On the role of dopamine receptors in the central regulation of human TSH

1981 ◽  
Vol 98 (4) ◽  
pp. 521-527 ◽  
Author(s):  
G. Delitala ◽  
L. Devilla ◽  
A. Canessa ◽  
F. D'Asta
Keyword(s):  
Dopamine Receptors ◽  
Blood Brain Barrier ◽  
Median Eminence ◽  
Normal Subjects ◽  
Acute Administration ◽  
Central Regulation ◽  
Before And After ◽  
Tsh Secretion ◽  
Substituted Benzamides

Abstract. The effects of acute administration of haloperidol (4 mg im) and pimozide (4 mg orally) on TSH and Prl secretion were studied in normal and hypothyroid man. The TRH-induced TSH secretion before and after pre-medication with pimozide and domperidone, a peripheral dopamine (DA) blocker, was also evaluated in a group of normal subjects. Haloperidol and pimozide induced a marked increment in serum Prl; mean Prl levels were still significantly elevated 12 h following pimozide administration. A small but significant TSH increase was observed following haloperidol and pimozide in normal as well as hypothyroid subjects. Both domperidone and pimozide significantly enhanced TRH-induced TSH release. In another experiment 3 women with primary thyroid failure received an infusion of DA (4 (μg/kg/min for 4 h) with and without domperidone administration. TSH and Prl levels were suppressed by DA, but the effect was completely abolished by domperidone. The results suggest that psychotrophic drugs, such as haloperidol and pimozide, can, like substituted benzamides, stimulate TSH release in man. Since domperidone and DA do not cross the blood-brain-barrier and domperidone significantly enhanced the TSH response to TRH, the data also support the hypothesis that human TSH is regulated by DA at the hypothalamus (median eminence) and/or pituitary level.

Pressor responses to norepinephrine in humans before and after corticosteroids

1962 ◽  
Vol 203 (5) ◽  
pp. 961-963 ◽  
Author(s):  
Mohinder P. Sambhi ◽  
Max H. Weil ◽  
Vasant N. Udhoji
Keyword(s):  
Human Subject ◽  
Normal Subjects ◽  
Adrenal Function ◽  
Variance Analysis ◽  
Acute Administration ◽  
Intravenous Injections ◽  
Pressor Responses ◽  
Before And After

Pressor responses produced by intravenous injections of graded doses of norepinephrine were recorded in ten normal subjects before and after pharmacologic doses of glucocorticoids. Two subjects had been pretreated with 9α-fluorocortisol. Although a considerable variation was found in the responsiveness to repeated norepinephrine injections, variance analysis demonstrated that administration of adrenal cortical hormones and their analogues did not significantly alter the response. These observations do not support the hypothesis that acute administration of corticosteroids in large doses potentiates the pressor effects of catecholamines in the human subject with normal adrenal function.

Aminophylline and human diaphragm strength in vivo

1990 ◽  
Vol 68 (6) ◽  
pp. 2591-2596 ◽  
Author(s):  
R. D. Levy ◽  
S. Nava ◽  
L. Gibbons ◽  
F. Bellemare
Keyword(s):  
Motor Units ◽  
Normal Subjects ◽  
Acute Administration ◽  
Transdiaphragmatic Pressure ◽  
Gastric Pressure ◽  
Significant Difference ◽  
Before And After ◽  
Normal Human ◽  
Twitch Characteristics

The transdiaphragmatic pressure (Pdi) twitch response to single shocks from supramaximal bilateral phrenic nerve stimulation was studied before and after acute intravenous infusions of aminophylline [14.9 +/- 3.1 (SD) micrograms/ml] in nine normal subjects. Stimulation was performed with subjects in the sitting position against an occluded airway from end expiration. Baseline gastric pressure and abdominal and rib cage configuration were kept constant. There was no significant difference in peak twitch Pdi from the relaxed diaphragm between control (38.8 +/- 3.3 cmH2O) and aminophylline (40.2 +/- 5.2 cmH2O) experiments. Other twitch characteristics including contraction time, half-relaxation time, and maximum relaxation rate were also unchanged. The Pdi-twitch amplitude at different levels of voluntary Pdi was measured with the twitch occlusion technique, and this relationship was found to be similar under control conditions and after aminophylline. With this technique, maximum Pdi (Pdimax) was calculated as the Pdi at which stimulation would result in no Pdi twitch because all motor units are already maximally activated. No significant change was found in mean calculated Pdimax between control (146.9 +/- 27.0 cmH2O) and aminophylline (149.2 +/- 26.0 cmH2O) experiments. We conclude from this study that the acute administration of aminophylline at therapeutic concentrations does not significantly affect contractility or maximum strength of the normal human diaphragm in vivo.

