Tachykinin neurokinin 3 receptor signaling in cholecystokinin-elicited release of oxytocin and vasopressin

2008 ◽  
Vol 294 (5) ◽  
pp. R1760-R1767 ◽  
Author(s):  
Gwendolen E. Haley ◽  
Francis W. Flynn

Neurokinin 3 receptor (NK3R) signaling has an integral role in the stimulated oxytocin (OT) and vasopressin (VP) release in response to hyperosmolarity and hypotension. Peripheral injections of cholecystokinin (CCK) receptor agonists for the CCK-A (sulfated CCK-8) and CCK-B (nonsulfated CCK-8) receptors elicit an OT release in rat. It is unknown whether NK3R contributes to this endocrine response. Freely behaving male rats were administered an intraventricular pretreatment of 250 or 500 pmol of SB-222200, a specific NK3R antagonist, or 0.15 M NaCl before an intraperitoneal or intravenous injection of CCK-8 (nonsulfated or sulfated) or 0.15 M NaCl. Blood samples were taken before intraventricular treatment and 15 min after intraperitoneal or intravenous injection, and plasma samples were assayed for OT and VP concentration. Intraperitoneal injection of both nonsulfated and sulfated CCK-8 significantly increased plasma OT levels and had no effect on plasma VP levels. Intravenous injection of sulfated CCK-8 stimulated an increase in plasma OT levels and did not alter plasma VP levels. However, intravenous injection of nonsulfated CCK-8 stimulated a significant increase in plasma levels of both OT and VP. No other studies have demonstrated CCK-8-stimulated release of VP in rat. NK3R antagonist did not alter baseline levels of either hormone. However, pretreatment of NK3R antagonist significantly blocked the CCK-stimulated release of OT in all CCK treatment groups and blocked VP release in response to intravenous injection of nonsulfated CCK-8. Therefore, central NK3R signaling is required for OT and VP release in response to CCK administration.

2007 ◽  
Vol 293 (2) ◽  
pp. R931-R937 ◽  
Author(s):  
Gwendolen E. Haley ◽  
Francis W. Flynn

Activation of the neurokinin 3 receptor (NK3R) by a receptor agonist, hypotension, and hyperosmolarity results in the internalization of NK3R expressed by magnocellular neurons and the release of vasopressin (VP) and oxytocin (OT) into the circulation. The contribution of NK3R activation to the release of VP and OT in response to hyperosmolarity and hypotension was evaluated by measuring the release of both hormones following pretreatment with a selective NK3R antagonist, SB-222200. Freely behaving male rats were given an intraventricular injection of either 0.15 M NaCl or 250, 500, or 1,000 pmol SB-222200, and then were administered an intravenous infusion of 2 M NaCl or 0.15 M NaCl ( experiment 1), or a bolus intra injection of 0.15 M NaCl or hydralazine (HDZ), a hypotension-inducing drug ( experiment 2). Blood samples were taken from indwelling arterial catheters at various time points for 1–2 h, both before and after treatments. Plasma VP and OT levels were determined by ELISA. Blockade of NK3R did not affect the baseline levels of either hormone. In contrast, pretreatment with SB-222200 significantly reduced (∼60%) or abolished the release of VP and OT, respectively, to 2 M NaCl infusion. HDZ-induced VP and OT release was eliminated by pretreatment with 500 pmol SB-222200. Therefore, NK3R activation contributes significantly to the systemic release of both VP and OT in response to osmotic and hypotensive challenges.


1996 ◽  
Vol 270 (3) ◽  
pp. E438-E444 ◽  
Author(s):  
D. H. Han ◽  
K. P. Kelly ◽  
G. W. Fellingham ◽  
R. K. Conlee

