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Query: UMLS:C0432222 (
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47,337
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To investigate the effects of dietary sodium on the peripheral dopaminergic mechanism, changes of unconjugated plasma dopamine(DA) and its related humoral factors were studied in 8 patients with essential hypertension(EH) and 8 age-matched normal controls(N) while they were receiving ordinary meals (Na, 130-180 mEq daily) followed by higher sodium (250-300 mEq daily) diets for a week. Plasma and urinary DA, norepinephrine(NE) and epinephrine(E) were measured by the highly sensitive COMT-mediated radioenzymatic procedure, which permits an accurate estimation of plasma DA as low as 5-6 pg/ml. Under high sodium diets, blood pressure and heart rate were not changed significantly in N and EH subjects. Urinary NE and E tended to decrease, while urinary DA increased significantly in both groups of subjects (p less than 0.05). There was a significant correlation between urinary sodium and DA (r = 0.590, p less than 0.001), but plasma DA failed to correlate significantly to urinary sodium or DA in all subjects. Plasma NE and E tended to decrease in both N and EH subjects, while plasma DA increased significantly (p less than 0.05) in EH from 7.2 +/- 0.8 pg/ml [mean +/-
SEM
] to 9.3 +/- 1.0 and slightly in N from 9.1 +/- 1.8 to 11.2 +/- 1.3. Plasma renin activity(PRA) and plasma aldosterone(PAC) were invariably decreased in all subjects, while plasma
prolactin
(PRL) remained unchanged. A significant correlation was observed between plasma DA and NE under ordinary meals (r = 0.733, p less than 0.01), but this correlation disappeared under high sodium diets. Plasma DA showed an inverse correlation to PAC (r = 0.351, p less than 0.05) under both dietary conditions. Upright posture induced a significant rise (p less than 0.05) in NE, E, DA, PRA and PAC with ordinary meals, but the responses of NE and PAC were apparently attenuated with high sodium diets. An intravenous injection of metoclopramide (MCP, 10 mg), a DA receptor antagonist, provoked a slight rise in plasma NE and DA with ordinary meals, of which responses were further enhanced with high sodium diets. MCP induced a definite rise in PAC and PRL in all subjects under both dietary conditions (p less than 0.01), while plasma E and PRA remained unchanged after MCP challenge. The results lend support to the view that unconjugated plasma DA could be a useful marker of peripheral dopaminergic activity, which might be a physiological regulator responsible for the suppression of aldosterone secretion and sympathetic nerve activity observed during high sodium intake.
...
PMID:[Effects of high sodium diet on dopaminergic mechanism in normal and hypertensive subjects]. 306 95
This study was designed to assess the effect of an altered level of serum oestrogen and progesterone on the
prolactin
(
PRL
) response to gonadotrophin releasing hormone (GnRH). Six normal women were studied in the early follicular phase and the mid-luteal phase of one cycle and five menopausal women were studied before and after treatment with progesterone. Blood samples were collected at 15 min intervals for 6 h after a basal collection period of 30 min. Intravenous boluses of GnRH (1 microgram, 10 micrograms and 50 micrograms) were given at 0, 2 and 4 h. Basal samples were assayed for 17 beta-oestradiol (E2), oestrone (E1) and progesterone (P); LH, FSH and
PRL
were measured in all samples. Serum
PRL
was significantly elevated in all groups after 10 micrograms of GnRH with maximum increments (+/-
SEM
) ranging from 3.9 +/- 1.3 micrograms/l in early follicular phase women to 14.7 +/- 4.7 micrograms/l in progesterone-treated menopausal women. The
PRL
response to GnRH was significantly greater in the luteal phase and in menopausal women compared to early follicular phase women. There was a significant correlation between the maximum
PRL
response and the maximum LH response to GnRH in all the women studied (r = 0.7; P less than 0.01). A significant correlation was also found between the maximum
PRL
response and the basal serum oestrogen concentration in the normal cycling women (r = 0.8; P less than 0.01), but not when the menopausal women were included in the analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:The effect of physiological changes in ovarian steroids on the prolactin response to gonadotrophin releasing factor. 308 91
