Selective activation of norepinephrine- and epinephrine-secreting chromaffin cells in rat adrenal medulla

1992 ◽  
Vol 263 (3) ◽  
pp. R716-R721 ◽  
Author(s):  
R. R. Vollmer ◽  
A. Baruchin ◽  
S. S. Kolibal-Pegher ◽  
S. P. Corey ◽  
E. M. Stricker ◽  
...  

The differential effects of insulin-induced hypoglycemia and cold exposure on adrenal medullary epinephrine (Epi) and norepinephrine (NE) cells were investigated in male Sprague-Dawley rats. In rats fasted overnight, insulin produced a marked hypoglycemia that resulted in a 70% decrease in adrenal medullary Epi content 3 h after the insulin was administered. No change in NE content was observed. Plasma Epi concentration was increased markedly after insulin, with a smaller increment in NE. In contrast, exposure to a 4 degrees C environment selectively reduced adrenal NE content, with the effect reaching statistical significance at 18 h. Cold exposure also led to a significant rise in plasma NE but not Epi. Both insulin-induced hypoglycemia and cold exposure significantly elevated adrenal dopamine, indicating that catecholamine synthesis was stimulated. Further evidence of enhanced catecholamine formation was the observation that inhibition of synthesis with alpha-methyl-p-tyrosine (AMT) greatly augmented the ability of insulin-induced hypoglycemia to selectively reduce adrenal medullary Epi content. Similarly, in cold-exposed animals, AMT pretreatment accelerated the NE depletion so that a significant decline was observed at 3 h. These results support the conclusion that the two major populations of adrenal catecholamine-secreting cells may be preferentially stimulated by different stressors. Moreover, augmented synthetic activity functions to maintain catecholamine stores in both Epi- and NE-secreting cells.

1973 ◽  
Vol 59 (3) ◽  
pp. 539-544 ◽  
Author(s):  
VARAPAN DANUTRA ◽  
MAUREEN E. HARPER ◽  
K. GRIFFITHS

SUMMARY Male Sprague—Dawley rats were injected (i.m.) daily for 10 days with 100 μg of either oestradiol-17β, diethylstilboestrol (DES), dl-dihydrodibutylstilboestrol (dl-DHBS) or meso-dihydrodibutylstilboestrol (meso-DHBS) in 0·2 ml sesame oil. After 10 days, the testicular tissue was removed and incubated simultaneously with [7α-3H]dehydroepiandrosterone and [4-14C]17α-hydroxyprogesterone. Less testosterone was synthesized by the testicular tissue from animals treated with oestradiol-17β, DES and meso-DHBS than by the controls or animals treated with dl-DHBS. The decreased synthetic activity was related to the decreased activity of both the 17β-hydroxysteroid dehydrogenase and 17α-pregnene-C17, 20-lyase enzyme systems. Prostatic tissue was also incubated with [7α-3H]testosterone. Administration of DES, oestradiol-17β or meso-DHBS increased the metabolism of testosterone by the prostatic tissue with a marked effect on the 5α-reductase enzyme system.


1993 ◽  
Vol 264 (3) ◽  
pp. F411-F414 ◽  
Author(s):  
J. A. Haas ◽  
A. A. Khraibi ◽  
M. A. Perrella ◽  
F. G. Knox

Systemic inhibition of nitric oxide synthesis with NG-monomethyl-L-arginine (L-NMMA) increases renal perfusion pressure (RPP) and urinary sodium excretion. Increased RPP has been proposed as one of the mechanisms for the natriuresis caused by intravenous infusion of L-NMMA. We tested the hypothesis that increases in renal interstitial hydrostatic pressure (RIHP) are required for the natriuresis of L-NMMA infusion. Experiments were performed in four groups of Sprague-Dawley rats in which partial aortic clamping and/or bilateral renal decapsulation was performed to control RPP and RIHP. Infusion of L-NMMA (15 mg/kg bolus + 500 micrograms.kg-1 x min-1 continuous infusion) increased RPP (delta+ 14 +/- 1 mmHg), RIHP (delta+ 3.6 +/- 0.7 mmHg), and fractional excretion of sodium (FENa; delta 2.4 +/- 0.6%, P < 0.005). When RPP was prevented from increasing by controlling RPP with an adjustable clamp around the suprarenal aorta, RIHP and FENa did not significantly change. When only RIHP was held constant by bilateral renal decapsulation, FENa was not significantly increased (delta+ 0.68 +/- 0.36%, not significant), despite a significant rise in RPP (delta+ 18 +/- 2 mmHg, P < 0.001). Control of both RPP and RIHP prevented the increase in FENa. Thus, when renal interstitial pressure was controlled, the infusion of L-NMMA did not result in an increase in FENa. These results demonstrate that an increase in RIHP is a necessary component in the natriuresis due to systemic infusion of L-NMMA.


