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Biomedical subjects

B Lutz-Bucher

Publications and source records attributed to B Lutz-Bucher.

At least 37 records · Page 2Linked to original sources
PubMed1989

Indirect relationship between vasopressin-induced secretion of ACTH and cyclic nucleotides in cultured anterior pituitary cells.

The present study examines whether a correlation exists between cyclic nucleotides and the mechanism of action of arginine vasopressin (AVP) on adrenocorticotropin hormone (ACTH) secretion from pituitary corticotrophs. Incubation of cultured anterior pituitary cells with 3-isobutyl-1-methylxanthine (IBMX) or Rolipram elevated the basal intracellular content of both adenosine 3':5'-cyclic monophosphate (cAMP) and guanosine 3':5'-cyclic monophosphate (cGMP) or cAMP alone, respectively. Both IBMX and Rolipram enhanced the AVP-stimulated secretion of ACTH in cultured anterior pituitary cells, but not in AtT-20 corticotrophs which lack functional AVP receptors. Rolipram was less potent than IBMX in this regard, which suggests a possible involvement of cGMP. In contrast, both drugs showed similar potency to stimulate CRF-induced ACTH secretion. Incubation of pituitary cells with atrial natriuretic factor elevated tissue cGMP levels and increased the ACTH response to AVP. The results of this study show that, although AVP fails to directly affect the levels of cAMP and cGMP in anterior pituitary cells, the stimulatory effect of AVP on ACTH secretion was modulated by the cellular cAMP content.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Stimulation by atrial natriuretic factor of cyclic GMP production in cultured anterior and intermediate pituitary tissues: evidence for a major contribution of proliferating nonendocrine cells.

Primary cultures of anterior and intermediate pituitary tissues were monitored immunocytochemically for the presence of endocrine and nonendocrine cells and simultaneously tested for their ability to produce cyclic GMP in response to atrial natriuretic factor (ANF). Cells cultured for 3 days and 6 days, in which nonendocrine (vimentin-positive) cells were found to rapidly overgrow the endocrine cells, showed a dramatic elevation in cyclic GMP production stimulated by ANF, with maximum stimulation 300-700% that seen in 1-day cultured cells. Also, ANF-induced accumulation of cyclic GMP in an enriched population of vimentin-positive cells appeared to closely match that triggered in a 3-day culture of anterior pituitary cells, emphasizing the major role played by nonendocrine cells and their ability to synthesize cyclic GMP. In contrast, in the homogeneous population of tumor corticotrophs AtT-20, there was a close relationship between cyclic GMP formation and cell density. It thus appears that contamination of primary cultures of anterior and intermediate pituitary tissues by proliferating nonendocrine cells (mainly fibroblasts), in which ANF-induced accumulation of cyclic GMP may be confused with that of the very secretory cells, leads to overestimation and masking of guanylate cyclase activity of endocrine cells.

Adrenocorticotropic Hormone↗
PubMed1989

Corticotropin-releasing factor-like immunoreactivity, arginine vasopressin-like immunoreactivity and ACTH-releasing bioactivity in hypothalamic tissue from fetal and neonatal sheep.

Corticotropin-releasing factor-like immunoreactivity (CRF-LI), arginine vasopressin-like immunoreactivity (AVP-LI) and ACTH-releasing bioactivity of hypothalamic tissue from 63- to 143-day-old ovine fetuses and from 7- and 150-day-old lambs have been assessed. CRF-LI and AVP-LI contents and concentrations increased steadily between 63 and 138 days of gestation, decreased at day 143 then rose again in postpartum animals. In terms of concentration, the AVP-LI/CRF-LI ratio remained close to 5 between 63 and 123 days of intrauterine life, decreased steadily in late gestation down to 1.2 at day 143 increased again in lambs. The total hypothalamic ACTH-releasing bioactivity increased 26-fold between 63 and 138 days of gestation and remained constant until day 143. The highest values were observed in 150-day-old-lambs. These data support the view that AVP and oCRF1-41 might be important hypothalamic factors involved in the regulation of ACTH release by the pituitary gland of the sheep fetus. In addition, they suggest that AVP is more important in young fetuses and lambs than in prepartum animals.

Aging↗
PubMed1988

Binding and effect of atrial natriuretic factor on cyclic GMP formation and alpha-MSH secretion of intermediate pituitary cells.