Hypogonadotropic hypogonadism due to a deficiency in hypothalamic gonadotropin-releasing hormone is common in female athletes ("hypothalamic amenorrhea"). It is not known, however, whether a similar phenomenon occurs in male athletes. We investigated the integrity of the hypothalamic-pituitary-gonadal axis in six highly trained male marathon runners (who were running 125 to 200 km per week). The mean (+/-
SEM
) frequency of spontaneous luteinizing hormone pulses was diminished in the runners, as compared with healthy controls (2.2 +/- 0.48 vs. 3.6 +/- 0.24 pulses per eight hours, P less than 0.05). The amplitude of the pulses was also low in the runners (0.9 +/- 0.24 vs. 1.6 +/- 0.15 mlU per milliliter; P less than 0.05), and the responses of luteinizing hormone to gradually increasing doses of exogenous gonadotropin-releasing hormone were decreased. Plasma testosterone levels were similar in the two groups and increased equally in response to an intramuscular injection of 2000 units of human chorionic gonadotropin. During short-term intense physical exercise (a treadmill run at 72 percent of maximal oxygen consumption for two hours), the plasma gonadotropin levels in the athletes remained stable, but significant elevations in plasma levels of cortisol,
prolactin
, and testosterone occurred. We conclude that highly trained male athletes, like their female counterparts, may have a deficiency of hypothalamic gonadotropin-releasing hormone. This condition may be caused by the prolonged, repetitive elevations of gonadal steroids and other hormones known to suppress gonadotropin-releasing hormone secretion that are elicited by their daily exercise.
...
PMID:Decreased hypothalamic gonadotropin-releasing hormone secretion in male marathon runners. 309 Apr 37
The mechanisms whereby growth hormone (GH) secretion is decreased in human obesity remain obscure. We studied the response of plasma GH and
prolactin
(
PRL
) to an I.V. dose of 0.5 mcg/kg of growth hormone releasing factor (GRF) in three groups of children: lean (N = 12), obese (N = 15) and GRF-deficient, i.e. children with complete GH deficiency on the basis of conventional provocative testing and evidence of hypothalamic dysfunction on the basis of thyrotropin-releasing hormone testing (N = 7). Mean (+/-
SEM
) peak plasma GH after GRF was blunted to the same extent in obese and in GRF deficient children (11.1 +/- 2.2 and 8.3 +/- 2.8 ng/ml) as compared to lean control children (34.7 +/- 4.7 ng/ml). The pattern of
PRL
response to GRF was however different in GRF deficient children, whose high basal
PRL
levels increased further after GRF injection, and in obese and lean children, who had n alpha acute change in
PRL
levels after GRF. Baseline plasma somatomedin C concentrations were low for age in GRF deficient children and tended to be high for age in obese children. On the basis of these discrepant patterns of response of
PRL
to GRF and plasma somatomedin C concentrations, we conclude that GRF deficiency does not account for the decreased GH secretion observed in obese children.
...
PMID:Evidence against growth hormone-releasing factor deficiency in children with idiopathic obesity. 309 43
Hyperprolactinaemia was found in 15 of 135 infertile patients with regular menstrual cycles, biphasic basal body temperature record and no galactorrhoea. In those 15 women, mean serum
prolactin
levels during the mid-follicular and mid-luteal phases of the menstrual cycle were 29.8 (
SEM
1.8) ng/ml and 29.5 (
SEM
1.3) ng/ml, respectively. Although serum FSH and LH levels were similar in normal and hyperprolactinaemic women, serum oestradiol level during the mid-follicular phase was subnormal in hyperprolactinaemic women (P less than 0.05). In contrast, serum oestradiol and progesterone levels during the mid-luteal phase and luteal phase length were similar in normoprolactinaemic and hyperprolactinaemic groups. The results suggest that hyperprolactinaemia is associated with defects of follicle development as measured by oestradiol production during the mid-follicular phase, but not with corpus luteum function as measured by progesterone production during the mid-luteal phase, and luteal phase length.
