Effect of acute administration of ethanol on beta-endorphin plasma level in ethanol preferring and non-preferring rats chronically treated with naltrexone

2006 ◽  
Vol 85 (1) ◽  
pp. 155-159 ◽  
Author(s):  
J ZALEWSKAKASZUBSKA ◽  
D GORSKA ◽  
W DYR ◽  
E CZARNECKA
Keyword(s):  
Plasma Level ◽  
Acute Administration ◽  
Beta Endorphin

Abnormal beta-endorphin and beta-lipotropin responses to TRH and LRH administration in primary and secondary affective disorders

1986 ◽  
Vol 112 (4) ◽  
pp. 481-486 ◽  
Author(s):  
E. Brambilla ◽  
F. Petraglia ◽  
F. Facchinetti ◽  
A. R. Genazzani
Keyword(s):  
Plasma Levels ◽  
Affective Disorders ◽  
Anterior Pituitary ◽  
Pituitary Hormone ◽  
Acute Administration ◽  
Beta Endorphin ◽  
Anterior Pituitary Hormone ◽  
Saline Administration ◽  
Hormone Responses ◽  
Primary Affective Disorders

Abstract. Anomalous anterior pituitary hormone responses to acute administration of TRH and LRH have previously been observed in patients with primary affective disorders (PAD), with TRH eliciting GH, FSH and LH rises, and LRH eliciting GH and Prl rises. We examined whether the same unusual responses were present also for beta-endorphin (β-EP) and beta-lipotropin (β-LPH) in 15 PAD patients, in 9 patients with secondary affective disorders (SAD), and in 7 controls. TRH (500 ug iv) elicited rises of β-EP plasma levels in 5 PAD and 2 SAD patients, and of β-LPH in 4 PAD and 3 SAD patients. LRH (150 ug iv) elicited rises of plasma β-EP levels in 2 PAD and 2 SAD patients, and of β-LPH in 5 PAD and 2 SAD patients. No rises of β-EP and β-LPH plasma levels were observed in PAD patients after saline administration, nor in the controls after TRH, LRH or saline administration.

Lack of Beta-Endorphin Plasma Level Rise in Oxytocin-Induced Labor

1985 ◽  
Vol 19 (3) ◽  
pp. 130-134 ◽  
Author(s):  
Andrea R. Genazzani ◽  
Felice Petraglia ◽  
Fabio Facchinetti ◽  
Paolo A. Galli ◽  
Annibale Volpe
Keyword(s):  
Plasma Level ◽  
Induced Labor ◽  
Beta Endorphin

Plasma and tissue kallikrein–kinin systems during acute administration of frusemide in normotensive and hypertensive humans

1991 ◽  
Vol 81 (3) ◽  
pp. 305-311 ◽  
Author(s):  
K. Peter Öhman ◽  
Bengt E. Karlberg
Keyword(s):  
Plasma Level ◽  
Urine Volume ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Primary Hypertension ◽  
Plasma Kallikrein ◽  
Acute Administration ◽  
Tissue Kallikrein ◽  
Kinin System ◽  
Hypertensive Patients

1. This study aims to further elucidate the role of the tissue and plasma kallikrein-kinin systems in blood pressure, electrolyte and volume homoeostasis. Components thereof and of the renin-angiotensin-aldosterone system were measured in conjunction with frusemide administration, in normotensive subjects and in patients with primary hypertension. 2. Frusemide increased plasma pre-kallikrein, angiotensin II and aldosterone concentrations and plasma renin activity, whereas the plasma level of tissue kallikrein remained unchanged. Basal values and the induced changes were similar in both groups. 3. Frusemide increased the urine volume and the excretion of Na+, K+, Mg2+, Cl−, aldosterone, prostaglandin E2 and tissue kallikrein. These changes were similar in both groups, but the total tissue kallikrein excretion was significantly lower in the hypertensive patients. Excretion of electrolytes and hormones was also measured during three 24 h urine collection periods and did not differ between the two groups. 4. Thus, acute administration of frusemide to hypertensive patients and normal subjects increased the plasma level of pre-kallikrein, possibly indicating less activation to kallikrein and subsequently less kinin generation in the blood stream. This also suggests a role for the plasma kallikrein-kinin system in the regulation of vascular tone and blood volume. Circulating tissue kallikrein does not seem to be acutely involved. 5. Urinary excretion of kallikrein is reduced in patients with primary hypertension after the administration of frusemide, apparently without affecting the renal excretory response.

