Role of catecholamines in regulating ovine median eminence blood flow

1990 ◽  
Vol 258 (5) ◽  
pp. R1242-R1249
Author(s):  
R. B. Page ◽  
M. Gropper ◽  
E. Woodard ◽  
J. Townsend ◽  
S. Davis ◽  
...  
Keyword(s):  
Blood Flow ◽  
Choroid Plexus ◽  
Median Eminence ◽  
Serum Prolactin ◽  
Dopamine Antagonist ◽  
Drug Infusion ◽  
Neural Lobe ◽  
Dopamine Infusion ◽  
D2 Agonist ◽  
Before And After

Blood flow was measured in the ovine median eminence and neural lobe before and after the intravenous infusion of dopamine (n = 7), the D1 agonist SKF 38393 (n = 4), the D2 agonist bromocriptine (n = 4), and the dopamine antagonist haloperidol (n = 5). It was also measured before and after the intracarotid infusion of dopamine into eight naive sheep and seven sheep pretreated with phenoxybenzamine. Radiolabeled microspheres were used to determine regional cerebral and regional neurohypophysial blood flows (RNHBF) in these 35 adult female sheep anesthetized with pentobarbital sodium. Samples for serum prolactin measurement by radioimmunoassay were obtained before and after drug infusion. Intravenous dopamine infusion did not change median eminence or neural lobe blood flow (RNHBF) but increased renal and choroid plexus blood flow. Intravenous haloperidol caused a significant fall in RNHBF and blood flow in choroid plexus, caudate nucleus, and kidneys. Intracarotid dopamine infusion decreased RNHBF but increased choroid plexus blood flow. RNHBF was significantly greater in the seven sheep pretreated with phenoxybenzamine than in the eight naive sheep. These findings do not support a role for dopamine in the regulation of median eminence blood flow. The last observation does add support to the hypothesis that norepinephrine or epinephrine interaction with alpha-receptors plays a role in the control of ovine median eminence blood flow and hence in the regulation of delivery of humoral messages from the brain to the anterior pituitary gland.

The effects of dopaminergic blockade on serum TSH and prolactin levels in thyrotoxicosis

1984 ◽  
Vol 106 (3) ◽  
pp. 330-335 ◽  
Author(s):  
S. Swart ◽  
B. P. O'Malley ◽  
J. Vora ◽  
D. B. Barnett ◽  
F. D. Rosenthal
Keyword(s):  
Significant Decline ◽  
Serum Prolactin ◽  
Control Group ◽  
Dopamine Antagonist ◽  
Serum Samples ◽  
Before And After ◽  
Dopaminergic Tone ◽  
Long Acting ◽  
Serum Tsh ◽  
Tsh Levels

Abstract. In the first part of this study, we have demonstrated that, in 7 patients with untreated thyrotoxicosis, a 7 day regime of the long acting dopamine antagonist metoclopramide (10 mg orally 8 hourly) produces more adequate dopaminergic blockade at pituitary level than a single oral 10 mg dose of the compound as assessed by serum prolactin responses. Subsequently, we have employed this protracted oral metoclopramide regime to evaluate the contribution of dopaminergic tone to the abnormal TSH and prolactin responsiveness of thyrotoxicosis. Serum TSH and prolactin responses to iv TRH (200 μg) were measured in 10 untreated thyrotoxic patients before and after a 7 day period of metoclopramide 10 mg orally 8 hourly. Ten euthyroid individuals were studied in similar fashion, their serum samples being analysed for prolactin levels alone, thus providing a control group for prolactin responsiveness to TRH, before and after metoclopramide. In the thyrotoxic patients basal TSH levels did not change as a consequence of metoclopramide therapy and the TSH response to TRH remained flat. Basal prolactin levels were similar in thyrotoxic and euthyroid individuals and the increase in prolactin, seen in both groups after metoclopramide, was smaller in the thyrotoxic group than in the euthyroid group. Prolactin responsiveness to TRH was significantly impaired in the thyrotoxic subjects as compared to euthyroid subjects. After metoclopramide there was a significant decline in prolactin responsiveness in the euthyroid group, and a similar, though insignificant, trend in the thyrotoxic patients. We conclude that in thyrotoxicosis dopaminergic tone plays no major part in the suppression of TSH levels, nor in the impaired prolactin responsiveness to TRH.