...
PMID:Serum gonadotrophin and sex steroid hormone levels during mid-follicular and mid-luteal phases in hyperprolactinaemic women with regular menstrual cycles. 310 71
Three experiments were conducted to determine serum growth hormone (GH) response of bull calves (N = 4; 83 kg body wt) to iv injections and infusions of human pancreatic GH-releasing factor 1-40-OH (hpGRF). Peak GH responses to 0, 2.5, 10, and 40 micrograms hpGRF/100 kg body wt were 7 +/- 3, 8 +/- 3, 18 +/- 7, and 107 +/- 55 (mean peak height +/-
SEM
) ng/ml serum, respectively. Only the response to the 40-microgram dose was greater (P less than 0.05) than the 0-microgram dose. Concentrations of
prolactin
in serum were not affected by hpGRF treatment. In calves injected with hpGRF (20 micrograms/100 kg body wt) at 6-hr intervals for 48 hr, GH increased from a mean preinjection value of 3.1 ng/ml serum to a mean peak response value of 70 ng/ml serum. Differences in peak GH response between times of injection existed within individual calves (e.g., 10.5 ng/ml vs 184.5 ng/ml serum). Concentrations of GH in calves infused continuously with either 0 or 200 micrograms hpGRF/hr for 6 hr averaged 7.4 +/- 3 and 36.5 +/- 11 ng/ml serum, respectively (P less than 0.05). Concentrations of GH oscillated markedly in hpGRF-infused calves, but oscillations were asynchronous among calves. We conclude that GH response of bull calves to hpGRF is dose dependent and that repeated injections or continuous infusions of hpGRF elicit GH release, although magnitude of response varies considerably. We hypothesize that differences in GH response to hpGRF within and among calves, and pulsatile secretion in the face of hpGRF infusion may be related to the degree of synchrony among exogenous hpGRF and endogenous GRF and somatostatin.
...
PMID:Growth hormone response of bull calves to growth hormone-releasing factor. 310 19
Hormone levels, physiologic parameters, electroencephalographic (EEG) activity, and changes in subjective feelings recorded using a nonverbal instrumental device were assessed following the double-blind intravenous administration of 500 micrograms of gonadotropin-releasing hormone (GnRH) or placebo to five normal males. Within 30 minutes of GnRH administration,
prolactin
(
PRL
) levels had risen by 4.3 +/- 1.2 ng/ml (mean +/-
SEM
) from a baseline of 8.5 +/- 0.9 ng/ml (overall increase P less than 0.005 vs. baseline, P less than 0.001 vs. placebo); maximally stimulated values had a mean of 16.7 +/- 2.3 ng/ml. The
PRL
elevations measured in absolute terms significantly correlated with increases in luteinizing hormone (LH) (r = 0.97) and follicle stimulating hormone (FSH) (r = 0.89). No changes in physiologic parameters or EEG activity occurred in response to GnRH, nor were any behavioral responses found. The increase in
PRL
following GnRH was specifically shown to be unrelated to experimental stress or the behavioral effects of GnRH.
...