Cholinergic modulation of GH secretion in acromegalic patients before and after pituitary surgery

1992 ◽  
Vol 127 (6) ◽  
pp. 489-493 ◽  
Author(s):  
Leon Fiszlejder ◽  
Olga Penacini ◽  
Susana Ratz ◽  
Adriana Oneto ◽  
Maria Storani ◽  
...  
Keyword(s):  
Area Under The Curve ◽  
Pituitary Surgery ◽  
Normal Subjects ◽  
Physiological Control ◽  
Gh Secretion ◽  
Pathophysiological Role ◽  
Before And After ◽  
Transsphenoidal Adenomectomy ◽  
Ghrh Test

Cholinergic neurotransmission exerts a physiological control on GH secretion. Pirenzepine (Pz), an antagonist of muscarinic receptors, by enhancing hypothalamic somatostatin release, inhibits stimulated GH secretion in normal subjects but not in acromegalic patients. To address the hypothesis that a feedback effect of GH hypersecretion can be involved in this condition, GH responses to GHRH 1–29, 1 μg/kg iv, with and without administration of Pz, 40mg iv before tests, were investigated in eight acromegalic patients, before and 20–30 days after transsphenoidal adenomectomy. Pz diminished (p<0.001) the incremental area under the curve (AUC) of GH responses to GHRH in seven normal controls. In contrast, GHRH responsiveness in untreated acromegalic patients was not affected by Pz. Postoperative basal GH levels decreased by 62.4±14.9% (p<0.01). Pz inhibited GH responses to GHRH (p<0.01). Furthermore, a direct relationship (r = 0.73, p<0.01) between basal concentrations and the AUC of GH responses following Pz plus GHRH-test was found. The finding that muscarinic receptor activity recovered after the reduction of serum GH basal levels by pituitary surgery lends support to the proposed pathophysiological role of GH excess as a possible determinant factor in cholinergicsomatostatinergic dysfunction in acromegaly.

ABNORMAL URINARY ANDROSTERONE/ETIOCHOLANOLONE RATIO IN HYPOTHALAMIC DISTURBANCES IN MAN

1968 ◽  
Vol 57 (4) ◽  
pp. 595-614 ◽  
Author(s):  
Svend G. Johnsen
Keyword(s):  
Considerable Increase ◽  
Testosterone Propionate ◽  
Normal Subjects ◽  
Gonadal Development ◽  
Endocrine Disorders ◽  
Central Regulation ◽  
Hormone Production ◽  
Androgen Metabolism ◽  
Before And After

ABSTRACT The urinary androsterone/etiocholanolone (A/E) ratio was determined in 233 normal subjects. Compared with these, a group of 28 cases of adiposo-genital dystrophy (a.-g. d.) in boys and men showed a very considerable increase in the A/E ratio. It is shown by analyses in 23 cases of primary testicular failure and male castration and in 17 cases of exogenous obesity that this change in a.-g. d. is not secondary to the main symptoms, i. e. obesity and hypogonadism; neither can it be explained on a thyroid basis. Studies of 2362 fractionated 17-KS-determinations performed in all kinds of endocrine disorders showed that an elevated A/E ratio is found in certain conditions all of which are of hypothalamic origin. Furthermore it was found that an elevated A/E ratio was present in verified organic damage of the hypothalamus. In a number of a.-g. d. cases the A/E ratio was followed up to 10 years through the puberal age. Usually the ratio remained unaffected by the great puberal rise in the excretion of A and E. In contrast to the others some patients showed a fall in the ratio during puberty and these usually showed satisfactory gonadal development. Determination of the A/E ratio before and after the administration of a large dose of testosterone propionate was done in 23 cases of hypothalamic dysfunction and in 22 other cases. The abnormal A/E ratios in hypothalamic cases were reproduced during the metabolism of exogenous testosterone, which shows that the abnormal ratios originate from an abnormal androgen metabolism and not from abnormal hormone production. The findings indicate that there is, in man, a central regulation of androgen metabolism in which the hypothalamus is involved. The diagnostic, pathogenetic and theoretical implications of the findings are discussed.