The present study shows for the first time that in proopiomelanocortin cells of the rat intermediate pituitary gland ANF binds to two receptor forms, with apparent molecular weights of 150K and 70K. Scatchard plots revealed specific and high affinity non-interacting sites, with a KD value of about 3 nM and a density of 7,000 sites/cell. The presence of these binding sites was further confirmed by autoradiographic studies. Activation of these receptors led to an increase in cellular content of cGMP, with half-maximal effect being elicited with about 5 nM ANF, while cAMP formation was unaltered. Alpha-MSH secretion of intermediate pituitary cells was unaffected by ANF, whether the cells were incubated in the absence or presence of corticotropin-releasing factor or bromocryptine. These data thus indicate the presence of multiple ANF receptor sites in the intermediate pituitary which are coupled to cell production of cGMP, but independent of alpha-MSH secretion.

Animals↗
PubMed1988

Characterization of high affinity receptor sites for atrial natriuretic factor in anterior pituitary gland: evidence for the existence of two receptor forms.

The present study shows that in rat anterior pituitary tissue atrial natriuretic factor (ANF) binds to two distinct receptor forms, with apparent molecular weights of about 166K and 58K. Binding assays carried out with (125I)-ANF revealed specific and high affinity non-interacting binding sites, with Ko values of 1-1.7 nM and a density of 10-15,000 sites/cell. rANF fragments (5-25), (5-27) and (5-28) exhibited apparent equipotency in displacing tracer binding, while fragment (13-28) and various other peptides were ineffective. ANF (5-25) was about 100-times less potent than ANF (8-33) in stimulating half-maximum pituitary cGMP production. These data indicate the presence of multiple binding sites for ANF in the pituitary gland and suggest that only part of these sites may be coupled to activation of guanylate cyclase.

Animals↗
PubMed1987

Evidence that AVP receptors in AtT-20 corticotrophs are not coupled to secretion of POMC-derived peptides.

This study reports the presence in AtT-20 corticotrophs of high affinity-low capacity receptors for arginine-vasopressin (AVP), whose binding capacity was considerably enhanced by the divalent metal ion nickel. These binding sites, when analyzed in the presence of nickel, showed high affinity for AVP, vasotocin and oxytocin, but recognized to a lesser extent the V2-agonist 1-deamino-AVP, as well as V1-antagonists. Surprisingly, AVP failed to alter secretion of proopiomelanocortin (POMC)-derived peptides from the cells or corticotropin-releasing factor (CRF)-induced cAMP synthesis, as reported in normal corticotrophs. Exposure of cells to CRF elicited an increase in mRNAPOMC levels, while, in contrast, AVP was without significant effect. It thus appears that in AtT-20 tumor cells, the AVP receptors are not coupled to either the biochemical or biological cellular response.

Adrenocorticotropic Hormone↗
PubMed1987

Characterization and modulation of corticotropin-releasing factor in the neurointermediate pituitary gland.

The present study attempts to determine whether part of the corticotropin-releasing factor (CRF)-like materials present in the 'posterior pituitary' is composed of authentic CRF and examines whether the concentration of that peptide may be modulated by circulating glucocorticoids. Analysis of crude extracts of neurointermediate lobes (NIL) of rat pituitaries by reverse-phase HPLC, coupled with a specific radioimmunoassay (RIA), revealed the presence of a major component eluting with the same retention time as rat CRF (rCRF) and, importantly, which was indistinguishable by RIA from the synthetic peptide. Also, two minor forms eluted earlier than rCRF upon HPLC; one of these forms matched the elution position of r[Met(O)21,38]CRF. All three species did show biological activity and stimulated ACTH release from pituitary cells. Essentially the same elution profile was generated by median eminence (ME) extracts. Immunoreactive CRF (CRFi) content of the NIL was about 3% of that of the ME and was found to undergo a significant increase as a result of long-term adrenalectomy while, in contrast, CRFi content of the ME was decreased. This effect of adrenalectomy was completely antagonized by dexamethasone treatment. This study thus provides strong evidence for the presence of authentic CRF within the NIL of the rat pituitary and also shows that tissue concentration of that peptide was modulated by glucocorticoids.

Adrenalectomy↗
PubMed1986

Vasopressin and oxytocin levels in human neonates. Relationships with the evolution of labour and beta-endorphins.

In order to find out whether arterial and venous cord levels of vasopressin (VP) and oxytocin (OT) might be linked to one or more obstetric parameters and to beta-endorphin (BEP) secretion, 42 successively delivered neonates were studied. Arterial and venous cord blood levels of these peptides were not statistically different whenever the neonates were born vaginally with or without foetal distress, after induction of labour by oxytocic drugs, or by elective caesarean section. BEP levels in cord and maternal blood do not seem to be linked with AVP or OT. The results of the group of infants born after uncomplicated vaginal delivery analyzed with regard to obstetric parameters, led to the following conclusions: arterial cord VP correlated with venous cord VP, with arterial cord OT and with the duration of membrane rupture; arterial cord OT correlated with venous cord OT and with the time taken by the cervix to dilate from 5 to 10 cm, suggesting that the foetal pituitary gland is sensitive to the evolution of labour.

