanged by age. These results suggest that the age-related increase of corticosterone production in female rats is associated with the stimulatory effect of PRL on ZFR cells and is due in part to an increase of cAMP generation.

3-Hydroxysteroid Dehydrogenases↗

PubMed1999

Caffeine can override the S-M checkpoint in fission yeast.

The replication checkpoint (or 'S-M checkpoint') control prevents progression into mitosis when DNA replication is incomplete. Caffeine has been known for some time to have the capacity to override the S-M checkpoint in animal cells. We show here that caffeine also disrupts the S-M checkpoint in the fission yeast Schizosaccharomyces pombe. By contrast, no comparable effects of caffeine on the S. pombe DNA damage checkpoint were seen. S. pombe cells arrested in early S phase and then exposed to caffeine lost viability rapidly as they attempted to enter mitosis, which was accompanied by tyrosine dephosphorylation of Cdc2. Despite this, the caffeine-induced loss of viability was not blocked in a temperature-sensitive cdc2 mutant incubated at the restrictive temperature, although catastrophic mitosis was prevented under these conditions. This suggests that, in addition to S-M checkpoint control, a caffeine-sensitive function may be important for maintenance of cell viability during S phase arrest. The lethality of a combination of caffeine with the DNA replication inhibitor hydroxyurea was suppressed by overexpression of Cds1 or Chk1, protein kinases previously implicated in S-M checkpoint control and recovery from S phase arrest. In addition, the same combination of drugs was specifically tolerated in cells overexpressing either of two novel S. pombe genes isolated in a cDNA library screen. These findings should allow further molecular investigation of the regulation of S phase arrest, and may provide a useful system with which to identify novel drugs that specifically abrogate the checkpoint control.

Amino Acid Sequence↗

PubMed1999

Antisense bcl-2 retrovirus vector increases the sensitivity of a human gastric adenocarcinoma cell line to photodynamic therapy.

The bcl-2 oncoprotein directly prolongs cellular survival by blocking apoptosis and its overexpression is associated with cellular resistance to killing by chemotherapeutic drugs and gamma-irradiation. Meanwhile, it has been shown that bcl-2 antisense oligonucleotide can induce apoptosis or increase toxicity of the treatment in tumors in vivo and in vitro. However, it is difficult to obtain stable transfection by this approach and there are no reports about the effect of an antisense bcl-2 on the sensitivity to oxidative stress induced by photodynamic therapy (PDT). Here we investigated the effect of an antisense bcl-2 RNA retrovirus vector transfer on the sensitivity of 2-butylamino-2-demethoxy-hypocrellin A (2-BA-2-DMHA) photosensitization in a human gastric adenocarcinoma MGC803 cell line. The results indicate that antisense bcl-2-infected MGC803 cells expressed exogenous antisense bcl-2 mRNA measured by reverse transcription polymerase chain reaction and significantly reduced bcl-2 protein determined by western blotting analysis. The decreased expression of bcl-2 protein was accompanied by increased phototoxicity and susceptibility to apoptosis induced by 2-BA-2-DMHA PDT. Our finding suggests that reduction of bcl-2 protein in gastric cancers, and possibly also in a variety of other tumors, may be a novel and rational approach to improve photosensitivity and the treatment outcome.

Adenocarcinoma↗

PubMed1998

Effects of aging on erythropoietin secretion in female rats.

The secretion of erythropoietin (EPO) in old (22 25 months), middle (mid)-aged (15-17 months), adult (6-7 months), and young (3 months) female rats was studied. Rats of different ages were bled by cardiac puncture for measuring plasma EPO, estradiol, and progesterone levels. The metabolic clearance rate of EPO was determined by a single-injection method. The effects of ovariectomy and replacement of estradiol (E) and/or progesterone (P) on plasma EPO concentration were also investigated. Analysis of direct effects of E and/or P on EPO from kidney tissues was carried out in an in vitro study. Plasma EPO levels were higher in both mid-aged and old rats than in young rats (P < 0.01). The metabolic clearance rate of EPO was also greater in adult, mid-aged and old rats than in young rats (P < 0.01). Ovariectomy increased rat plasma EPO concentration which might be inhibited by E (P < 0.01), P (P < 0.01), or E and P (P < 0.05) replacement. Neither E (10(-10) or 10(-9) M) nor P (10(-8) or 10(-7) M) alone altered EPO release from kidney tissue in vitro. Combination of E (10(-10) M) and P (10(-8) x or 10(-7) M) stimulated the EPO release from kidney tissue (P < 0.01). These data suggest that the mechanism of the secretion of EPO by kidneys in female rats during aging is ovarian steroid hormones independent.