Regional neurohypophyseal blood flow and its control in adult sheep

1981 ◽  
Vol 241 (1) ◽  
pp. R36-R43 ◽  
Author(s):  
R. B. Page ◽  
D. J. Funsch ◽  
R. W. Brennan ◽  
M. J. Hernandez
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
White Matter ◽  
Arterial Blood Pressure ◽  
Median Eminence ◽  
Vascular System ◽  
Neural Lobe ◽  
Adult Sheep ◽  
Blood Flows ◽  
Arterial Blood

Regional neurohypophyseal and cerebral blood flows were measured by the radiolabeled microsphere technique in 30 adult sheep under light barbiturate anesthesia. Regional blood flows were determined under basal conditions. The responses of regional blood flow to alterations in arterial PCO2 and to changes in arterial blood pressure wee also determined. In addition, the relationship between regional neurohypophyseal blood flow and neurosecretory activity as judged by plasma arginine vasopressin levels was assessed. Under basal conditions median eminence blood flow averaged 461 ml.100 g-1.min-1 and did not significantly differ from neural lobe blood flow (436 ml.100 g-1.min-1). Blood flow in the neurohypophysis was about 8 times cortical and 16 times white matter blood flow in these animals. Median eminence and neural lobe blood flow proportionately increased far less than regional cortical or white matter blood flow under conditions of hypercarbia. With alteration of arterial blood pressure, regional neurohypophyseal blood flow remained constant beyond the limits of cerebral autoregulation. The neurohypophysis demonstrates a degree of blood flow homeostasis that exceeds that of any other brain area studied. Although the neurohypophysis is a diverticulum of the brain, its vascular system forms a unique functional as well as a unique anatomic unit.

Dopaminergic regulation of 18-hydroxycorticosterone and aldosterone secretion in man

1983 ◽  
Vol 102 (2) ◽  
pp. 258-264 ◽  
Author(s):  
James R. Sowers ◽  
Frances W. J. Beck
Keyword(s):  
Circadian Rhythm ◽  
Plasma Renin ◽  
Serum Prolactin ◽  
Dopamine Antagonist ◽  
Aldosterone Secretion ◽  
Dopamine Infusion ◽  
Dopaminergic Mechanisms ◽  
Normal Males ◽  
Dopaminergic Regulation ◽  
Corticosteroid Secretion

Abstract. This study was designed to investigate dopaminergic mechanisms involved in the control of corticosteroid secretion. Plasma renin activity (PRA), prolactin, cortisol, corticosterone, 11-deoxycorticosterone, 18-hydroxycorticosterone (18-OHB) and aldosterone responses to metoclopramide 10 mg iv in the presence of a vehicle or dopamine (3 μg/kg/min) infusions, or domperidone 10 mg iv were evaluated in 10 normal males. Metoclopramide, and the peripheral dopamine antagonist, domperidone both resulted in rises in serum prolactin levels. Metoclopramide, but not domperidone, resulted in parallel rises in plasma 18-OHB and aldosterone levels. Dopamine infusion markedly inhibited prolactin, 18-OHB and aldosterone responses to the central and peripheral dopamine antagonist metoclopramide. Administration of the dopamine agonist, bromocriptine, 2.5 mg three times a day for 4 days suppressed (P < 0.01) mean 24 h plasma 18-OHB levels from 22.1 ± 2.1 to 15.8 ± 1.5 ng/dl. These results suggest that dopaminergic mechanisms modulate the secretion of 18-OHB and aldosterone. The circadian rhythm of 18-OHB secretion is not dependent on dopaminergic mechanisms.

