Production of corticosterone and testosterone in scorbutic mutant rats: difference of in vivo production between adrenal gland and testis

1991 ◽  
Vol 124 (4) ◽  
pp. 425-433 ◽  
Author(s):  
Haruki Fukuda ◽  
Yasuhiro Ito ◽  
Ryouji Hirota ◽  
Motomu Tsuji ◽  
Hiroshi Mori
Keyword(s):  
Ascorbic Acid ◽  
Adrenal Gland ◽  
Steroid Hormones ◽  
Mutant Strain ◽  
Seminal Vesicles ◽  
Plasma Acth ◽  
Chronic Stimulation ◽  
Testosterone Levels ◽  
Stimulation Of

Abstract. Effects of deficiency in ascorbic acid on in vivo production of corticosterone and testosterone were examined using a mutant strain of rats unable to synthesize ascorbic acid. The adrenal weight of scorbutic rats was larger, and corticosterone levels in plasma and adrenal tissues were higher than those of ascorbic acid-supplied (ascorbutic) rats. Acute and chronic stimulation with ACTH increased corticosterone levels in both ascorbutic and scorbutic rats. In contrast, weights of seminal vesicles and ventral prostates in unstimulated scorbutic rats were smaller, and testosterone levels in plasma and testicular tissues were lower than those in ascorbutic rats. Acute stimulation with hCG increased testosterone levels only slightly in plasma and not in testicular tissues of scorbutic rats, when testosterone levels in ascorbutic rats reached a maximum. Chronic stimulation with hCG increased testosterone levels remarkably in both ascorbutic and scorbutic rats. These findings seem to indicate that ascorbic acid is not essential for the synthesis of steroid hormones. The scurvy seems to increase plasma ACTH levels secondary to the stress, resulting in the stimulation of the adrenals. In contrast, a prolonged deficiency in ascorbic acid appears to decrease plasma gonadotropin levels, and may reduce the sensitivity of testes to gonadotropins.

Selective autonomic stimulation of canine trachealis with dimethylphenylpiperazinium

1981 ◽  
Vol 51 (2) ◽  
pp. 428-437 ◽  
Author(s):  
A. R. Leff ◽  
N. M. Munoz
Keyword(s):  
Adrenal Gland ◽  
Contractile Response ◽  
Sympathetic Innervation ◽  
Adrenergic Stimulation ◽  
Parasympathetic Ganglia ◽  
Regional Administration ◽  
Adrenal Secretion ◽  
Stimulation Of

The response of canine tracheal muscle to autonomic stimulation with 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) was studied isometrically in 39 dogs in vivo. Intra-arterial (ia) DMPP (2.5 X 10(-4) to 2.5 X 10(-2) mg/kg) caused selective dose related contraction [maximum 30.1 +/- 6.5 gram-force (gf)/cm] due to regional stimulation of parasympathetic ganglia. This contraction was blocked by regional administration of atropine 10(-3) mg/kg ia and hexamethonium 5 X 10(-2) mg/kg ia. Nonselective intravenous (iv) administration of DMPP 2.5 X 10(-2) mg/kg caused parasympathetic tracheal contraction [+13.4 +/- 1.64 gf/cm] followed by later sympathetic relaxation [-11.8 +/- 2.3 gf/cm]; 0.5 mg/kg iv atropine abolished contraction but did not affect relaxation. The role of the adrenal gland vs. direct sympathetic innervation in producing tracheal relaxation after sympathetic stimulation was also studied. Tracheal relaxation to 2.5 X 10(-2) mg/kg iv DMPP was -18.2 +/- 4.0 gf/cm before adrenalectomy (ADX) and -4.3 +/- 0.9 gf/cm afterward (P less than 0.001). In contrast, tracheal contraction resulting from alpha-adrenergic stimulation after 2.5 X 10(-2) mg/kg iv DMPP in beta-blocked (BB) dogs was not significantly altered by ADX. At 2.5 X 10(-1) mg/kg iv DMPP, the alpha-adrenergic contractile response was still 70% of the response prior to ADX. We conclude that sympathetic tracheal relaxation in dogs is predominantly mediated by circulating catecholamine from the adrenal gland, but that alpha-adrenergic contraction after BB results predominantly from direct sympathetic innervation and is not greatly augmented by adrenal secretion. We also report a new method for selective stimulation of airway cholinergic nerves in vivo without systemic effects.