Aging↗

PubMed1998

SB202190, a selective inhibitor of p38 mitogen-activated protein kinase, is a powerful regulator of LPS-induced mRNAs in monocytes.

Inhibitors of p38 mitogen-activated protein kinase (p38) have been reported to block tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) production in monocytes at the level of mRNA translation. Yet, several studies document that p38 can phosphorylate and activate specific transcription factors. Thus, to understand better the role of p38 during monocyte activation, we sought to determine the extent to which p38 is required for lipopolysaccharide (LPS)-induced gene expression. For this, differential mRNA display was used to identify LPS-induced genes whose expression was blocked by SB202190, a specific inhibitor of p38. A partial screen identified 10 genes in monoyctes induced 4- to 74-fold by LPS. Of these, genes encoding interferon-induced gene 15, neuroleukin, radiation-inducible immediate-early gene-1, A20, IL-1beta, and superoxide dismutase were suppressed >50% by SB202190. LPS-induced gene activation was not blocked by cycloheximide, indicating that synthesis of intermediate proteins was not required. SB202190 blocked gene induction by 50% when present between 41 and 123 nM, consistent with the potency of this compound as a p38 inhibitor. Furthermore, the ability of SB202190 to block gene activation was stimulus-dependent. LPS and interferon-alpha (IFN-alpha) both up-regulated neuroleukin mRNA, but only LPS-induced neuroleukin mRNA was suppressed by SB202190. In contrast, TNF-alpha and LPS both induced IL-8 mRNA, and induction by either TNF-alpha or LPS was blocked by SB202190. These data were consistent with the ability of LPS and TNF-alpha, but not IFN-alpha, to activate p38 in monocytes. The results provide pharmacological evidence that p38 may be a key mediator of inducible gene expression in monocytes, but its role is stimulus and gene specific.

Calcium-Calmodulin-Dependent Protein Kinases↗

PubMed1998

Purification and activation of recombinant p38 isoforms alpha, beta, gamma, and delta.

p38 is a proline-directed serine/threonine kinase that is activated by inflammatory cytokines and cellular stress. At present, four isoforms of p38 have been identified and termed alpha, beta, gamma, and delta. We expressed each p38 homolog in Escherichia coli and purified the recombinant isoforms. p38alpha and C-terminal Flag-tagged p38beta were purified by Q-Sepharose fast flow, hydroxyapatite, and Q-Sepharose high-performance chromatography. His-tagged p38gamma was purified using Ni2+-NTA resin followed by Mono Q chromatography. Glutathione S-transferase-Flag p38delta was purified using M2 affinity agarose and gel-filtration chromatography. Upstream activators of p38, constitutively active (ca) MKK3 and MKK6, were also cloned, purified, and used to activate each p38 isoform. p38 alpha, gamma, and delta were phosphorylated by both MKK6 and caMKK3. p38beta was phosphorylated only by MKK6. Mass spectrometry analysis and kinase assays showed that MKK6 was the superior reagent for phosphorylating and activating all p38 isoforms.

Activating Transcription Factor 2↗

PubMed1998

The beta2-agonist salbutamol affects the expression of phospholamban and both isoforms of SERCA in canine skeletal muscle and blocks changes in these induced by neuromuscular stimulation.