To determine the combined sympathoadrenal effects of cocaine and exercise in awake animals, rats were assigned to one of four treatment groups: saline-rest (SR), saline-exercise (SE), cocaine-rest (CR), and cocaine-exercise (CE). Venous blood samples from jugular catheters were obtained at -40, 0-4, 7, 10, 13, 16, 19, 26, and 36 min after intravenous injection of cocaine (5 mg/kg) or saline and the simultaneous onset of a 16-min treadmill run (26 m/min, 10% grade). CE increased plasma epinephrine (24.2 nM at 16 min), norepinephrine (28.0 nM at 10 min), and lactate (11.2 mM at 4 min) to levels 2-5 times greater than either treatment (SE and CR) alone (P<0.05) and 11-35 times higher that SR. Blood glucose values were significantly depressed in CE (-33% vs. SE) but increased in CR (+26% vs. SR). Plasma cocaine peaked < 2 min after injection in both CR and CE, and the peak was 69% higher in CE (P<0.05); however, the plasma elimination half-life (12-14 min) was not different. These results indicate that the combined effect of the two sympathoadrenal stimulants, exercise and cocaine, amplify the catecholamine responses to levels far greater than when each stimulant is used alone.


2019 ◽  
Vol 7 (22) ◽  
pp. 3781-3785
Author(s):  
Fajar Apollo Sinaga ◽  
Urip Harahap ◽  
Jansen Silalahi

BACKGROUND: Maximal physical activity can produce an imbalance between reactive oxygen species (ROS) and antioxidants which are possibly related to fatigue and tissue injury. One of the natural sources that contain antioxidants is virgin coconut oil (VCO). AIM: This study aimed to determine the protective effects antioxidant of virgin coconut oil (VCO) treatment on urea and creatine level on maximum physical activity METHODS: This study used 24 healthy male rats. The rats were divided into four groups, randomly consisted of six rats in each group. The control group (P0) was given 2 mL water, the treatment groups (VCO-1, VCO-2, and VCO-4) were given VCO 1 mL/200 gBW, 2 mL/200 gBW and 4 ml/200 gBW, respectively, per day using gavage spuit. After 28 days, the rats were forced to perform maximal activity by putting the rats in water with no exit. Blood samples were collected immediately after the maximum physical activity. The urea, creatinine, malondialdehyde and glutation peroxidase level was then measured. RESULTS: This study used 24 healthy male rats. The rats were divided into four groups randomly consisted of six rats in each group. The control group (P0) was given 2 mL water, the treatment groups (VCO-1, VCO-2, and VCO-4) were given VCO 1 mL/200 gBW, 2 mL/200 gBW and 4 ml/200 gBW, respectively, per day using gavage spuit. After 28 days, the rats were forced to perform the maximal activity by putting the rats in water with no exit. Blood samples were collected immediately after the maximum physical activity. The urea, creatinine, malondialdehyde and glutathione peroxidase level was then measured. CONCLUSION: The results of this study indicate that virgin coconut oil is effective in the prevention of oxidative stress following maximum physical activity.


2022 ◽  
Vol 16 (1) ◽  
pp. 27-34
Author(s):  
Anitsah Fiqardina ◽  
◽  
Yulia Yusrini Djabir ◽  
Arif Santoso ◽  
Syafira Nurul Salsabil ◽  
...  

Background: Levofloxacin is a fluoroquinolone antibiotic that has broad-spectrum antimicrobial activity, but it may induce kidney dysfunction. Clove oil (Oleum caryophylli) has antioxidant properties that may alleviate levofloxacin toxicity. This study aimed to examine the protective effect of clove oil on levofloxacin-induced nephrotoxicity in rat animal models. Methods: A total of 24 male rats were divided into 6 groups. One group did not receive levofloxacin to serve as the control. The treatment groups received a single daily administration of levofloxacin (93 mg/kg) with either placebo or clove oil (10 mg/kg, 25 mg/kg, or 50 mg/kg per body weight) pre-treatment. Another group received Curcuma extract pre-treatment as a comparison. Blood samples were withdrawn after 28 days of treatment to measure serum biomarkers (urea and creatinine), and the kidneys were removed to measure renal Malondialdehyde (MDA) and histopathological analysis. Results: The results showed that clove oil pre-treatment at a dose of 10 mg/kg was able to reduce renal MDA and serum biomarker levels (P<0.05). The effect was similar to that found in Curcuma-treated rats. In addition, clove oil (10 mg/kg) was also found to ameliorate renal histopathological damage due to levofloxacin. Conclusion: Based on biomarker and histopathological analysis, clove oil pre-treatment in rats provides a nephroprotective effect against levofloxacin toxicity.