scholarly journals Ascorbic acid, metal ions and the superoxide radical

1976 ◽  
Vol 155 (3) ◽  
pp. 697-700 ◽  
Author(s):  
B Halliwell ◽  
C H Foyer
Keyword(s):  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Bovine Serum Albumin ◽  
Metal Ions ◽  
Bovine Serum ◽  
Superoxide Radical ◽  
Alkaline Ph ◽  
Ph Values ◽  
Stimulation Of

1. No evidence could be found for production of the superoxide radical, O2-, during autoxidation of ascorbic acid at alkaline pH values. Indeed, ascorbate may be important in protection against O2- genat-d in vivo. 2. Oxidation of ascorbate at pH 10.2 was stimulated by metal ions. Stimulation by Fe2+ was abolished by superoxide dismutase, probably because of generation of O2- during reduction of O2 by Fe2+, followed by reaction of O2- with ascorbate. EDTA changed the mechanism of Fe2+-stimulated ascorbate oxidation. 3. Stimulation of ascorbate oxidation by Cu2+ was also decreased by superoxide dismutase, but this appears to be an artifact, since apoenzyme or bovine serum albumin showed similar effects.

Lipopolysaccharide is able to bypass corticotrophin-releasing factor in affecting plasma ACTH and corticosterone levels: evidence from rats with lesions of the paraventricular nucleus

1992 ◽  
Vol 133 (2) ◽  
pp. 231-236 ◽  
Author(s):  
I. J. Elenkov ◽  
K. Kovács ◽  
J. Kiss ◽  
L. Bertók ◽  
E. S. Vizi
Keyword(s):  
Hpa Axis ◽  
Paraventricular Nucleus ◽  
Physiological Responses ◽  
Plasma Acth ◽  
Experimental Conditions ◽  
Corticotrophin Releasing Factor ◽  
Adrenal System ◽  
Lps Treatment ◽  
Stimulation Of

ABSTRACT Stimulation of the immune system or experimental conditions (bacterial lipopolysaccharide (LPS) treatment) provoke a broad spectrum of physiological responses. It was recently shown that one of them is the activation of the hypothalamic-pituitary-adrenal (HPA) axis. The mechanism and the site or sites through which LPS stimulates the HPA axis are not well understood. To establish whether the effect of bacterial LPS is related in vivo to the presence of hypothalamic hypophysiotrophic peptides (corticotrophin-releasing factor-41, arginine vasopressin, etc.), plasma ACTH and corticosterone levels were monitored in intact and sham-operated rats, and in rats with paraventricular nucleus lesions in order to remove the main source of these neuropeptides. Evidence was obtained that 4 h after treatment, LPS was able to activate the hypophysial-adrenal system in the absence of hypophysiotrophic neuropeptides of paraventricular origin. It is suggested that, in vivo, LPS could have a direct effect on the pituitary gland or that it acts through an extrapituitary, non-paraventricular pathway to activate the HPA axis. Journal of Endocrinology (1992) 133, 231–236

scholarly journals Effect of adrenomedullin infusion on basal and stimulated aldosterone secretion in conscious sheep with cervical adrenal autotransplants

2000 ◽  
Vol 166 (2) ◽  
pp. 389-399 ◽  
Author(s):  
R Salemi ◽  
JG McDougall ◽  
KJ Hardy ◽  
EM Wintour
Keyword(s):  
Adrenal Gland ◽  
Zona Glomerulosa ◽  
Cortisol Secretion ◽  
Aldosterone Secretion ◽  
Stimulation Experiments ◽  
Gland Function ◽  
Conscious Sheep ◽  
Stimulation Of

In vivo and in vitro studies have shown conflicting effects of adrenomedullin (ADM) on the secretion of steroid hormones from the adrenal gland. While some investigators report no effect of this peptide on the output of various hormones, others have reported both stimulatory and inhibitory roles for ADM. We have shown that basal aldosterone secretion rate (ASR), in conscious sheep with cervical adrenal autotransplants, did not change when ADM was infused directly into the adrenal arterial supply. While not affecting basal ASR, ADM did produce pronounced increases in adrenal blood flow (BF). This elevation of BF in association with ADM infusion was seen in all subsequent experiments. When aldosterone output was acutely stimulated by angiotensin II (AngII), potassium chloride (KCl) and adrenocorticotrophic hormone (ACTH), ADM was seen to drastically reduce the secretion of aldosterone with all agonists studied. After pre-exposure to ADM, all three agonists increased ASR but the magnitude of the responses were somewhat blunted. ADM did not have the same effect on cortisol secretion stimulated by ACTH, suggesting that the ability of this peptide to influence adrenal gland function is limited to the zona glomerulosa. In conditions of chronic elevation of aldosterone levels, such as in Na deficiency, ADM did not display the same inhibitory abilities seen in the acute stimulation experiments. Hence, ADM has been shown to have a direct, inhibitory role on the acute stimulation of aldosterone by AngII, KCl and ACTH while not affecting basal or chronic aldosterone secretion or cortisol secretion stimulated by ACTH.