1982 ◽  
Vol 30 (4) ◽  
pp. 323-330 ◽  
Author(s):  
D M Williams ◽  
R Gillett ◽  
J E Linder

Changes in neutrophil precursor populations in the bone marrow and their alkaline phosphatase reactivity following an inflammatory stimulus were studied in the rat using an osmiophilic method. Seven groups each of 3 Sprague-Dawley rats received subcutaneous injections of turpentine, and femoral marrow was examined at intervals up to 72 hr. Depletion of mature neutrophils resulted in an increased first in the myeloblast-promyelocyte compartment and at 48-72 hr in the myelocyte-metamyelocyte population. By 72 hr replenishment of the mature neutrophil marrow population had begun. Within 6 hr marked acceleration of cytoplasmic maturation was evident, together with accelerated synthetic activity, manifested by marked dilatation of the rough endoplasmic reticulum and an enlarged Golgi. Together with these changes there was an increase in the number of alkaline phosphatase reactive cells, which was evident first in the myeloblast-promyelocyte population at 2 hr. An absolute increase in the amount of enzyme reaction product associated with individual cells was also seen.


1996 ◽  
Vol 270 (2) ◽  
pp. R404-R412 ◽  
Author(s):  
J. R. Mathiasen ◽  
E. R. Larson ◽  
M. A. Ariano ◽  
C. D. Sladek

We have exposed primary dispersed hypothalamic cultures from 14-day-old fetal Sprague-Dawley rats to substances known to either elevate adenosine 3',5'-cyclic monophosphate (cAMP) levels or increase vasopressin (VP) secretion. The levels of VP in the medium collected from the cultures were determined by radioimmunoassay, and the number of neurophysin (NP)-positive cells after immunohistochemistry was counted. cAMP-elevating agents, 3-isobutyl-1-methylxanthine (200 microM) and forskolin (25 microM), in combination (I-F) maintained NP synthesis and VP secretion in 19-day cultures. I-F replacement by K+ (28 mM), isoproterenol (10 microM), glutamate (10 microM), or bicuculline (10 microM) during the last week of culture resulted in maintenance of NP expression and transient stimulation of VP secretion, but these agents did not induce NP expression independently of I-F treatment. In contrast, exposure to the dopamine D1 agonist SKF-38393 (10 microM) significantly increased NP expression independently and after replacement of I-F. Dopamine D1A receptors were detected by immunofluorescence on NP-expressing cells, providing a morphological basis for this response. These results suggest a role for D1A receptors in the regulation of VP gene expression.


Author(s):  
Prajwal Pradeep Thakre ◽  
Michael D. Sunshine ◽  
David D. Fuller

Repeated short episodes of hypoxia produces a sustained increase in phrenic nerve output lasting well beyond AIH exposure (i.e., phrenic long term facilitation, pLTF). Pretreatment with ampakines, drugs which allosterically modulate AMPA receptors, enables a single brief episode of hypoxia to produce pLTF, lasting up to 90 min after hypoxia. Here we tested the hypothesis that ampakine pretreatment would enhance the magnitude of pLTF evoked by repeated bouts of hypoxia. Phrenic nerve output was recorded in urethane-anesthetized, mechanically ventilated and vagotomized adult male Sprague-Dawley rats. Initial experiments demonstrated that ampakine CX717 (15 mg/kg, intravenous) caused an acute increase in phrenic nerve inspiratory burst amplitude reaching 70±48% baseline (BL) after 2 min (P=0.01. This increased bursting was not sustained (2±32%BL at 60 min, P=0.9). When CX717 was delivered 2 min prior to a single episode of isocapnic hypoxia (5-min, PaO2 = 44±9 mmHg) facilitation of phrenic nerve burst amplitude occurred (96±62%BL at 60 min, P<0.001). However, when CX717 was given 2 min prior to three, 5-min hypoxic episodes (PaO2 = 45±6 mmHg) pLTF was attenuated and did not reach statistical significance (24±29%BL, P=0.08). In the absence of CX717 pretreatment, pLTF was observed after three (74±33%BL at 60 min, P<0.001) but not one episode of hypoxia (1±8%BL at 60 min, P=0.9). We conclude that pLTF is not enhanced when ampakine pretreatment is followed by repeated bouts of hypoxia. Rather, the combination of ampakine and a single hypoxic episode appears to be ideal for producing sustained increase in phrenic motor output.


1960 ◽  
Vol 198 (2) ◽  
pp. 375-380 ◽  
Author(s):  
John P. Hannon ◽  
David A. Vaughan

Liver and muscle tissue from male Sprague-Dawley rats, exposed to 5 ± 1°C for 3–4 weeks, were assayed for the activities of selected glycolytic enzymes. When compared to control animals maintained at 25 ± 1°C, the cold-exposed animals showed an increase in liver glucose-6-phosphatase, an increase in liver and muscle glucokinase, a decrease in glucose-6-phosphate and 6-phosphogluconic dehydrogenase in both liver and muscle, and an increase in the rate of pyruvate formation from 3-phosphoglycerate in liver tissue. Assays of liver and muscle phosphoglucomutase, total liver and muscle phosphorylase and phosphorylase a and b in muscle failed to show any cold effect. The results indicate the cold-exposed rat has the enzyme capacities for: an increased utilization of free glucose, an increased glycogenolysis either to free glucose to pyruvate and an increased gluconeogenesis. They also indicate a decreased hexose monophosphate shunt activity. Little evidence could be found to indicate an epinephrine-induced activation of phosphorylase in the cold-exposed animals.