Cesarean Section↗
PubMed1986

Modulation by Leu-enkephalin of peptide release from perifused neurointermediate pituitary. II. Inhibition of calcium-mediated secretion of alpha-MSH and beta-endorphin.

The present study examines the effect of opiates on alpha-MSH and beta-endorphin release from perifused neurointermediate rat pituitaries, as stimulated by various secretagogues for which Ca ions and/or cAMP serve as messengers. alpha-MSH release stimulated by high K+ concentrations (5-min pulses) and veratridine depolarization, which is closely dependent on Ca2+ fluxes, was abolished by both Leu-enkephalin and beta-endorphin. A dose-response relationship between inhibition of alpha-MSH secretion and the concentration of Leu-enkephalin, with ED50 approximately 10(-9) M, was observed. High K+-induced release of beta-endorphin was likewise blunted by Leu-enkephalin. The stimulatory effect of the Ca2+ ionophore A 23187 was inhibited in a similar way as was that of CRF, which requires both Ca2+ fluxes and cAMP formation. The antagonist naloxone not only reversed the action of opiates, but also enhanced spontaneous hormonal output. In contrast, the effects of l-isoproterenol and forskolin, for which cAMP serves as a primary messenger, were unaffected in the absence of extracellular Ca ions and, also, in the presence of Leu-enkephalin. We conclude that opioid peptides may exert a direct inhibitory influence on the release of both alpha-MSH and beta-endorphin and do so by interfering with the Ca2+ messenger system. In addition, these data also suggest the existence of an opiate-opiate negative feedback mechanism.

Animals↗
PubMed1986

Central nervous system control of pituitary vasopressin receptors: evidence for involvement of multiple factors.

The regulation of pituitary vasopressin (VP) receptor concentration was investigated in rats with antero-lateral cuts (ALC) placed around the hypothalamus, as well as in Brattleboro homozygotes (HO) that genetically suffer from a lack of AVP. Hypothalamic ALCs caused a reduction in (3H)-AVP binding, while counteracting the dramatic fall in binding that normally occurs after adrenalectomy. Surprisingly, in HO rats, long-term adrenalectomy did cause pituitary AVP receptor number to decrease to an extent similar to that seen in normal rats. However, the receptor disappeared twice as rapidly in heterozygote controls than in HO animals, with calculated half-lives of 1.1 and 2.0 days, respectively. In HO, chronic administration of VP reduced receptor concentration by about 80%, while the same dose of oxytocin (OT) produced only a 20-30% reduction. Whereas dexamethasone injections did reverse the depressing effect of adrenalectomy on pituitary AVP receptors, they failed to enhance binding in sham-operated controls, treated or not with VP; thereby suggesting a central site of action of the steroid. In contrast, in rats with hypothalamic ALCs (i.e. with the pituitary lacking central control), corticosterone implants did antagonize the reduction in receptor density caused by adrenalectomy. We conclude that the pituitary AVP receptor system lies mainly under control of the central nervous system, through a mechanism of action that not only seems to imply AVP and OT, but probably also some other hypothalamic factor(s). Glucocorticoids appear to exert a dual effect, acting indirectly through negative feedback control of neuropeptide release and, possibly, also directly on the pituitary to regulate binding sites.

Adrenalectomy↗
PubMed1985

Specific receptors for vasopressin in the pituitary gland: evidence for down-regulation and desensitization to adrenocorticotropin-releasing factors.

Specificity of binding of 3H-labeled arginine vasopressin [( 3H]AVP), down-regulation of receptors, and desensitization were studied in anterior pituitary glands of both Wistar and Brattleboro rats. Studies using both crude membrane fractions and isolated cells of anterior pituitaries revealed the presence of a single population of binding sites with a Kd of approximately 1 nM. The receptor recognized the following peptides, with AVP = lysine vasopressin = vasotocin greater than oxytocin = 1-deamino-(8-D-AVP) greater than d-(CH2)5-Tyr-(Me)-Val4-AVP greater than 1-deaminopenicillamine-(Val4-D-Arg8)VP. Neither corticotropin-releasing factor (CRF) nor any of the neuropeptides tested, including AVP ring and tail fragments, competed for tracer binding. Increased extracellular vasopressin levels due to chronic injections or long term adrenalectomy decreased receptor density by 80%, while oxytocin was less effective than AVP. Comparing binding data in Brattleboro homozygotes and heterozygotes revealed that AVP levels within the physiological range could down-regulate pituitary receptors as well. This could not be caused by occupation of sites by endogeneous vasopressin, since injection of large doses of peptide decreased tracer binding by less than 10%. Loss of pituitary receptors reduced 1) enhancement by AVP of CRF-induced cAMP accumulation, 2) intrinsic CRF-like activity and 3) synergistic effect of AVP on ACTH secretion elicited by CRF. This study thus provides evidence for the presence of highly specific vasopressin receptors in the anterior pituitary, which may undergo homologous down-regulation and desensitization in terms of cAMP production and ACTH release.