scholarly journals Chronic Stimulation of the Autophagy-inducing Ingredient of Areca Nut Promotes Tumor Growth In Vivo Through Up-regulation of Tumoral Autophagy

2019 ◽  
Vol 40 (1) ◽  
pp. 221-227
Author(s):  
CHANG-TA CHIU ◽  
SHYUN-YEU LIU ◽  
CHING-YU YEN ◽  
BANG-YEN LIU ◽  
ZI-YU SUN ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Areca Nut ◽  
Chronic Stimulation ◽  
Stimulation Of

scholarly journals Reversal of right ventricular failure by chronic α1A-subtype adrenergic agonist therapy

2019 ◽  
Vol 316 (1) ◽  
pp. H224-H232 ◽  
Author(s):  
Patrick M. Cowley ◽  
Guanying Wang ◽  
Philip M. Swigart ◽  
Anaha Raghunathan ◽  
Nikitha Reddy ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Therapeutic Target ◽  
Adrenergic Receptors ◽  
Chronic Stimulation ◽  
Pulmonary Artery Constriction ◽  
Rv Function ◽  
Fractional Shortening ◽  
Stimulation Of

Right ventricular (RV) failure (RVF) is a serious disease with no effective treatment available. We recently reported a disease prevention study showing that chronic stimulation of α1A-adrenergic receptors (α1A-ARs), started at the time of RV injury, prevented the development of RVF. The present study used a clinically relevant disease reversal design to test if chronic α1A-AR stimulation, started after RVF was established, could reverse RVF. RVF was induced surgically by pulmonary artery constriction in mice. Two weeks after pulmonary artery constriction, in vivo RV fractional shortening as assessed by MRI was reduced by half relative to sham-operated controls (25 ± 2%, n = 27, vs. 52 ± 2%, n = 13, P < 10−11). Subsequent chronic treatment with the α1A-AR agonist A61603 for a further 2 wk resulted in a substantial recovery of RV fractional shortening (to 41 ± 2%, n = 17, P < 10−7 by a paired t-test) along with recovery of voluntary exercise capacity. Mechanistically, chronic A61603 treatment resulted in increased activation of the prosurvival kinase ERK, increased abundance of the antiapoptosis factor Bcl-2, and decreased myocyte necrosis evidenced by a decreased serum level of cardiac troponin. Moreover, A61603 treatment caused increased abundance of the antioxidant glutathione peroxidase-1, decreased level of reactive oxygen species, and decreased oxidative modification (carbonylation) of myofilament proteins. Consistent with these effects, A61603 treatment resulted in increased force development by cardiac myofilaments, which might have contributed to increased RV function. These findings suggest that the α1A-AR is a therapeutic target to reverse established RVF. NEW & NOTEWORTHY Currently, there are no effective therapies for right ventricular (RV) failure (RVF). This project evaluated a novel therapy for RVF. In a mouse model of RVF, chronic stimulation of α1A-adrenergic receptors with the agonist A61603 resulted in recovery of in vivo RV function, improved exercise capacity, reduced oxidative stress-related carbonylation of contractile proteins, and increased myofilament force generation. These results suggest that the α1A-adrenergic receptor is a therapeutic target to treat RVF.

scholarly journals Changes in cyclic AMP level of rat thyroid by acute and chronic stimulation of thyrotropin in vivo.

1976 ◽  
Vol 23 (2) ◽  
pp. 157-163 ◽  
Author(s):  
YASUKO NAKAMURA ◽  
MITSUO SUZUKI ◽  
ISAO KOBAYASHI ◽  
YONOSUKE SHIMOMURA ◽  
TADAO KAKEGAWA
Keyword(s):  
Cyclic Amp ◽  
Chronic Stimulation ◽  
Rat Thyroid ◽  
Stimulation Of
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