scholarly journals Effect of repeated treatment with topiramate on voluntary alcohol intake and beta-endorphin plasma level in Warsaw alcohol high-preferring rats

2012 ◽  
Vol 225 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Jadwiga Zalewska-Kaszubska ◽  
Bartosz Bajer ◽  
Dorota Gorska ◽  
Dariusz Andrzejczak ◽  
Wanda Dyr ◽  
...  
Keyword(s):  
Plasma Level ◽  
Alcohol Intake ◽  
Repeated Treatment ◽  
Beta Endorphin

Comparison of renal excretion of rubidium and potassium

1959 ◽  
Vol 197 (6) ◽  
pp. 1297-1302 ◽  
Author(s):  
Arthur S. Kunin ◽  
Earl H. Dearborn ◽  
Belton A. Burrows ◽  
Arnold S. Relman
Keyword(s):  
Glomerular Filtration Rate ◽  
Plasma Level ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Excretion ◽  
Acute Administration ◽  
Rubidium Chloride ◽  
Anesthetized Dogs ◽  
Renal Clearances

The simultaneous renal clearances of rubidium and potassium were studied during the infusion of solutions of rubidium chloride into intact anesthetized dogs. The effects of prior loading with potassium were studied, as were also the responses to acute administration of acetazoleamide and meralluride. It was observed that the clearance of rubidium was usually slightly less than that of potassium and tended under most circumstances to vary in parallel with it. During infusion of RbCl the clearance of rubidium was usually less than the glomerular filtration rate and was independent of plasma level when the latter was varied from 1.0 to 5.0 mEq/l. However, net secretion of rubidium, as well as of potassium, could be demonstrated during periods of reduced filtration rate following administration of acetazoleamide. In the present experiments there was no evidence of interionic competition, but this possibility has not been critically tested. It is concluded that rubidium and potassium are probably handled by similar, if not identical, tubular mechanisms. The secretion of rubidium appears to be slower than that of potassium.

Central alpha-activation by clonidine reduces plasma level of beta-endorphin in patients with essential hypertension

Life Sciences ◽  
1985 ◽  
Vol 37 (16) ◽  
pp. 1461-1467 ◽  
Author(s):  
K. Yasunari ◽  
Y. Kanayama ◽  
M. Kohno ◽  
K. Murakawa ◽  
T. Kawarabayashi ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Plasma Level ◽  
Beta Endorphin

Acute administration of tumour necrosis factor-α or interleukin-1-α does not mimic the hypoketonaemia associated with sepsis and inflammatory stress in the rat

1992 ◽  
Vol 82 (2) ◽  
pp. 205-209 ◽  
Author(s):  
Rhys D. Evans ◽  
Vera Ilic ◽  
Dermot H. Williamson
Keyword(s):  
Plasma Level ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Ketone Bodies ◽  
Interleukin 1 ◽  
Acute Administration ◽  
Tumour Necrosis Factor Α ◽  
Glycerol Level ◽  
Factor Α ◽  
Necrosis Factor

1. Administration of tumour necrosis factor (cachectin) and of interleukin-1-α increased the plasma level of non-esterified fatty acids in fed rats, and in the case of interleukin-1-α the blood glycerol level was also increased, suggesting stimulation of adipose tissue lipolysis. There were parallel increases in the plasma level of triacylglycerols. Neither cytokine had significant effects on blood or liver total ketone body (acetoacetate plus 3-hydroxybutyrate) concentrations. 2. In starved rats, the higher plasma non-esterified fatty acid concentration was not increased further by the cytokines. The plasma triacylglycerol level was increased, although the absolute change was less than in fed rats. The ketonaemia associated with starvation tended to be increased by the cytokines, but this was only significant in the case of interleukin-1-α. Parallel changes occurred in hepatic ketone bodies. 3. It is concluded that tumour necrosis factor-α and interleukin-1-α are not responsible for the hypoketonaemia associated with sepsis or other inflammatory states.

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