Adrenalectomy↗
PubMed1985

Vasopressin secretion as a possible target of the gamma-aminobutyric acid-mediated component of the corticosteroid feedback effect.

The inhibition of gamma-aminobutyric acid (GABA) synthesis did not interfere with the suppressive effect of dexamethasone on the stress-induced rise of plasma corticosterone levels in vasopressin-deficient homozygous Brattleboro rats. In dexamethasone-treated heterozygous rats corticosterone and vasopressin secretion increased after stress provided GABA synthesis was inhibited. The results indicate that inhibition of corticotrophin secretion by corticosteroids may in part be mediated by enhancement of GABA synthesis and a consequent inhibition of vasopressin release.

3-Mercaptopropionic Acid↗
PubMed1984

Endocrine concomitants of sweating and sweat depression.

The effect of humid heat (Ta = 43 degrees C, Pa = 32 Torr) on sweat rate, plasma renin activity and plasma levels of aldosterone and antidiuretic hormone (ADH) was studied in four male subjects before and after repeated heat exposures. Over-sweating and sweat drippage followed by hidromeiosis were observed in three subjects during initial heat exposure. With repeated humid heat exposures increased sweat rates were accompanied by a more intense sweat depression (hidromeiosis) in all four subjects. In our conditions, no changes in plasma levels of aldosterone and ADH or plasma renin activity were observed with hidromeiosis. Plasma renin activity was slightly depressed by repeated exposures, whereas plasma volumes were enhanced, with no significant changes in plasma Na or K. The results suggest that neither ADH nor the components of the renin-angiotensin aldosterone system are involved in the hidromeiotic phenomenon.

Adult↗
PubMed1984

Paradoxical involvement of glucocorticoid receptors in the aldosterone-induced impairment of ACTH secretion from perifused pituitary glands.

The present investigation was aimed at examining whether interaction of aldosterone with specific mineralocorticoid receptors at the level of the pituitary gland may account for the inhibitory effect of that steroid on ACTH secretion. By using pituitaries from neonatal rats, which we show to completely lack specific mineralocorticoid receptors but to contain a functional glucocorticoid receptor system, we demonstrated the persistence of aldosterone-induced inhibition of ACTH release from perifused glands. Conversely, when the glucocorticoid receptors sites were blocked in pituitaries from mature rats by means of a potent antiglucocorticoid (RU 38486), thus leaving unaltered mineralocorticoid binder, aldosterone no longer dampened hormonal output. We conclude that the latter steroid affected corticotropic activity by interacting not with its proper and specific receptor, but rather with the glucocorticoid binding sites.

Adrenocorticotropic Hormone↗
PubMed1984

Modulation by leu-enkephalin of peptide release from perifused neurointermediate pituitary. I. Selective effect on potassium-, veratridine- and isoproterenol-stimulated secretion of vasopressin.

This study examines the effect of leu-enkephalin on K+, veratridine and isoproterenol stimulation of vasopressin (AVP) release from perifused neurointermediate pituitaries of rats. As opposed to catecholamine-evoked release of peptide, the secretory response to high K+ and veratridine involves Ca2+ influx, as the effect of both factors was blocked by Ca-chelation and the channel blocker D 600. Leu-enkephalin was found to antagonize AVP secretion induced by K+ and veratridine depolarization, by acting through a naloxone-sensitive receptor system. In contrast, the opiate failed to significantly affect isoproterenol-stimulated release of AVP, which we show to be correlated to cAMP accumulation in pure neurohypophyseal tissue. These results support the view that opiates modulate AVP secretion triggered by depolarization of nerve terminals by regulating Ca2+ fluxes.

Animals↗
PubMed1983

Characterization of specific receptors for vasopressin in the pituitary gland.

The present paper reports new findings concerning interaction of [3H]-Arginine-vasopressin with putative receptors in rat anterior pituitary gland. It shows the presence of a single type of receptor sites, with a limited binding capacity and a dissociation constant of nearly 1nM. The parent neurohormone oxytocin revealed weak affinity as compared with vasopressin [Ki = 100nM and Ki = 1nM, respectively]. None of the various peptides tested and, especially corticotropin-releasing factor CRF, competed for binding. Receptor characteristics appeared to be unaffected by lack of circulating vasopressin in Brattleboro rats presenting complete deficiency in synthesis of that peptide.

Angiotensin II↗