2019 ◽  
Vol 22 (5) ◽  
pp. 326-332
Author(s):  
Sarah Shin ◽  
No Soo Kim ◽  
Young Ah Kim ◽  
Hea Ry Oh ◽  
Ok-Sun Bang

Background: Traditionally, Phragmitis rhizoma has been prescribed to relive a fever, vomiting, dysuria, and constipation, and to promote secretion of fluids. In addition, recent studies have reported its efficacy as a diuretic and antiemetic. Our previous study demonstrated that the Phragmitis rhizoma aqueous extract (EPR) ameliorates docetaxel (DTX)-induced myelotoxicity. Aim and Objective: This study was aimed to investigate the effects of EPR on the pharmacokinetics of DTX in Sprague–Dawley rats. Materials & Methods: The animals received an intravenous injection of DTX (5 mg/kg) with or without oral EPR (100 mg/kg) pretreatment for 1 or 6 days. The pharmacokinetics of plasma DTX was analyzed using an ultra-performance liquid chromatography-tandem mass spectrometry system, and pharmacokinetic parameters were estimated via noncompartmental analysis. Results: Relative to the control group (DTX alone), EPR pretreatment did not affect significantly the overall profiles of plasma DTX levels. Consecutively pretreated EPR for 6 days slightly altered AUC0-t and Cmax of DTX by 122 and 145.9%, respectively, but these data did not reach the threshold of statistical significance (p > 0.05). Conclusion: These results indicate that DTX exposure may not be affected by EPR treatment at the dose level used in this study, suggesting that oral EPR can be used safely when taken with intravenously injected DTX. However, further studies under the stringent conditions are needed when chronic treatment of EPR and anticancer drug.


2014 ◽  
Vol 116 (10) ◽  
pp. 1308-1314 ◽  
Author(s):  
Toru Kawada ◽  
Meihua Li ◽  
Can Zheng ◽  
Shuji Shimizu ◽  
Kazunori Uemura ◽  
...  

We tested whether 6-wk vagal stimulation (VS) treatment improved open-loop baroreflex function in rats after myocardial infarction (MI). The following three groups of Sprague-Dawley rats were examined: normal control (NC, n = 9), MI with no treatment (MI-NT, n = 8), and MI treated with VS (MI-VS, n = 7). Under anesthesia, a stepwise input ranging from 60 to 180 mmHg was imposed on isolated carotid sinus baroreceptor regions, while the responses in splanchnic sympathetic nerve activity (SNA) and arterial pressure (AP) were measured. The response range of percent SNA was greater in the MI-VS than in the MI-NT group (63.8 ± 4.9% vs. 33.1 ± 3.8%, P < 0.01). The slope of the AP response to percent SNA was not different between the MI-VS and MI-NT groups (0.611 ± 0.076 vs. 0.781 ± 0.057 mmHg/%). The difference in the response range of AP between the MI-VS and MI-NT groups did not reach statistical significance (40.7 ± 6.2 vs. 26.4 ± 3.5 mmHg). In conclusion, the 6-wk VS treatment significantly improved the baroreflex control of SNA, but the effect was limited for the baroreflex total-loop function due to the lack of significant improvement in the AP response to percent SNA.


2005 ◽  
Vol 22 (4) ◽  
pp. 501-507 ◽  
Author(s):  
JOHN WELLARD ◽  
DONALD LEE ◽  
KRISZTINA VALTER ◽  
JONATHAN STONE

The current study aims to assess the vulnerability of photoreceptors in rat retina to variations in tissue oxygen levels. Young adult Sprague-Dawley rats were exposed to air with the concentration of oxygen set at 10% (hypoxia), 21% (room air, normoxia), and four levels of hyperoxia (45%, 65%, 70%, and 75%), for up to 3 weeks. Their retinas were then examined for cell death, using the TUNEL technique. Hypoxia (10% oxygen) for 2 weeks caused a limited but significant rise in the frequency of TUNEL+ (dying) cells in the retina, the great majority (> 90%) being located in the outer nuclear layer (ONL). Hyperoxia also induced an increase in the frequency of TUNEL+ cells, again predominantly in the ONL. The increase rose with duration of exposure, up to 2 weeks. At 2 weeks exposure, the increase was limited yet significant at 45% oxygen, and maximal at 65%. Where the frequencies of TUNEL+ cells were high, it was evident that photoreceptor death was maximal in the midperipheral retina. The adult retina is vulnerable to maintained shifts in oxygen availability to the retina, both below and above normal. The vulnerability is specific to photoreceptors; other retinal neurons appeared resistant to the exposures tested. Shifts in retinal oxygen levels caused by variations in ambient light, by the persistence of light through the normally dark (night) half of the day–night cycle, or by depletion of the photoreceptor population, may contribute to photoreceptor death in the normal retina.


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