scholarly journals Antipsychotics increase steroidogenic enzyme gene expression in the rat brainstem

2021 ◽  
Author(s):  
Katarzyna Bogus ◽  
Małgorzata Żarczyńska ◽  
Artur Pałasz ◽  
Aleksandra Suszka-Świtek ◽  
John J. Worthington ◽  
...  
Keyword(s):  
Gene Expression ◽  
Term Treatment ◽  
Sprague Dawley ◽  
Steroidogenic Enzyme ◽  
Enzyme Gene ◽  
Brain Functions ◽  
Sprague Dawley Rats ◽  
Long Term Treatment ◽  
Rat Brainstem

Abstract Background Neurosteroids are involved in several important brain functions and have recently been considered novel players in the mechanic actions of neuropsychiatric drugs. There are no reports of murine studies focusing on the effect of chronic neurosteroid treatment in parallel with antipsychotics on key steroidogenic enzyme expression and we therefore focused on steroidogenic enzyme gene expression in the brainstem of rats chronically treated with olanzapine and haloperidol. Methods and results Studies were carried out on adult, male Sprague–Dawley rats which were divided into 3 groups: control and experimental animals treated with olanzapine or haloperidol. Total mRNA was isolated from homogenized brainstem samples for RealTime-PCR to estimate gene expression of related aromatase, 3β-HSD and P450scc. Long-term treatment with the selected antipsychotics was reflected in the modulation of steroidogenic enzyme gene expression in the examined brainstem region; with both olanzapine and haloperidol increasing aromatase, 3β-HSD and P450scc gene expression. Conclusions The present findings shed new light on the pharmacology of antipsychotics and suggest the existence of possible regulatory interplay between neuroleptic action and steroidogenesis at the level of brainstem neuronal centres.

Role of antiglucocorticoid RU 486 on dexamethasone-induced hypertension in rats

1989 ◽  
Vol 256 (5) ◽  
pp. E682-E685 ◽  
Author(s):  
M. Kalimi
Keyword(s):  
Blood Pressure ◽  
Term Treatment ◽  
Sprague Dawley ◽  
Ru 486 ◽  
Sprague Dawley Rats ◽  
Long Term Treatment ◽  
Term Administration ◽  
Slight Elevation

This study was conducted to investigate whether hypertension induced by long-term in vivo administration of dexamethasone in rats could be prevented by the newly synthesized potent antiglucocorticoid drug RU 486. Subcutaneous implantation of 5 mg of dexamethasone pellets in Sprague-Dawley rats resulted in a rapid increase in the blood pressure that remained elevated during the 3 wk of experimental observation. RU 486 (50 mg) administered alone surprisingly showed slight elevation of blood pressure over untreated control animals. However, the blood pressure leveled off to control levels over the next 2 wk. Interestingly, a 50-mg RU 486 pellet implanted along with 5 mg of dexamethasone effectively prevented the dexamethasone-induced increase in blood pressure. RU 486 administered together with dexamethasone prevented dexamethasone-induced diuresis and urinary Na+ excretion. However, RU 486 was unable to reverse the weight loss or involution of thymus observed by long-term treatment with dexamethasone alone. No abnormalities were found in either kidneys or hearts in any of the treated groups under microscopic examination. These results suggest that RU 486 successfully prevented the hypertension produced by the long-term administration of dexamethasone in male Sprague-Dawley rats.

scholarly journals Modulatory effect of olanzapine on SMIM20/phoenixin, NPQ/spexin and NUCB2/nesfatin-1 gene expressions in the rat brainstem

2021 ◽  
Author(s):  
Artur Pałasz ◽  
Piotr Żarczyński ◽  
Katarzyna Bogus ◽  
Kinga Mordecka-Chamera ◽  
Alessandra Della Vecchia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mrna Expression ◽  
Mrna Level ◽  
Brain Structures ◽  
Term Treatment ◽  
Sprague Dawley ◽  
Gene Expressions ◽  
Alternative Mode ◽  
Long Term Treatment ◽  
Rat Brainstem

Abstract Background Phoenixin, spexin and nesfatin-1 belong to a family of newly discovered multifunctional neuropeptides that play regulatory roles in several brain structures and modulate the activity of important neural networks. However, little is known about their expression and action at the level of brainstem. The present work was, therefore, focused on gene expression of the aforementioned peptides in the brainstem of rats chronically treated with olanzapine, a second generation antipsychotic drug. Methods Studies were carried out on adult, male Sprague–Dawley rats that were divided into 2 groups: control and experimental animals treated with olanzapine (28-day-long intraperitoneal injection, at dose 5 mg/kg daily). All individuals were killed under anesthesia and the brainstem excised. Total mRNA was isolated from homogenized samples of both structures and the RT-PCR method was used for estimation of related SMIM20/phoenixin, NPQ/spexin and NUCB2/nesfatin-1 gene expression. Results Long-term treatment with olanzapine is reflected in qualitatively different changes in expression of examined neuropeptides mRNA in the rat brainstem. Olanzapine significantly decreased NPQ/spexin mRNA expression, but increased SMIM20/phoenixin mRNA level in the rat brainstem; while NUCB2/nesfatin-1 mRNA expression remained unchanged. Conclusions Olanzapine can affect novel peptidergic signaling in the rat brainstem. This may cautiously suggest the presence of an alternative mode of its action.

scholarly journals Osteosarcoma in Sprague-Dawley rats after long-term treatment with teriparatide (human parathyroid hormone (1-34))