2008 ◽  
Vol 295 (4) ◽  
pp. R1158-R1167 ◽  
Author(s):  
Gwendolen E. Haley ◽  
Francis W. Flynn

Tachykinin neurokinin 3 receptor (NK3R) signaling has a broad role in vasopressin (VP) and oxytocin (OT) release. Hydralazine (HDZ)-induced hypotension activates NK3R expressed by magnocellular neurons, increases plasma VP and OT levels, and induces c-Fos expression in VP and OT neurons. Intraventricular pretreatment with the specific NK3R antagonist, SB-222200, eliminates the HDZ-stimulated VP and OT release. NK3R are distributed in the central pathways conveying hypotension information to the magnocellular neurons, and the NK3R antagonist could act anywhere in the pathways. Alternatively, the antagonist could act at the NK3R expressed by the magnocellular neurons. To determine whether blockade of NK3R on magnocellular neurons impairs VP and OT release to HDZ, rats were pretreated with a unilateral PVN injection of 0.15 M NaCl or SB-222200 prior to an intravenous injection of 0.15 M NaCl or HDZ. Blood samples were taken, and brains were processed for VP/c-Fos and OT/c-Fos immunohistochemistry. Intravenous injection of 0.15 M NaCl did not alter plasma hormone levels, and little c-Fos immunoreactivity was present in the PVN. Conversely, intravenous injection of HDZ increased plasma VP and OT levels and c-Fos expression in VP and OT magnocellular neurons. Intra-PVN injection of SB-222200 prior to an intravenous injection of HDZ significantly decreased c-Fos expression in both VP and OT neurons by ∼70% and attenuated plasma VP and OT levels by 33% and 35%, respectively. Therefore, NK3R signaling in magnocellular neurons has a critical role for the release of VP and OT in response to hypotension.


1986 ◽  
Vol 113 (3) ◽  
pp. 317-322 ◽  
Author(s):  
F. López ◽  
D. Gónzalez ◽  
E. Aguilar

Abstract. To analyze a possible direct action of serotonin (5-hydroxytryptamine) at pituitary level in GH secretion, two experimental models were used: hypophysectomized autografted rats and perifused pituitaries. Adult male rats were hypophysectomized and their own pituitaries placed under the right kidney capsule. Ten days later an intra-atrial cannula was inserted. The next day, blood samples were obtained before and every 10 min during a 2 h period after the injection of saline or 5-hydroxytryptamin (1 or 2 mg/kg iv). Plasma volume was replaced with saline. Both doses of 5-hydroxytryptamine elicit a strong release of GH, the effect being dose-dependent. In pituitaries perifused with 5-hydroxytryptamine (100 μm during 115 min or 1, 10 and 100 μm during 15 min), a significant release of GH was also observed. These results suggested that 5-hydroxytryptamine may stimulate GH secretion through a direct pituitary action.


2005 ◽  
Vol 187 (3) ◽  
pp. 369-378 ◽  
Author(s):  
C K Hilleson-Gayne ◽  
J A Clapper

To further delineate the role of estradiol in the IGF system an experiment was conducted to determine the dosage of the aromatase inhibitor, anastrozole, needed to decreases serum concentrations of estradiol-17β (E2) in maturing boars. A second experiment was conducted to determine if administration of anastrozole to growing boars decreased serum concentrations of E2 and affected components of the serum and anterior pituitary gland (AP) IGF system vs untreated boars and barrows. In Experiment 1, 12 crossbred boars (292 days, 158 kg) were administered either 0, 1 or 10 mg/day anastrozole (n=4/group) beginning on day 1. Blood samples were collected every 7–14 days. Mean serum concentrations of E2 were decreased (P < 0·05) in the 10 mg group vs the 0 and 1 mg groups by day 36; however, no difference (P > 0·05) existed between the 0 and 1 mg groups. In Experiment 2, 24 crossbred boars and 12 barrows (101 days, 44 kg) were stratified by litter to one of three treatment groups (n=12): boars administered 10 mg/day anastrozole, boars administered 0 mg/day, and barrows administered 0 mg/day. Blood samples were collected and pigs were weighed on day 0 and every 14 days thereafter, then killed on day 84 when blood and APs were collected. The 10 mg/day pigs were fed the anastrozole-amended diet beginning on day 1. Mean serum concentrations of E2 did not differ (P > 0·05) between the 10 mg/day pigs and 0 mg/day pigs on day 0; however, on day 15 through to 84 mean serum concentrations of E2 were greater (P < 0·05) in 0 mg/day pigs than in the 10 mg/day pigs. Mean percentage increase in serum concentrations of IGF-I was greater (P < 0·05) in untreated boars than anastrozole-treated boars and barrows from day 58 through to 84. Mean percentage of basal IGF-I increased (P < 0·05) from day 29 through to 84 in untreated boars. Mean relative amounts of AP IGF-binding protein (IGFBP)-2 and -5 were less (P < 0·01) in 10 mg/day pigs than in the 0 mg/day pigs, but each was greater (P < 0·01) than in barrows administered 0 mg/day. These results indicate anastrozole administered at a dosage of 10 mg/day suppresses serum concentrations of E2 in pigs. Administration of anastrozole to boars reduced the percentage increase in serum concentrations of IGF-I and relative amounts of AP IGFBP-2 and -5. These data further support a role for E2 in regulating components of the IGF system in pigs.


