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F Musajo

Publications and source records attributed to F Musajo.

At least 19 recordsLinked to original sources
PubMed1996

Intra-adrenal 11 beta-hydroxysteroid dehydrogenase plays a role in the regulation of corticosteroid secretion: an in vitro study in the rat.

The expression of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) has been demonstrated in the adrenal glands, but until now little attention has been paid on its possible physiologic action. In-situ perfused rat adrenals released under basal conditions, in addition to mineralo- and glucocorticoids, notable amounts of 11-dehydrocorticosterone (DH-B), the inactive form to which corticosterone (the main glucocorticoid in rodents) is converted by 11 beta-HSD. The addition to the perfusion medium of glycyrrhetinic acid, a specific inhibitor of 11 beta-HSD, strongly reduced DH-B release and simultaneously evoked a moderate rise in both mineralo- and glucocorticoid output. The bolus administration of ACTH strikingly enhanced mineralo- and glucocorticoid secretion, but it significantly depressed DH-B release Rat adrenal microsome preparations possessed 11 beta-HSD activity, that was inhibited by glycyrrhetinic acid. Conversely, ACTH was without any apparent effect, a finding indicating that the in vivo observed ACTH-induced inhibition of adrenal 11 beta-HSD activity is mediated by an indirect mechanism whose elucidation requires further investigation. In conclusion, our present findings suggest that adrenal 11 beta-HSD plays a role in the regulation of steroid secretion in rats under both basal and stimulated conditions.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1996

Adrenomedullin stimulates steroid secretion by the isolated perfused rat adrenal gland in situ: comparison with calcitonin gene-related peptide effects.

Adrenomedullin (ADM), a vasodilatatory peptide contained in adrenal medulla, was found to induce a dose-dependent increase in aldosterone (ALDO) and corticosterone (B) release by the in situ perfused rat adrenal gland, along with a rise in the flow rate of the perfusion medium. The minimal effective dose for ALDO response was three and two orders of magnitude less than those able to evoke B and medium flow rate responses. Calcitonin gene-related peptide (CGRP), another vasodilatatory peptide contained in adrenal medulla and showing a slight homology in its amino acid sequence with ADM, elicited similar effects. CGRP (8-37), a specific antagonist of CGRP1 receptors, annulled all the effects of both ADM and CGRP, whereas l-alprenolol, a beta-adrenoceptor antagonist, partially reversed only ALDO response to the peptides. In light of these findings the following conclusions are drawn: i) ADM and CGRP stimulate rat adrenals in vivo to release B by raising blood flow rate; ii) ADM and CGRP enhance ALDO secretion via an indirect mechanism probably requiring the release of catecholamines by medullary chromaffin cells; and iii) the effects of ADM and CGRP on the rat adrenal gland are mediated by a common receptor of the CGRP1 subtype.

Adrenal Glands↗
PubMed1993

Arginine-vasopressin release mediates the aldosterone secretagogue effect of neurotensin in rats.

Acute and chronic systemic administrations of neurotensin (NT) and arginine-vasopressin (AVP) significantly increases plasma aldosterone concentration (PAC) in rats. Deamino-Pen1, Val4, D-Arg8-vasopressin (AVP-A), a potent AVP antagonist, completely reversed both acute and chronic aldosterone secretagogue actions of NT and AVP. AVP-A acute administration did not affect basal PAC, while chronic AVP-A treatment significantly lowered it. Taken together our findings suggest that both NT and AVP exert a marked aldosterone secretagogue effect in rats, and that the mechanism underlying NT action may involve the stimulation of AVP release. Moreover, they indicate that endogenous AVP plays an essential role in the maintenance of the mineralocorticoid secretory capacity of rat zona glomerulosa.

Aldosterone↗
PubMed1993

Evidence that endogenous arginine-vasopressin (AVP) is involved in the maintenance of the growth and steroidogenic capacity of rat adrenal zona glomerulosa.

A 7-day subcutaneous infusion with the AVP antagonist [Deamino-Pen1, Val4, D-Arg8]-vasopressin (AVP-A; 3 nmol.kg-1 x min-1) significantly lowered plasma aldosterone concentration in rats, without affecting the plasma levels of ACTH and corticosterone. Prolonged AVP-A treatment caused a marked atrophy of adrenal zona glomerulosa (ZG) and its parenchymal cells, without inducing any significant change in zona fasciculata morphology. Isolated ZG cells from AVP-A-infused rats evidenced a notable decrease in both their basal and maximally-stimulated aldosterone production. The simultaneous infusion of rats with AVP (3 nmol.kg-1 x min-1) completely reversed all these effects of AVP-A. These findings suggest that endogenous AVP may be specifically involved in the maintenance of the growth and steroidogenic capacity of rat adrenal ZG. Moreover, they seem to indicate that under basal conditions the pituitary-adrenal-glucocorticoid axis is independent of AVP release.

Adrenocorticotropic Hormone↗
PubMed1992

Direct secretagogue effect of corticotropin-releasing factor on the rat adrenal cortex: the involvement of the zona medullaris.

CRF dose-dependently enhanced corticosterone (B) secretion by rat adrenal slices including both cortex and medulla. Conversely, CRF did not exert any B response by fragments of adrenocortical autotransplants, which are completely deprived of chromaffin tissue. However, autotransplant quarters exhibited a dose-dependent response to ACTH qualitatively similar to that of adrenal slices, although markedly less intense. The maximal B response of adrenal slices to CRF (10(-8) M) was completely annulled by corticotropin-inhibiting peptide (10(-6) M), a competitive inhibitor of ACTH, which totally blocked the secretory response to ACTH (10(-8) M) of both kinds of preparations. ACTH immunoreactivity was present in the adrenal gland of control rats, but was undetectable in autotransplanted adrenocortical nodules. Moreover, adrenal fragments mainly composed of chromaffin tissue released detectable amounts of ACTH in response to high concentrations of CRF (10(-8)/10(-6) M). These findings suggest that chromaffin medullary cells play a pivotal role in the direct adrenocortical secretagogue effect of CRF, probably by releasing ACTH, which, in turn, may evoke, in a paracrine manner, the glucocorticoid response.

Adrenal Cortex↗
PubMed1992

The influence of environmental pressure on retentiveness of prosthetic crowns: an experimental study.

To determine the effect of pressure variations on the retention of prosthetic crowns, 36 identical, cast metal crowns were fixed to simulated, epoxy resin crown preparations with zinc oxyphosphate cement. Eighteen specimens were placed in a hyperbaric chamber and subjected to 15 cycles of simulated immersion at 30 m and decompression, as usually carried out by scuba divers. The untreated specimens served as controls. When the force required to dislodge the crowns was measured, the treated crowns were dislodged at about one third the load that was required to dislodge the control group, indicating that a statistically significant decrease in cement strength follows pressure variations.

Atmospheric Pressure↗