Effects of hypophysectomy, adrenalectomy and (-)-propranolol on ethanol-induced decrease in plasma amino acids.

T Eriksson; T Magnusson; A Carlsson; M Hagman; R Jagenburg; S Edén

doi:10.1007/bf00503819

Home/Archive/PubMed

PubMed · 7322213

Effects of hypophysectomy, adrenalectomy and (-)-propranolol on ethanol-induced decrease in plasma amino acids.

T Eriksson·T Magnusson·A Carlsson·M Hagman·R Jagenburg·S Edén

View original source ↗Export metadata ↓

Abstract

In previous studies we have demonstrated that an acute dose of ethanol cause an immediate decrease in most plasma amino acids in both man and rat. This effect of ethanol is partly inhibited by the beta-adrenergic antagonist (-)-propranolol, partly by adrenalectomy or hypophysectomy and almost completely by a combination of adrenalectomy with (-)-propranolol. This finding suggests an involvement of both beta-adrenergic mechanisms and steroids from the adrenal cortex in the ethanol-induced decrease in plasma amino acids.

Explore related subjects

Adrenalectomy Amino Acids Animals Ethanol Hypophysectomy Male Propranolol Rats Rats, Inbred Strains Tryptophan Tyrosine Journal Article Research Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

T Eriksson, T Magnusson, A Carlsson, M Hagman, R Jagenburg, S Edén. 1981. Effects of hypophysectomy, adrenalectomy and (-)-propranolol on ethanol-induced decrease in plasma amino acids.. https://doi.org/10.1007/bf00503819

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Regulation by glucocorticoids and osmolality of expression of ROMK (Kir 1.1), the apical K channel of thick ascending limb.

Mechanisms of regulation of ROMK channel mRNA and protein expression in medullary thick ascending limb (MTAL) were assessed in rat MTAL fragments incubated for 7 h. ROMK mRNA was quantified by quantitative RT-PCR and ROMK protein by immunoblotting analysis of crude membranes. Medium hyperosmolality (450 mosmol/kgH(2)O; NaCl plus urea added to isoosmotic medium) increased ROMK mRNA (P < 0.04) and protein (P < 0.006), and 10 nM dexamethasone also increased ROMK mRNA (P < 0.02). Hyperosmolality and dexamethasone had no additive effects on ROMK mRNA. NaCl alone, but not urea or mannitol, reproduced the hyperosmolality effect on ROMK mRNA. 1-Deamino-(8-d-arginine) vasopressin (1 nM) or 0.5 mM 8-bromo-cAMP had no effect per se on ROMK mRNA and protein. However, 8-bromo-cAMP abolished the stimulatory effect of dexamethasone on ROMK mRNA in the isoosmotic but not in the hyperosmotic medium (P < 0.004). In in vivo studies, the abundance of ROMK protein and mRNA increased in adrenalectomized (ADX) rats infused with dexamethasone compared with ADX rats (P < 0.02). These results establish glucocorticoids and medium NaCl concentration as direct regulators of MTAL ROMK mRNA and protein expression, which may be modulated by cAMP-dependent factors.

Adrenalectomy↗

PubMed2003

Mechanisms underlying the cardiovascular responses to spinal dopamine receptor stimulation by apomorphine in anesthetized rats.

The present study investigated the mechanisms by which intrathecal (i.t.) apomorphine affects mean aortic pressure and heart rate in anesthetized rats. In saline-pretreated rats, upper thoracic (T2-T4) i.t. administration of apomorphine (48 microg/rat) induced immediate and significant hypotension and bradycardia. These responses were unaffected by intravenous (i.v.) methylatropine (1 mg/kg) or bilateral vagotomy, while they were prevented by i.t. lidocaine (25 microl at 1%) or i.v. hexamethonium (30 mg/kg). However, i.v. atenolol (1.5 mg/kg) suppressed the apomorphine-induced bradycardia without affecting the hypotension in either intact or bivagotomized rats. Bilateral adrenalectomy had no effect upon both maximal hypotensive and bradycardic responses to apomorphine (48 microg/rat at the T9-T10 level). These results suggest that hypotensive and bradycardic responses to i.t. apomorphine are due to an action in the spinal cord, presumably on sympathetic preganglionic neurons. These responses are dissociated and seem to result from withdrawal of sympathetic outflow to the vasculature and to the heart, respectively.

Adrenalectomy↗

PubMed2003

Transabdominal laparoscopic adrenalectomy.

Laparoscopic adrenalectomy has become the standard technique for the surgical removal of the adrenal gland at many centers worldwide. Functional adrenal tumors such as aldosteronoma, glucocorticoid, androgen/estrogen-producing adenomas, and small-to-moderate sized solitary pheochromocytomas are amenable to removal via a laparoscopic approach. The advantages of laparoscopic adrenalectomy over open adrenalectomy are well documented and include a shorter hospital stay, a decrease in postoperative pain, shorter interval between surgery and return to preoperative activity level, and improved cosmesis. Various laparoscopic approaches to the adrenal gland have been described. Among these are the lateral transabdominal, anterior transabdominal, lateral retroperitoneal, and posterior retroperitoneal approaches. Each of these methods has specific advantages and disadvantages. This article reviews the transperitoneal approach to laparoscopic adrenalectomy, and discusses indications, operative technique, and a survey of the available literature.

Adrenalectomy↗