1985 ◽  
Vol 65 (3) ◽  
pp. 627-630 ◽  
Author(s):  
L. A. BATE ◽  
R. R. HACKER ◽  
M. B. KREUKNIET

Blood samples were collected from five pregnant sows from day 111 postbreeding to farrowing and from their piglets at regular intervals between birth and 48 h. The time between birth and first suckling (BTS) was recorded for each piglet. Maternal serum testosterone (T) levels were detectable only at the beginning of parturition and were highly correlated (r = 0.83) with litter BTS. Serum T levels of male and female piglets were similar at birth. In male piglets the T levels increased to a peak 2 h after birth and decreased gradually thereafter. In contrast, the T levels of female piglets declined rapidly after birth to baseline levels. The BTS of female piglets was shorter than that of male piglets. Body weight of males was higher than that of females and was influenced by litter size. These results suggest that the higher serum T levels of male piglets may have a detrimental effect on their teat-seeking ability. Key words: Serum testosterone, sex, piglets, teat-seeking ability, sow


Author(s):  
Siska Siska ◽  
Franciscus D. Suyatna ◽  
Abdul Mun'im ◽  
Anton Bahtiar

Based on previous reports, the combination of captopril and celery could reduce blood pressure in hypertensive patients. This study aimed to investigate the changes of blood pressure, urine volume, sodium, and potassium level, due to concomitant administration of captopril with celery extract orally in male rats induced by 4% NaCl. The blood pressure was measured using a non-invasive tail method. The urine and blood were collected, and the sodium, potassium concentration, and cumulative urine volume were measured. The combination of 5 mg/kgBW of captopril and 40 mg/kgBW of celery extract decreased the blood pressure in hypertensive rats better than 5 mg/kgBW of captopril alone. The fell in blood pressure was followed by an increase in urine volume. Urinary and serum sodium, serum potassium levels tended to increase in all treatment groups, but not significantly different from the healthy group. Urinary potassium levels tended to decrease except in the combined 5 mg/kgBW of captopril and 40 mg/kgBW of celery extract. In conclusion, oral administration of a combination of 5 mg/kgBW captopril and 40 mg/kgBW celery extract decreased the blood pressure to the standard value in NaCl-induced hypertension rats.Keywords: Apium graveolens, captopril, celery, hypertension, pharmacodynamic


1978 ◽  
Vol 79 (1) ◽  
pp. 85-89 ◽  
Author(s):  
J. A. M. MATTHEIJ ◽  
J. J. M. SWARTS

The occurrence of circadian variations in the concentration of prolactin in the plasma of 6- to 9-month-old male rats has been assessed in animals exposed to light for 14 h/day (lights on 06.00–20.00 h). Blood samples were obtained after decapitation, or from individual rats at regular intervals via a permanent cannula. Care was taken to limit stress during sampling. The concentration of prolactin in the plasma was significantly lower between 07.00 and 15.00 h than at other times. Between 15.00 and 20.00 h (during the light period), the concentration of prolactin was significantly higher in comparison with the preceding period, or with the remainder of the 24 h period. During the night, the concentration fluctuated, probably because of episodic releases of the hormone. The possible physiological significance of a circadian rhythm in the plasma concentration of prolactin and the implications for endocrine experimentation are discussed briefly.


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