2012 ◽  
Vol 37 (3) ◽  
pp. 617-629 ◽  
Author(s):  
Atsushi Watanabe ◽  
Shigeki Yoneyama ◽  
Mikio Nakajima ◽  
Norihiro Sato ◽  
Ryoko Takao-Kawabata ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Term Treatment ◽  
Human Parathyroid Hormone ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Long Term Treatment

Abstract P053: Enhanced Exercise Capacity By Muscadine Grape Extract Treatment Is Only Evident In Older Hypertensive Female Rats And Is Independent Of Blood Pressure

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Nildris Cruz Diaz ◽  
A'ja V Duncan ◽  
Wayne Graham ◽  
Brian Westwood ◽  
Patricia E. Gallagher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Exercise Capacity ◽  
Physical Performance ◽  
Term Treatment ◽  
Female Rats ◽  
Sprague Dawley ◽  
Grape Extract ◽  
Long Term Treatment ◽  
Muscadine Grape

Physical performance and systolic blood pressure (SBP) during aging in normotensive female Sprague-Dawley (SD) and hypertensive (mRen2)27 transgenic rats were assessed following long-term treatment with a Muscadine Grape Extract (MGE, Piedmont Research and Development Corp). MGE was administered at a dose of 0.2 mg/mL in the drinking water starting at 14 weeks (wks) of age with an endpoint at 70 wks of age (total time of treatment of 56 wks). At 20-, 40- and 70-wks of age, physical performance (exercise capacity in seconds and workload in grams - meters) was determined using a treadmill at a velocity of 17 cm/second with a 5% incline. SBP was determined by tail-cuff plethysmography in trained rats. There were no significant differences in physical performance between SD and (mRen2)27 female rats at any age despite the higher SBP in the (mRen2)27 rats at all ages. Long-term treatment with MGE had no significant effect on physical performance or SBP in SD rats at any age. In contrast, MGE treatment markedly increased exercise capacity (40 wks: 1615 ± 166 vs 4943 ± 442 seconds, p<0.01, n = 4-9; 70 wks: 2520 ± 374 vs 4117 ± 245 seconds, p<0.01, n = 4-8) and workload (40 wks: 4579 ± 490 vs 14730 ± 1353 grams - meters, p<0.01, n = 4-9; 70 wks: 8338 ± 1340 vs 13659 ± 933 grams - meters, p<0.01, n = 4-8) at the later ages in female (mRen2)27 rats, while there was no effect on SBP (20 wks: 167 ± 4 vs 173 ± 4 mm Hg, n = 4-6; 40 wks: 177 ± 8 vs 170 ± 7 mm Hg, n = 6-7; 70 wks:154 ± 6 vs 172 ± 6 mm Hg, n = 5) at any age. These data suggest that MGE treatment is effective in improving physical performance only in hypertensive female rats and may be independent of changes in blood pressure. The benefit of MGE in the older hypertensive female may reflect reductions in vascular stiffness and oxidative stress. Support: Chronic Disease Research Fund, Hypertension & Vascular Research Center

Long-term captopril treatment restores natriuresis after carotid baroreceptor activation in the SHR

1997 ◽  
Vol 273 (1) ◽  
pp. R70-R79
Author(s):  
J. P. Valentin ◽  
S. A. Mazbar ◽  
M. H. Humphreys
Keyword(s):  
Renal Plasma Flow ◽  
Renal Nerves ◽  
Sprague Dawley ◽  
Wky Rats ◽  
Sprague Dawley Rats ◽  
Long Term Treatment ◽  
Bilateral Carotid ◽  
Wistar Kyoto ◽  
Captopril Treatment

In anesthetized Sprague-Dawley rats, intermittent bilateral carotid artery traction (BilCAT) caused a transient decrease in mean arterial pressure (MAP) of 28 +/- 3 mmHg and led to a progressive increase in sodium excretion (UNaV) that nearly doubled 45-90 min after initiation of the repetitive application of BilCAT (P < 0.001). This natriuresis was accompanied by an increase in glomerular filtration rate (GFR) from 2.70 +/- 0.3 to 3.2 +/- 0.3 ml/min (P < 0.001), no change in renal plasma flow [clearance of p-aminohippurate (PAH)], and an increase in the fractional excretion of lithium. Rats with bilateral renal denervation exhibited neither natriuresis nor an increase in GFR in response to BilCAT despite similar vasodepression caused by the maneuver. Normotensive Wistar-Kyoto (WKY) rats responded to BilCAT like Sprague-Dawley rats, whereas spontaneously hypertensive rats (SHR) exhibited an exaggerated vasodepressor response to BilCAT (-51 +/- 3 mmHg) without increasing either UNaV or GFR. Separate groups of WKY and SHR were treated from 4 wk of age with captopril added to the drinking water at a concentration of 1 g/l. At 12-14 wk, both groups had lower MAP compared with untreated animals. Captopril treatment did not alter either the natriuretic response or the increase in GFR seen in untreated WKY after BilCAT, and the maneuver produced equivalent degrees of vasodepression as in controls. However, treated SHR now responded to BilCAT with increases in both UNaV and GFR that closely resembled the responses seen in Sprague-Dawley and WKY rats. These results suggest that BilCAT produces natriuresis through a pathway dependent on the renal nerves. This pathway does not function in untreated SHR despite similar vasodepression. Long-term treatment with captopril restores this reflex pathway in SHR, lending support to the concept that angiotensin II is critically linked to heightened sympathetic nerve activity and abnormal sodium metabolism in this strain.

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