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Biomedical subjects

J A Tresguerres

Publications and source records attributed to J A Tresguerres.

At least 19 recordsLinked to original sources
PubMed2003

Growth hormone and aging.

In elderly people, vascular alterations and degenerative alterations of the Central Nervous System (CNS) are two of the most common reasons for illness and death. Lipid pattern modifications and menopause in women are some of the causes for the appearance of these alterations. Vascular endothelium is in part responsible for vascular homeostasis, through the production of several vasoactive factors. Growth hormone (GH) exerts effects on the CNS and on the vascular endothelium, since GH deficient subjects exhibit endothelium-dependent alterations, which recover under substitutive GH treatment. Growth hormone has important actions on lipid metabolism that also play a role on vascular and endothelial function. Moreover, cardiac function improves when GH is associated to angiotensin II receptor blockers. Elderly people exhibit a physiological GH deficiency that could affect their vascular and cerebral functions. A study was carried out using old Wistar rats to clarify the effects of GH on the vessels under chronic "in vivo" conditions. The response to various vasoactive substances in aortic rings has been evaluated. An increase in the aortic media thickness was seen in old rats, which showed also a reduction in the vasodilator response to isoprenaline as compared to young animals. GH treatment partially restored the vasodilator response and reduced media thickness. Neuronal population was reduced in the hypocampus of old rats as compared to young ones and GH treatment was able to significantly enhance the number. Neurotransmitters were measured in several cerebral areas to establish differences between young and old GH-treated or untreated animals. Glutamine, Arginine and Aspartate were reduced in old animals whereas Citruline was increased. GH treatment restored in all cases the levels corresponding to young rats.

Aged↗
PubMed2001

Circadian urinary 6-sulphatoxymelatonin, cortisol excretion and locomotor activity in airline pilots during transmeridian flights.

Airline pilots divided into two groups of age (over and under 50 years) were studied before, during and after westbound (Madrid-Mexico City-Madrid, n = 12) and eastbound (Madrid-Tokyo-Madrid, n = 21) flights. A group of 10 age-matched people staying in Madrid were submitted to the same tests and served as a control group. Changes in urinary 6-sulphatoxymelatonin (6-aMTs) and free cortisol excretion (determined in 6-hr intervals) were measured by radioimmunoassay. Using wrist actigraphy, the circadian locomotor activity rhythm (LAR) was also monitored. Maximal baseline excretion of 6-aMTs occurred between 00:00 and 12:00 hr and maximal excretion of cortisol took place between 6:00 and 12:00 hr in the control group. Analysed globally, older pilots exhibited significantly lower values of 6-aMTs than younger ones. In both flight directions, pilots maintained the pattern of excretion of 6-aMTs, corresponding to baseline. The return flight to Madrid from Mexico and Tokyo coincided with a maximum in 6-aMTs excretion. Pilots kept the cortisol pattern found in the control group, with those over 50 years of age exhibiting significantly lower cortisol values than the younger ones. A 7-hr delay in acrophase of LAR after 2 days in Mexico City was found after cosinor analysis, and similar pre-flight values were found after returning to Madrid. An 8-9-hr acrophase advance of LAR was observed after arriving in Tokyo, with acrophase on the post-return flight day still being advanced 3 4 hr as compared to pre-flight values. Decreases in the amplitude of LAR in older pilots were found at Mexico City, as well as at Tokyo stopover and on post-flight day. Data confirm the occurrence of internal desynchronization in airline crewmembers after transmeridian flights.

Adult↗
PubMed2001

GH gene expression in the submaxillary gland in normal and Ames dwarf mice.

High local GH-releasing hormone (GHRH) levels are capable of inducing transdifferentiation in salivary cells to synthesize GH. However, the factors implicated in this process remain unknown. To study this subject, normal and Ames dwarf mice were implanted in the submaxillary gland with a slow release pellet releasing 21 microgram GHRH (1-29)-NH(2)/day for 2 months. Control animals received placebo pellets at the same site. After 60 days, heart blood was collected and submaxillary glands were removed. Circulating levels of GH and IGF-I were significantly decreased (P<0.05) in dwarf mice in comparison with controls, and GHRH treatment did not modify either of these two parameters. Controls carrying GHRH pellets showed a significantly higher GH content (P<0.05) in the submaxillary gland than the placebo-treated normal mice. There were no differences between the IGF-I concentrations of placebo- and GHRH-treated salivary tissue from normal mice. Analysis of GH mRNA by RT-PCR followed by Southern blot revealed that GH transcripts were present in the salivary gland samples carrying the placebo pellets in both normal and dwarf mice. The expression of GH was significantly (P<0.05) increased by the GHRH pellets in salivary tissue from normal mice, but not in submaxillary glands from dwarf mice. Pit-1 mRNA was not detected in the GHRH-treated glands of normal and dwarf mice by RT-PCR or by Southern blot. Using these highly sensitive methods, we have been able to detect the transcription of both GH and Pit-1 in pituitaries from Pit-1-deficient Ames dwarf mice. The present experiment demonstrates that salivary tissue synthesizes GH when it is exposed to the influence of GHRH. Both basal and GHRH-induced salivary GH expression appear to be independent of Pit-1.