Portal vascular route from hypophysial stalk/neural lobe to adenohypophysis

1980 ◽  
Vol 239 (5) ◽  
pp. R463-R469 ◽  
Author(s):  
A. J. Baertschi
Keyword(s):  
Blood Flow ◽  
Median Eminence ◽  
General Circulation ◽  
Circulatory Arrest ◽  
Constant Current ◽  
Extracellular Potassium ◽  
Neural Lobe ◽  
Capillary Networks ◽  
Anterior Dorsal ◽  
Current Spread

Adenohypophysis, neural lobe, stalk, and median eminence are interconnected by capillary networks and portal vessels, but the directions of blood flow are not clearly understood. To test the hypothesis that peptides released from the hypothalamohypophysial tract (HHT) may reach the adenohypophysis, the HHT of anesthetized rats were stimulated electrically with 5-s trains of constant current (400 microA) biphasic impulses (0.2-1 ms) at 30 Hz, and extracellular potassium activity was recorded in various parts of the hypothalamohypophysial complex with microelectrodes (2- to 4-micrometer tip). Within HHT and neural lobe, K+ increased without delay (within 30 ms) from 2.20 +/- 0.25 (meq/l, mean +/- SE) and 2.65 +/- 0.40 to 4.50 +/- 0.60 and 7.60 +/- 0.85, respectively. Within the anterior dorsal regions of the adenohypophysis (AAH), K+ increased from 3.00 +/- 0.25 to 5.05 +/- 0.35, but with a delay of 1-4 s. Within the posterior regions of the dorsal adenohypophysis, the increase was barely significant (P < 0.1) and was delayed by 4-10 s. K+ responses in AAH to nicotine and HHT stimulation were abolished by circulatory arrest; thus K+ responses were not due to current spread or passive diffusion. Coagulation of long portal vessels did not diminish K+ responses in AHH. Results suggest that peptides released from HHT are not only secreted into the general circulation, but may reach the adenohypophysis through a portal vascular route.

Regional neurohypophysial and hypothalamic blood flow in rats during hypercapnia

1988 ◽  
Vol 255 (2) ◽  
pp. R295-R302
Author(s):  
R. M. Bryan ◽  
C. L. Myers ◽  
R. B. Page
Keyword(s):  
Blood Flow ◽  
Paraventricular Nucleus ◽  
Median Eminence ◽  
Adrenergic Receptors ◽  
Supraoptic Nucleus ◽  
Regional Cerebral Blood ◽  
Neural Lobe ◽  
Arterial Pco2 ◽  
Alpha Adrenergic Receptors ◽  
Fractional Concentration

Regional cerebral blood flow (rCBF) was measured in the neurohypophysis and hypothalamus in normocapnic and hypercapnic rats using [14C]isopropyliodoamphetamine. Rats were surgically prepared using nitrous oxide and halothane and placed in plaster restraining casts. Hypercapnia was produced by increasing the fractional concentration of inspired CO2 (FICO2). rCBF in normocapnic rats was higher in the paraventricular nucleus, supraoptic nucleus, median eminence, and neural lobe than rates previously measured by use of diffusible tracers. During hypercapnia blood flow increased linearly with arterial PCO2 (PACO2) in all regions except the median eminence and neural lobe, which were not affected by hypercapnia. When rats were pretreated with phentolamine (1 mg/kg) to block the alpha-adrenergic receptors, blood flow in the median eminence and neural lobe increased significantly during hypercapnia. We conclude that blood flow in the cell bodies of the paraventricular nucleus and supraoptic nucleus is regulated differently during hypercapnia than blood flow in the nerve terminals in the median eminence and neural lobe. Furthermore, vasodilation produced by increased CO2 is offset by alpha-receptor stimulation in the median eminence and neural lobe.

