Search PubMed⌕ Search

Biomedical subjects

K Tasaka

Publications and source records attributed to K Tasaka.

At least 253 records · Page 14Linked to original sources
PubMed1984

Site of negative feedback action of estrogen on gonadotropin secretion in normal women.

We have reported that iv administration of conjugated estrogens results in no significant change in the plasma LH-RH level during the negative feedback phase of LH, suggesting that estrogen does not suppress LH by decreasing hypothalamic LH-RH. To determine the site of estrogen action during the negative feedback phase, we studied the pituitary response to a small amount of LH-RH after estrogen administration in normal cyclic women in the mid-follicular phase. The pituitary responses to an iv bolus of 2.5 micrograms of synthetic LH-RH were evaluated by measuring serum LH and FSH 2 h before and 8 h after administration of 20 mg of conjugated estrogens (Premarin). The mean levels of serum LH and FSH were significantly (p less than 0.05) decreased 8 h after the injection. The peak responses of LH and FSH to LH-RH were also significantly (p less than 0.05) reduced after Premarin administration. These findings suggest that the negative feedback effect of estrogen on gonadotropin secretion is caused by its direct suppression on the pituitary response to LH-RH.

Adult↗
PubMed1984

Impaired LH-RH release by estrogen in women with sulpiride-induced hyperprolactinemia.

The effects of hyperprolactinemia on the release of immunoreactive luteinizing hormone-releasing hormone (LH-RH) and luteinizing hormone (LH) in response to iv injection of 20 mg conjugated estrogens (Premarin) were studied. Five normal cycling women were injected with Premarin on the morning of the 7th day of the first cycle (control cycle), and then the plasma levels of LH-RH, LH, and prolactin (PRL) were determined every 8 to 16 hours for 72 h. Two months later, the same women received 200 mg of oral sulpiride daily for 8 days from the 3rd day of the cycle (sulpiride treated cycle), and then the same protocol as in the control cycle was applied. Mean (+/- SE) plasma levels of PRL on day 7 in the sulpiride treated cycle were significantly higher than those in the control cycle (118 +/- 24 ng/ml vs. 14 +/- 4 ng/ml, p less than 0.001). After estrogen injection, the mean percent increases in immunoreactive LH-RH at 32 h (control: 71 +/- 38% vs. sulpiride: 6 +/- 36%) and 40 h (154 +/- 38% vs. -5 +/- 21%) and in LH at the 48 h (175 +/- 89% vs. 57 +/- 57%) and 56 h (99 +/- 32% vs. 7 +/- 21%) were significantly (p less than 0.01 or p less than 0.05) suppressed in the sulpiride cycle. These data suggest that the impaired positive feedback effect of estrogen on LH-release in hyperprolactinemic anovulatory women may be caused, at least in part, by disturbed LH-RH release.

Adult↗
PubMed1984

Absence of effect of the peptide PHI-27 on LH release in vitro.

The effects of PHI-27, a peptide of the glucagon-secretion family, on luteinizing hormone (LH) release and on LH-releasing hormone (LH-RH)- or estradiol-induced LH release were examined in a sequential double chamber perifusion system by perifusing the pituitary alone or in sequence with the mediobasal hypothalamus (MBH) from normal female rats in diestrus. PHI at 10(-7) M had no significant effect on LH release from the pituitary in series with the MBH. Moreover, on perifusion of the pituitary alone with medium containing 10(-7) M PHI, LH release induced by 20 ng/ml LH-RH from the pituitary was not significantly different from that without PHI. Furthermore, PHI had no effect on estradiol-induced LH release from the pituitary in sequence with the MBH. These data indicate that PHI has no effect on LH release in vitro.

Animals↗
PubMed1984

Hydrocortisone elicits the effect of clomiphene citrate on luteinizing hormone-releasing hormone release in vitro.

The effect of hydrocortisone on the release of luteinizing hormone (LH) and LH-releasing hormone (LRH) in response to clomiphene citrate (clomiphene) were examined in a sequential double chamber perifusion system by perifusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were perifused in sequence with medium containing 5 X 10(-6) M hydrocortisone, a significant release in LH (100- 150% increase, P less than 0.01-P less than 0.05) was observed 40 min after the administration of 3 X 10(-8) mol clomiphene. Clomiphene had no effect on LH release from the pituitary when perifused in series with the MBH without basal hydrocortisone infusion. Administration of clomiphene did not cause a significant increase in LH from the pituitary perifused alone, with or without medium containing hydrocortisone. The concentration of LRH in the efflux was significantly increased 40 min after clomiphene administration when MBH was perifused with medium containing hydrocortisone, whereas clomiphene had no effect when perifused with medium only. These data indicate that hydrocortisone stimulates the effect of clomiphene on LRH release from the hypothalamus, which in turn induces LH release from the pituitary.