Analysis of Variance↗
PubMed2000

Growth hormone response to long-term GH-RH administration in lambs.

The pattern of long-term GHRH administration capable of stimulating GH release without depleting pituitary GH content has been investigated using two experimental approaches. In experiment 1, recently weaned male lambs were treated for 3 weeks as follows: Group A) control; B) subcutaneous (sc) continuous infusion of GHRH (1200 mg/day) using a slow release pellet; C) the same as B plus 1 daily sc injection of long acting somatostatin (SS) (octreotide, 20 mg) ; D) 3 daily sc GHRH (250 mg) injections ; E) 2 daily sc injections of GHRH (250 mg) and 2 of natural SS (250 mg). In experiment 2, recently weaned male lambs were continuously GHRH-treated using sc osmotic minipumps (900 mg/day) alone or combined with a daily sc injection of octreotide (20 mg) for 4 weeks. Basal plasma GH levels were increased after chronic pulsatile GHRH treatment but not after any kind of continuous GHRH administration. This increment was maintained during the 3 weeks of experimentation and appeared accompanied by a pituitary GH content similar to controls. A marked GH response to the iv GHRH challenge was observed in controls and in lambs receiving both types of continuous sc GHRH infusions, whereas pulsatile sc GHRH-treated animals did not respond to the iv GHRH challenge in the first and second weeks of the study but did so in the third week of treatment. These data demonstrate that long-term pulsatile GHRH administration is capable of stimulating GH release in growing male lambs, without producing pituitary desensitization.

Analysis of Variance↗
PubMed2000

Recombinant human growth hormone enhances tibial growth in peripubertal female rats but not in males.

OBJECTIVE: A novel non-invasive technique termed microknemometry, which allows daily leg length measurement, was used to investigate the growth promoting effect of growth hormone (GH) on peripubertal rats. We compared the effect of different patterns of recombinant human (rh) GH administration to peripubertal male rats with the effect produced by two daily administrations of the same amount of rhGH to peripubertal female rats or adult male rats. Another group of peripubertal male rats was also submitted to a 3-day period of starvation, in order to study catch-up growth during refeeding and to determine whether this process could be stimulated by exogenous GH administration. RESULTS: GH treatment was unable to stimulate tibial growth or weight gain in peripubertal males, whereas a clear growth promoting effect was observed in female rats and also in adult male rats. Starvation caused a dramatic body weight loss, and a reduction in tibial growth rate. Peripubertal male rats gained body weight faster than unstarved animals during refeeding, although recovery was not complete after nine days. Tibial growth, however, was resumed at the same speed as in normally fed males. This means that no catch-up effect was observed after refeeding in animals either with or without GH treatment. CONCLUSIONS: During peripuberty, normal male rats grow at a maximal speed that cannot be further increased by exogenous GH treatment, whereas age-matched female rats or older males grow at a slower rate than peripubertal males. Thus, exogenous rhGH administration is capable of enhancing growth velocity.

Aging↗
PubMed1999

Parotid gland tissue is able partially to assume pituitary functions under the influence of hypothalamic factors: in vivo and in vitro studies.

To test whether salivary tissue can secrete pituitary hormones, female Sprague-Dawley rats were hypophysectomized (hypox) and the following were transplanted to the sella turcica: parotid gland (group 3, n=33), adrenal gland (group 4, n=30), muscle (group 5, n=24). Group 2 (n=21) had the sella turcica filled with dentist's cement. In addition a group of rats (group 1, n=22) remained intact as controls. All groups were followed for 8 months. Daily vaginal smears showed normal cyclicity in controls and constant dioestrus in all hypox groups. Blood samples, taken once every 30 days before and after LHRH stimulation, showed significantly lower (P<0.001) plasma LH values in all hypox groups compared with controls. In group 3, a gradual and significant increase (P<0.05) was observed in the LH response to LHRH in parallel with a partial recovery of oestrous smears. No LH modification was observed in the other hypox groups. Plasma prolactin (PRL) levels were also very low in all hypox groups and were unaltered throughout the study. At the end of the experiments, half the animals were killed by decapitation and the hypothalamic-pituitary areas carefully dissected, homogenized and analysed for LH and PRL content. The remaining animals were perfused with 4% paraformaldehyde to obtain fixing of the whole body tissues. Hypothalamic and transplant areas were carefully dissected, frozen, cut and submitted to immunochemical procedures. LH content in the graft of group 3 animals was markedly (P<0.001) lower than in the control pituitary, but significantly higher (P<0.05) than in the other hypox groups. Immunochemistry showed LH and PRL positive cells in the graft of group 3 animals, whereas neither positive cells, nor LH content were observed in the parotid gland in situ. Experiments were completed with in vitro cultures of parotid glands in the presence or absence (controls) of synthetic hypothalamic hormones or rat hypothalamic extracts. After 1.5 weeks of culture, a significantly higher LH concentration (P<0.05) was observed in the wells treated with synthetic hypothalamic hormones (216+/-46 pg/ml vs 41+/-6 pg/ml in controls). When hypothalamic extracts were used, the LH levels increased more markedly (1834+/-190 pg/ml vs 36+/-6 pg/ml in controls) and those values were maintained during 3 weeks of culture. Immunostaining of these cultures showed a positive LH reaction in the epithelial cells found in the hypothalamic extract-treated wells. Both in vivo and in vitro studies confirm the transdifferentiation of parotid gland tissue to pituitary hormone-producing cells under hypothalamic influence.