PMID:Effect of gonadotropin-releasing hormone on prolactin levels in males unrelated to stress or behavioral changes. 311 3
Plasma
prolactin
(
PRL
) responses to several exogenous agents are variable in patients with prolactinomas. In this study the factors determining the responsiveness to exogenous stimuli were investigated in 35 patients with prolactinomas. Among these patients, 14 patients were responder (greater than 150% increase of basal value) to TRH, sulpiride (DA D2-receptor blocker) and arginine, and remaining 21 were non-responder to these three agents. Plasma TSH responses to sulpiride, an indirect indicator of hypothalamic dopaminergic tone on pituitary gland, were similar between responder (delta TSH: M +/-
SEM
; 5.3 +/- 0.2 microU/ml) and non-responder (delta TSH: 5.6 +/- 0.2 microU/ml), and were greater than those in normal subjects (delta TSH: 0.7 +/- 0.2 microU/ml, n = 18) (P less than 0.001). The plasma
PRL
responses to dopaminergic agents (L-dopa, CB-154, dopamine) were greater in responders than in non-responders (% of basal: L-dopa, 33.7 +/- 3.7% vs 51.6 +/- 5.6% at 150 min, P less than 0.05; CB-154, 16.5 +/- 2.6% vs 30.9 +/- 2.8% at 6 hr, P less than 0.05; dopamine, 31.7 +/- 5.6% vs 44.9 +/- 4.3% at 90 min, P less than 0.05). When all patients were divided into microadenoma (n = 12) and macroadenoma patients (n = 23), there were no differences in plasma
PRL
responses to these agents between the two groups. Again, there were no differences in the duration of illness between the responder and non-responder patients (61.9 +/- 13.7 vs 54.1 +/- 12.0 months). During the short term CB-154 treatment (7.5mg/day for 3 approximately 5 weeks) in 8 responders and 15 non-responders, all responder patients showed normalization of plasma
PRL
levels, while such normalization was observed in only 6 non-responder patients. These results suggest that in prolactinoma patients variable responsiveness to several exogenous agents are depending on the sensitivity to several exogenous agents are depending on the sensitivity of prolactinoma itself, regardless of the endogenous hypothalamic dopaminergic tone, tumor size or duration of the illness.
...
PMID:[The properties of prolactin secretion in patients with prolactin secreting pituitary adenomas]. 312 84
Plasma levels of LH, FSH,
prolactin
(
PRL
), and testosterone (T) were assessed in six normal men following administration of a pharmacologic dose of gonadotropin releasing hormone (GnRH) (500 micrograms iv over a one-min period) with concomitant oral administration of either ethanol (0.695 g/kg of body weight over a 15-min period) or ethanol placebo. Acute ethanol administration had no effect on the response of either LH or FSH to GnRH.
PRL
levels increased following GnRH and administration of both ethanol and ethanol placebo. Ethanol administration enhanced the T response to GnRH (p less than 0.001 vs placebo). During the placebo condition, T levels did not rise significantly until 100 min after GnRH administration, at which time the mean increment over baseline was 101 +/- 20 ng/dl (+/-
SEM
). In contrast, following ethanol intake, T levels were significantly elevated within 30 min after GnRH administration, at which time the mean increment over baseline was 187 +/- 42 ng/dl. The mean T increments were 304 +/- 62 and 472 +/- 77 ng/dl, respectively, 60 and 105 min following GnRH and ethanol administration. The increase in T levels following acute ethanol intake and concomitant gonadotropin stimulation is in contrast to the well-documented effect of chronic ethanol intake on suppression of testosterone synthesis by testicular Leydig cells.
...
PMID:Acute ethanol administration enhances plasma testosterone levels following gonadotropin stimulation in men. 312 15
We found, by radioimmunoassay, that thyrotropin-releasing-hormone (TRH) was present in human
prolactin
(
PRL
)-secreting adenomas (mean: 89 +/- 45 (
SEM
) fmol/mg proteins) and was released by perifused adenomatous cells at levels varying from 5 to 60 fmol/10(6) cell/2 min. TRH release was increased in the presence of dopamine (DA) 10(-6) M but was not modified by the presence of somatostatin (SRIH) 10(-6) M.
...
PMID:[Release of thyrotropin releasing hormone (TRH) from human prolactin-secreting pituitary adenoma cells. Modulation by dopamine]. 312 91
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