Chronic administration of salbutamol induced expression of hybrid fibers in canine skeletal muscles. Fast-twitch fibers expressed SERCA2a (the slow-twitch isoform of sarcoplasmic reticulum Ca2+-ATPase) and slow-twitch fibers expressed SERCA1 (the fast-twitch isoform of the Ca2+-ATPase). The proportion of fibers that became hybrid increased from a small percentage in the control muscles to 30% in the predominantly fast-twitch latissimus dorsi and to 45% in the predominantly slow-twitch vastus intermedius. In contrast to this response by the SERCA genes the phospholamban gene response was muscle specific. The fraction of fibers that expressed phospholamban decreased slightly in the latissimus dorsi while increasing moderately in the vastus intermedius. The effects of chronic neurostimulation of the latissimus dorsi on SERCA1, SERCA2a and phospholamban levels were mostly blocked by salbutamol. While 100% of fibers from neurostimulated muscles expressed phospholamban, only 51% of the fibers from the neurostimulated and salbutamol-treated muscles expressed it. In the neurostimulated muscle, very few muscle fibers expressed SERCA1a while 61% of the fibers that received salbutamol expressed it, albeit as hybrid fibers. The levels of SERCA2a in response to these interventions were just the opposite. In the neurostimulated muscle 37.5% of fibers were hybrid and 62.5% expressed SERCA2a only. With co-administration of neurostimulation and salbutamol, 61.3% of fibers were hybrid and 38.7% expressed SERCA2a only.

Adrenergic alpha-2 Receptor Agonists↗

PubMed1998

Effects of methanol extract of Chansu on hypothalamic-pituitary-testis function in rats.

Chansu, a galenical preparation of the dried white venom of Chinese Bufo bufo gargarizans, is one of the major components of Kyushin, a traditional Chinese medicine. Kyushin is reported to have a cardiotonic effect that has been suggested to be due to the action of bufadienolides such as bufalin and cinobufagin. Recently, we found that administration of bufalin in male rats diminished the luteinizing hormone (LH) response to gonadotropin-releasing hormone (GnRH) and the secretion of testosterone both in vivo and in vitro. These observations suggest that Chansu may possess hypogonadal effects in male rats. In the present study, the effects of the methanol extract of Chansu on hypothalamic-pituitary-testicular function in male rats were examined. Crude Chansu was extracted by methanol and purified by a Sep-Pak C18 column. No activity of bufalin, cinobufagin, estradiol, or digoxin in purified methanol extract was detected; all Chansu used in this study was the purified methanol extract. A single intravenous injection of Chansu resulted in a decrease of the basal (20% to 55%) and human chorionic gonadotropin (hCG)-induced (35% to 40%) levels of plasma testosterone and the GnRH-induced level of plasma LH (25% to 30%). Administration of Chansu in vitro decreased basal and hCG-stimulated testosterone production by 60% to 70% and 40% to 60%, respectively, as well as spontaneous and forskolin- or 3-isobutyl-1-methylxanthine (IBMX)-induced accumulation of adenosine 3',5'-cyclic monophosphate (cAMP) by 30% to 45% in rat testicular interstitial cells. Although LH release by rat anterior pituitary glands was diminished, GnRH release by the rat mediobasal hypothalamus was enhanced by administration of Chansu in vitro. These results suggest that the bufalin-free extracts of Chansu inhibit testosterone secretion in rats, in part, due to (1) a decreased production of testicular cAMP, (2) a decreased response of testosterone to gonadotropin, and (3) a reduction of the LH response to GnRH.

Animals↗

PubMed1998

Inhibitory effect of digoxin on testosterone secretion through mechanisms involving decreases of cyclic AMP production and cytochrome P450scc activity in rat testicular interstitial cells.

1. In vivo and in vitro experiments were performed to examine inhibitory effects of digoxin on testosterone secretion and to determine possible underlying mechanisms. 2. A single intravenous injection of digoxin (1 microg kg(-1)) decreased the basal and human chorionic gonadotropin (hCG)-stimulated plasma testosterone concentrations in adult male rats. 3. Digoxin (10(-7) - 10(-4) M) decreased the basal and hCG-stimulated release of testosterone from rat testicular interstitial cells in vitro. 4. Digoxin (10(-7) - 10(-4) M) also diminished the basal and hCG-stimulated production of cyclic 3':5'-adenosine monophosphate (AMP) and attenuated the stimulatory effects of forskolin and 8-Br-cyclic AMP on testosterone production by rat testicular interstitial cells. 5. Digoxin (10(-4) M) inhibited cytochrome P450 side chain cleavage enzyme (cytochrome P450sec) activity (conversion of 25-hydroxy cholesterol to pregnenolone) in the testicular interstitial cells but did not influence the activity of other steroidogenic enzymes. 6. These results suggest that digoxin inhibits the production of testosterone in rat testicular interstitial cells, at least in part, via attenuation of the activities of adenylyl cyclase and cytochrome P450sec.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1998

Effects of ovarian steroid hormones and thyroxine on calcitonin secretion in pregnant rats.