Lowering of serum T3 and rise in reverse T3 induced by glucagon infusion in anaesthetized dogs

1987 ◽  
Vol 116 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Udaya M. Kabadi ◽  
Lester Dragstedt
Keyword(s):  
Normal Saline ◽  
Normal Subjects ◽  
Reverse T3 ◽  
Significant Fall ◽  
Before And After ◽  
Serum T3 ◽  
Saline Administration ◽  
Glucagon Injection ◽  
Control Study

Abstract. We recently demonstrated that lowering of T3 and a rise in rT3 observed in non-thyroidal illnesses could be induced by glucagon infusion in normal subjects without altering T4, Free T4 (FT4) and T3 resin uptake (T3RU) values suggesting that altered T4 metabolism may be mainly responsible for those changes. To further assess the role of altered T4 metabolism in these changes during induction of hyperglucagonaemia, we studied glucose, T4, FT4, T3RU, T3, and rT3 concentrations before and after iv glucagon injection (0.5 mg) for up to 3 h in 6 anaesthetized dogs, since thyroxinebinding globulin (TBG) concentration is known to be extremely low in dogs. A control study was conducted with iv normal saline (0.5 ml) injection. T4, FT4 and T3RU remained unchanged during both studies. A significant fall was noted in T3 with glucagon (ΔT3, 0.23 ± 0.06 nmol/l vs 0 ± 0.03 nmol/l with normal saline; P < 0.01). rT3 rose markedly following glucagon infusion (ΔrT3, 0.04 ± 0.011 nmol/l vs −0.017 ± 0.006 nmol/l with normal saline; P < 0.01). Moreover, areas under the curves for T3 and rT3 were markedly increased during glucagon infusion when compared to saline administration (P < 0.01 for both comparisons). Therefore, this study suggests that changes in T3 and rT3 concentrations observed in non-thyroidal illnesses may be attributed to hyperglucagonaemia and may be secondary to altered T4 metabolism as reflected by lowered T3/T4 and increased rT3/T4 ratio.

Ratio of Inhibited-to-Activated Pallidal Neurons Decreases Dramatically During Passive Limb Movement in the MPTP-Treated Monkey

2000 ◽  
Vol 83 (3) ◽  
pp. 1760-1763 ◽  
Author(s):  
T. Boraud ◽  
E. Bezard ◽  
B. Bioulac ◽  
C. E. Gross
Keyword(s):  
Macaca Fascicularis ◽  
Normal Animal ◽  
Normal Subjects ◽  
Neuronal Population ◽  
Limb Movement ◽  
Medial Part ◽  
Before And After ◽  
Drug Naïve ◽  
State 1

Mink advanced the hypothesis in 1996 that the role of the basal ganglia (BG) is primarily one of focused selection; the encouragement of motor mechanisms inducing a desired movement and the inhibition of competing mechanisms. This would imply, in normal subjects, a ratio of inhibited-to-activated (I/A) movement-related globus pallidus pars internalis (GPi) neurons <1 and a drastic decrease of this ratio in the parkinsonian state. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication should therefore decrease the specificity of the response of this neuronal population. To test this working hypothesis we studied the activity of GPi neurons in response to passive limb movement in the normal and the parkinsonian monkey. Extracellular unit recordings monitored any correlation between passive limb movements and eventual modifications of the neuronal activity of the GPi in two calm, awake, and drug naive monkeys ( Macaca fascicularis) before and after MPTP intoxication. In the normal animal, arm- and leg-related neurons were located in clusters in the medial part of the GPi. The I/A ratio was 0.22. Most GPi cells were linked to a single joint. In the MPTP-treated monkey, the number of movement-related neurons increased, the I/A ratio dropped significantly to 0.03, and most responding cells were linked to several joints. These data, which cannot be explained by the classic “box” model, endorse Mink's hypothesis.

Interaction of captopril and ibuprofen on glomerular and tubular function in humans

1990 ◽  
Vol 259 (2) ◽  
pp. F233-F238
Author(s):  
M. Allon ◽  
C. B. Pasque ◽  
M. Rodriguez
Keyword(s):  
Renal Plasma Flow ◽  
Urine Volume ◽  
Normal Subjects ◽  
Acute Administration ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Water Handling ◽  
Patients With Heart Failure ◽  
Before And After ◽  
Opposing Effects