Animals↗
PubMed1984

Involvement of norepinephrine in pituitary LH release induced by oestradiol in vitro.

The direct effects of oestradiol-17 beta (E2) on pituitary luteinizing hormone (LH) release and the role of norepinephrine (NE) in E2-induced gonadotrophin release were examined in a sequential double chamber perifusion system by perifusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normally cycling female rats. Administration of E2 induced significant release (70-160% increase, P less than 0.05) of LH from the pituitary of rats in pro-oestrus, but not in other stages of the oestrous cycle. When the MBH and the pituitary were perifused in sequence, E2 induced significant release of LH in all stages of the oestrous cycle except oestrus. When the pituitary from rats in dioestrus II was perifused alone with medium containing 200 ng/ml NE, significant release of LH (80-170% increase, P less than 0.05) was observed after the administration of E2. The E2-induced LH release in pro-oestrus was completely abolished by perifusion with medium containing diethyldithiocarbamate, an inhibitor of NE synthesis. These findings suggest that NE may be involved in changes of pituitary responsiveness in LH secretion to oestrogen during the rat oestrous cycle.

Animals↗
PubMed1984

Excitatory and inhibitory effects of H1-blockers on isolated bullfrog spinal cords.

Effects of pyrilamine and diphenhydramine on isolated spinal cords of bullfrogs were studied in order to clarify the mechanisms of depressant and stimulant actions of H1-blockers on the central nervous system. Pyrilamine and diphenhydramine depressed both the DR-VRP and DR-DRP. Pyrilamine and diphenhydramine also suppressed L-glutamate-induced depolarization of the motoneurones, but they did not depress GABA depolarization at the dorsal root terminals. By switching the perfusate to drug-free Ringer solution, depressed amplitudes of DR-VRP were suddenly increased over the control level (rebound phenomenon). The rebound increase of DR-VRP was inhibited by either tetrodotoxin or D-600. These results suggest that the rebound phenomenon may be due to the effect of H1-blockers 1) inhibiting transmitter release participating in presynaptic inhibition and 2) inducing a rapid recovery from the depressed influx of Na+ and Ca2+ into motoneurones.

Animals↗
PubMed1983

Analgesic activity of certain tripeptide-beta-phenethylamide analogs.

Studies of the analgesic effect of tripeptide-beta-phenethylamides are described, and their structure-activity relationship is discussed. SD-25, which has a methyl group at R2, and a hydroxymethyl group at R3 of beta-phenethylamide, was the most potent one of the 8 analogs tested.

Analgesia↗
PubMed1983

Compound 48/80-induced permeability change in liposomal membrane.

The action of compound 48/80 (a mixture of condensation products of p-methoxy-N-methylphenethylamine with formaldehyde) on liposomal membranes was studied by means of K+-loaded liposomes and a K+ ion-selective electrode. Prompt efflux of K+ was detected when 48/80 was added to the negatively charged liposome suspension, while the monomer of 48/80, p-methoxy-N-methylphenethylamine, did not release K+ from the same liposomes. The mechanism for the action of 48/80 is discussed in comparison with that of a polymyxin, well known as an antibiotic acting on bacterial membranes.

Kinetics↗
PubMed1983

Histamine release inhibition and prevention of the decrease in membrane fluidity induced by certain anti-allergic drugs: analysis of the inhibitory mechanism of NCO-650.

NCO-650 exerted a dose-dependent inhibition of histamine release from isolated rat mast cells without affecting the Ca-uptake and intracellular cAMP levels. When the membrane stabilizing action of NCO-650 was investigated with the liposomes prepared by various phospholipids with or without cholesterol, it became clear that compound 48/80 decreases the order parameter of liposomes and NCO-650 inhibits the decrease of order parameter. Histamine release from histamine-containing liposomes was brought about by compound 48/80 at concentrations higher than 0.5 micrograms/ml, and pretreatment of the liposomes with NCO-650 inhibited histamine release due to compound 48/80. The incorporation of NCO-650 in the liposomes was effective in abolishing the phase transition of the lipid bilayer membranes from crystalline gel to liquid crystalline phases, and decreased the phase transition temperature. Those changes in the lipid bilayer membranes correspond to those displayed by incorporation of cholesterol in the liposomes. An increase of permeability of lipid membrane by compound 48/80 may be due to partial loosening of the lipid order; NCO-650 rigidified the liposome membrane and as a result of this, it decreased histamine release.