133Xe-DSPECT: Normalwerte von zerebraler Ruhedurchblutung und Reservekapazität

1987 ◽  
Vol 26 (05) ◽  
pp. 192-197 ◽  
Author(s):  
T. Kreisig ◽  
P. Schmiedek ◽  
G. Leinsinger ◽  
K. Einhäupl ◽  
E. Moser
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Correlation Coefficient ◽  
Regional Cerebral Blood Flow ◽  
Regression Line ◽  
Reserve Capacity ◽  
Regional Cerebral Blood ◽  
Quantitative Measurements ◽  
Before And After

Using the 133Xe-DSPECT technique, quantitative measurements of regional cerebral blood flow (rCBF) were performed before and after provocation with acetazolamide (Diamox) i. v. in 32 patients without evidence of brain disease (normals). In 6 cases, additional studies were carried out to establish the time of maximal rCBF increase which was found to be approximately 15 min p. i. 1 g of Diamox increases the rCBF from 58 ±8 at rest to 73±5 ml/100 g/min. A Diamox dose of 2 g (9 cases) causes no further rCBF increase. After plotting the rCBF before provocation (rCBFR) and the Diamox-induced rCBF increase (reserve capacity, Δ rCBF) the regression line was Δ rCBF = −0,6 x rCBFR +50 (correlation coefficient: r = −0,77). In normals with relatively low rCBF values at rest, Diamox increases the reserve capacity much more than in normals with high rCBF values before provocation. It can be expected that this concept of measuring rCBF at rest and the reserve capacity will increase the sensitivity of distinguishing patients with reversible cerebrovascular disease (even bilateral) from normals.

Pituitary responses to a dopamine antagonist at different times of the day in normal women

1982 ◽  
Vol 100 (4) ◽  
pp. 481-485 ◽  
Author(s):  
F. R. Pérez-López ◽  
C. M. González-Moreno ◽  
M. D. Abós ◽  
J. A. Andonegui ◽  
R. H. Corvo
Keyword(s):  
Serum Prolactin ◽  
Dopamine Antagonist ◽  
Hormonal Changes ◽  
Healthy Women ◽  
Serum Lh ◽  
Normal Women ◽  
The Times ◽  
Serum Tsh

Abstract. In order to determine whether or not pituitary responsiveness to the dopaminergic antagonist clebopride changes during the nyctohemeral cycle, 10 healthy women with regular cycles were given 1 mg of clebopride orally at 09.00 h and 24.00 h with at least a 5 day interval between each test. In addition, 5 of the women were given a placebo instead of clebopride at midnight to evaluate the spontaneous hormonal changes. During the 24.00 h test the women had significantly higher P < 0.05) mean TSH basal levels. Serum prolactin (Prl) increased significantly (P < 0.001) after clebopride administration while these changes did not occur when placebo was used instead of clebopride at midnight. The Prl response to clebopride was qualitatively similar at 09.00 h and at 24.00 h. Clebopride given at midnight induced a significant increase (P < 0.05) in serum TSH while this change did not occur when the drug was given at 09.00 h or when placebo was given at midnight. The administration of clebopride resulted in no discernible alterations in serum LH, FSH or GH in either the 09.00 h or the 24.00 h tests. Thus, Prl responses to clebopride were similar in the morning and at midnight, TSH significantly increased after clebopride at midnight whereas this did not occur when the drug was given in the morning, and no significant changes were induced in LH, FSH or GH at the times studied.

Blood pressure, heart rate, and adrenal catecholamines prior to ventricular fibrillation

1961 ◽  
Vol 201 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Noel M. Bass ◽  
Vincent V. Glaviano
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Ventricular Fibrillation ◽  
Coronary Occlusion ◽  
Marked Decrease ◽  
Mean Blood Pressure ◽  
Plasma Adrenaline ◽  
Acute Coronary Occlusion ◽  
Before And After

Heart rate, mean blood pressure, adrenal blood flow, and adrenal plasma adrenaline and noradrenaline were compared before and after ligation of the anterior descending coronary artery in dogs anesthetized with chloralose. One group of 12 dogs responded to acute coronary occlusion with a sudden and marked decrease in mean blood pressure (mean, 31%) and heart rate (mean, 18%) followed by an early onset (mean, 227 sec) of ventricular fibrillation. Another group of nine dogs responded with slight decreases in mean blood pressure (mean, 13%) and heart rate (mean, 5%), during which time ventricular fibrillation occurred late (mean, 30 min) or not at all. While the two groups were statistically different in mean blood pressure and heart rate, the minute output of adrenal catecholamines in either group was not found to be related to the early or late occurrence of ventricular fibrillation.

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