In the present study, the roles of ovarian steroid hormones and thyroxine (T4) in regulating the secretion of calcitonin (CT) in pregnant rats were examined. The levels of plasma progesterone, pre- and post-CaCl2 plasma CT, and recovery time of plasma CT and calcium after calcium challenge were greatest in midterm pregnant rats. The levels of basal plasma progesterone, CT, calcium, and recovery time of plasma CT after calcium challenge were less in late pregnant rats, but basal plasma estradiol was highest in late pregnancy. The concentrations of plasma T4 were gradually decreased in rats during pregnancy. Regardless of the presence of estradiol, administration of progesterone in ovariectomized (Ovx) rats resulted in an increase of plasma T4 as well as the basal and calcium-induced secretion of CT. Administration of estradiol alone did not alter the CaCl2-induced levels but decreased the post-CaCl2 levels of plasma calcium in Ovx rats. The basal levels of plasma CT were decreased in Ovx rats treated with T4. These results suggest that the hypercalcitoninemia in midterm pregnant rats is due to an increased secretion of progesterone. Hypocalcitoninemia in late pregnant rats, however, is due in part to lower plasma calcium.

Animals↗

PubMed1998

Age-related differences in the secretion of calcitonin in female rats.

The mechanism that causes hypercalcitonemia in female rats and is associated with aging was investigated. Young (3 mo), adult (8 mo), middle-aged (12 mo), and old (21 mo) rats were infused with CaCl2 and were bled from a jugular catheter after a CaCl2 challenge. To mimic some of the hormonal changes caused by aging, the anterior pituitary (AP)-grafted ovariectomized rats with hyperprolactinemic syndrome were used to mimic the physiological status of aging. The rat thyroid gland was incubated with or without ovine prolactin (oPRL; 40 or 80 ng/ml) at 37 degreesC for 30 min. Old rats possessed the lowest levels of plasma estradiol and progesterone yet had the highest levels of plasma prolactin and calcitonin (CT) compared with young, adult, and middle-aged rats. The basal release of thyroid CT in vitro in thyroid glands gradually increased with age. Compared with cortex (CX)-grafted rats, the AP-grafted rats possessed higher levels of plasma PRL, basal and CaCl2-induced levels of plasma CT, and the release of thyroid CT in thyroid glands. After stimulation with oPRL, the in vitro release of thyroid CT increased in both CX- and AP-grafted rats. These results suggest that the hypersecretion of CT in old rats is due at least in part to hyperprolactinemia.

Aging↗

PubMed1998

Disturbed small intestinal motility in the late rat pregnancy.

We investigated whether various periods of pregnancy might disturb rat gastrointestinal motility. When the proestrus of female rats occurred, they were housed with male rats. Motility studies were conducted on day 7 (first period), day 14 (second) and day 21 (third) of pregnancy, respectively. After the orogastric feeding of radiochromium marker, rats were sacrificed 15 min later. Gastric emptyings of pregnant rats measured at various periods did not differ from the nonpregnant diestrus controls. The geometric center represented intestinal transits in the first, second and third periods of pregnancy and controls were (mean+/-SEM) 4.54+/-0.25, 4.47+/-0.17, 3.61+/-0.27 and 4.98+/-0.13, respectively (p < 0.01) while their plasma progesterone levels were 15.6+/-2.6, 18+/-1.4, 7.1+/-0.5 and 8.6+/-0.4 ng/ml, respectively (p< 0.01). This shows that late pregnancy inhibits small intestinal transit, whereas gastric emptying remains unchanged. Altered progesterone during pregnancy is not a main mediator to disturb intestinal transit.

Animals↗