Animals↗
PubMed1983

Absence of effect of danazol on estrogen-induced luteinizing hormone release from rat hypothalamo-pituitary axis in vitro.

The effects of danazol on luteinizing hormone (LH) release by estradiol (E2) were examined in a sequential double chamber superfusion system by superfusing the mediobasal hypothalamus (MBH) and pituitary excised from normal female rats in diestrus. Administration of 3x10(-13) mole E2 caused a significant (p less than 0.05) increase of LH (80-220% above the pre-injection level) from the pituitary in series with MBH superfused with Medium 199 alone or Medium 199 containing 10(-4)M danazol. These data indicate that acute administration of danazol does not affect estrogen-induced LH release in rats.

Animals↗
PubMed1983

Epileptogenic activity of cephalosporins in rats and their structure-activity relationship.

The epileptogenic properties of 10 cephalosporins and penicillin G were compared by intraventricular application to rats. At doses greater than 32 micrograms per head, cefazolin provoked tremendous seizure signs, a spike-and-wave complex appeared in close succession for more than 30 min, and severe convulsions were observed repeatedly. Reactions to cefotiam, ceftezole, and cephaloridine were almost equal to reactions to penicillin. No epileptogenic signs were observed on EEGs, and no behavioral symptoms were observed after administration of 1,000 micrograms of cephalexin and cephradine per head. Reactions to cephapirin, cefmetazole, cephalothin, and ceftizoxime exhibited less marked epileptogenic features; activity was diminished in that order on EEGs and in behavioral signs. Compounds substituted with two different heterocyclic rings at position 7 (R1) and position 3 (R2) of 7-aminocephalosporanic acid were potent in producing epileptogenic signs both on EEGs and in behaviors. Compounds substituted with a heterocyclic ring at either position of 7-aminocephalosporanic acid were less potent. Compounds such as ceftizoxime, cephalexin, and cephradine, substituted at R2 with small groups, were almost incapable of producing epileptogenic activity. This may indicate that the substitution of a heterocyclic ring at position 3 will provoke the convulsive actions.

Animals↗
PubMed1983

Estrogen induces the release of luteinizing hormone-releasing hormone in normal cyclic women.

The plasma concentrations of immunoreactive LRH, LH, and FSH were determined by RIA every 6 h until 72 h after iv administration of conjugated estrogens during the midfollicular phase. The percentage change in LH from the preinjection level showed a biphasic pattern after the injection of conjugated estrogens, i.e. significant suppression (-70%) from 6-42 h after the injection, followed by a rebound increase with a peak (+150%) at 56 h. Plasma FSH after the injection also showed a biphasic pattern. The plasma immunoreactive LRH levels were unchanged until 32 h after the injection, but then increased significantly (P less than 0.02) to 160% of the preinjection level at 42 h and then decreased rapidly. These data indicate that 1) estrogen administration results in increases in plasma immunoreactive LRH and LH, and the peak of plasma LRH precedes that of gonadotropin; and 2) the negative feedback effect of estrogen on gonadotropin secretion may not be mediated through LRH.

Adult↗
PubMed1983

Sodium induces oxytocin release from superfused rat pituitary.

The effects of various osmotic agents on the release of oxytocin were examined in a superfusion system. Oxytocin was released significantly from the rat pituitary by superfusion with medium of an osmolality of 350 mOsm/kg H2O adjusted with NaCl, regardless of the presence of the rat hypothalamus. Media adjusted to an osmolality of 350 mOsm/kg H2O with sucrose, glucose, urea or mannitol had no effect on oxytocin release from the hypothalamo-pituitary complex. Medium containing excess Na2SO4 induced significant release of oxytocin from the pituitary without the hypothalamus. The administration of tetraethylammonium chloride had no oxytocin secretion. These data suggest that oxytocin release from the pituitary is influenced by the level of sodium ion rather than the osmotic pressure.

Animals↗