Renal hemodynamics and tubular solute and water handling were evaluated in normal subjects during water diuresis, before and after the acute administration of captopril, ibuprofen, or the combination of both drugs. The glomerular filtration increased after captopril administration but did not change after ibuprofen alone or in combination with captopril. Renal plasma flow increased with captopril alone and captopril plus ibuprofen but did not change after ibuprofen alone. Urine volume and Na excretion increased with captopril and decreased after ibuprofen; coadministration of ibuprofen attenuated the tubular effects produced by captopril alone. FELi, fractional delivery of solute to the distal nephron, and FELi-FENa, fractional distal reabsorption of solute, both significantly increased after captopril and decreased after ibuprofen but did not change with the combined regimen. (FELi-FENa)/FELi, fractional reabsorption of distally delivered Na, significantly decreased after captopril and increased after ibuprofen but remained unchanged after captopril plus ibuprofen. Thus captopril and ibuprofen have opposing effects on tubular Na and water handling, which are attenuated by the addition of the other drug. This interaction may have clinical relevance in patients with heart failure or hypertension, in whom captopril is used to enhance Na and water diuresis.

Role of kinins in pain and hyperalgesia: psychophysical studies in a patient with kininogen deficiency

1992 ◽  
Vol 83 (3) ◽  
pp. 337-341 ◽  
Author(s):  
Srinivasa N. Raja ◽  
James N. Campbell ◽  
Richard A. Meyer ◽  
Robert W. Colman
Keyword(s):  
Pain Threshold ◽  
Matched Control ◽  
Normal Subjects ◽  
Thenar Eminence ◽  
Control Subjects ◽  
Intradermal Administration ◽  
Heat Pain Threshold ◽  
Before And After ◽  
Psychophysical Studies

1. Bradykinin is considered to be an important mediator of pain and hyperalgesia associated with injury and inflammation. Psychophysical studies were conducted in a patient with complete kininogen deficiency to determine whether the absence of bradykinin was associated with abnormalities in pain sensibility. Pain evoked by heat stimuli to the thenar eminence was tested before and after a localized burn, which has been shown to cause hyperalgesia in normal subjects. In addition, pain evoked by intradermal administration of bradykinin (0.1–10 μg) to the forearm and the effects of bradykinin on pain induced by heat stimuli were studied. The patient rated the intensity of pain evoked by all heat stimuli relative to the pain induced by a 3s 45°C stimulus. 2. The patient's heat pain threshold (45°C) in the glabrous skin was similar to that of age-matched control subjects (n = 5) and to that previously observed in younger control subjects. 3. The burn resulted in a decrease in pain threshold and an increase in pain induced by suprathreshold stimuli. The magnitude of hyperalgesia was within the range observed in the age-matched control subjects and in younger control subjects. Thus, kinins are not essential for the development of hyperalgesia after heat injury. 4. In control subjects, intradermal injections of bradykinin produced pain and hyperalgesia to heat stimuli. In the patient, intradermal bradykinin injections induced minimal pain and no hyperalgesia to heat stimuli. Thus, congenital absence of kininogens may be associated with a deficiency in bradykinin receptors.

ADRENAL AND OVARIAN TESTS IN FEMALE HIRSUTISM

1967 ◽  
Vol 55 (4) ◽  
pp. 685-696 ◽  
Author(s):  
J. Reforzo-Membrives ◽  
D. Z. Rocca ◽  
C. L. Enriori ◽  
S. C. Mazza
Keyword(s):  
Adrenal Cortex ◽  
Fixed Ratio ◽  
Normal Subjects ◽  
Polycystic Ovaries ◽  
Dexamethasone Treatment ◽  
Before And After ◽  
Menstruating Women ◽  
Normal Women ◽  
Androgenic Steroids

ABSTRACT The role of the adrenal cortex and the ovary in hirsutism was studied by estimating the urinary neutral 17-ketosteroids before and after suppression with dexamethasone, and following the administration of HCG to patients while still on dexamethasone treatment. Studies were performed in 11 non hirsute normally menstruating women, 16 women with hirsutism and polycystic ovaries (PO), as demonstrated by gynaecography, and 56 women with hirsutism (H). Before adrenal suppression the 17-ketosteroids were higher in women with PO and H. After dexamethasone administration, the 17-ketosteroids decreased to more uniform levels similar to those found in normal women. Following stimulation with HCG, the 17-ketosteroids were higher in the former two groups than in normal subjects. In normal women there was no correlation between the values before and after dexamethasone while in women with PO and H a positive correlation was found. The differences between values before and after dexamethasone increased proportionately to the values found before dexamethasone administration; this correlation was more evident in the PO and H groups. The correlation of values after dexamethasone and after HCG administration was statistically significant in patients with PO and H, but not in normal women. No differences were found between women with PO and H. These results suggest that there is an increased production by the adrenal cortex and the ovary of androgenic steroids in women with PO and H with no fixed ratio between the contribution of each organ.

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