Adrenal Glands↗
PubMed1999

Salivary gland is capable of GH synthesis under GHRH stimulation.

Twelve female rats weighing approximately 150 g received in the submaxillary gland a pellet capable of releasing 3.5 microg GHRH/h for 60 days. Another eight sex- and weight-matched animals received placebo pellets in the same place. After two months the animals were killed, heart blood was collected and pituitary and submaxillary glands were carefully dissected. Pituitary GH content in both placebo- and GHRH-treated animals showed similar values, but plasma GH and IGF-I levels were significantly lower in the animals carrying GHRH pellets (P<0.03); these animals also had a significantly higher GH content in the submaxillary gland (19.2+/-8 ng/mg protein) compared with the placebo-treated group (1.1+/-0.3 ng/mg protein). GH mRNA was present only in the submaxillary gland of GHRH-treated rats as determined by PCR-Southern blot and by in situ hybridization methods. It is concluded that high local GHRH levels are capable of inducing transdifferentiation in submaxillary gland cells to synthesize GH.

Animals↗
PubMed1999

Effect of long-term GHRH and somatostatin administration on GH release and body weight in prepubertal female rats.

In order to find a chronic GHRH administration capable of stimulating growth rate without depleting pituitary GH content, prepubertal female rats were subcutaneously (sc) treated with GHRH (1-29)-NH2 and somatostatin (SS). In experiment 1, the rats received sc injections of GHRH and cyclic natural SS for 19 days. In the second study, female rats were continuously treated during 21 days with GHRH, using a slow release pellet, alone or combined with one daily injection of long acting SS (octreotide). In experiment 1, body weight was significantly increased when GHRH was administered at the highest daily dosage (1200 microg/day), accompanied by an slight increment in pituitary GH content. Hypothalamic SS concentrations decreased when GHRH or SS were administered alone whereas the combined treatment with both peptides did not modify this parameter, which suggests the existence of a balance between the chronic actions of both peptides on hypothalamus. In experiment 2, the continuous infusion of GHRH increased plasma GH levels and tended to enhance pituitary GH content. Nevertheless, GHRH effect was not effective enough to increase body weight. By adding one daily injection of SS both GHRH effects on the pituitary gland were abolished. Our study indicates that female rats retain responsiveness to chronic GHRH and SS treatments at both pituitary and hypothalamic levels.

Animals↗
PubMed1998

Sexual dimorphism in growth as measured by microknemometry: different responses to GH deficiency and exogenous GH administration.

To monitor growth, a novel noninvasive leg length measurement technique, called microknemometry, which allows daily observation of tibial growth rate, was used. The rat exhibits a striking sex-related difference in postpubertal growth. Exogenous GH administration results in a sexually dimorphic response, affecting growth in normal young female rats but not in males. Here we investigated how chronic GH deficiency affects male and female rat growth patterns. The degree of growth rate recovery was investigated after exogenous GH administration to chronically deficient males and females. The deficiency was induced by neonatal monosodium glutamate (MSG) treatment. Since the neonatal gonadal environment plays an important role in the dimorphic growth pattern, neonatal androgenization of female rats with testosterone or neonatal feminization of male rats by castration was performed and the growth pattern monitored. MSG treatment decreased pituitary GH content and plasma IGF I levels in both sexes, but caused a less marked reduction of female rat tibial growth and body weight gain than in males. Additionally, only MSG-treated males showed decreased pituitary LH content, so that the dimorphic action of MSG on the gonadal axis may contribute to the observed differences in growth rate. GH administration was able to increase leg length in all MSG-treated rats but was more effective in females, despite a similar restoration of plasma IGF I levels in both sexes. Although neonatal castration of male rats resulted in a reduction of tibial growth rate and body weight, and neonatal testosterone administration to female rats caused a slight increase in body weight, a complete modification of the gender-dependent growth pattern was not achieved, indicating that appropriate steroid environment is also needed in puberty and adulthood.

Animals↗
PubMed1996

Differential catch-up in body weight and bone growth after short-term starvation in rats.

Catch-up or compensatory growth is known as a physiological phenomenon. However, most studies of catch-up growth were based on measurements of body weight, whereas changes in longitudinal bone growth remained largely undescribed. The present study describes the dynamics of both weight and longitudinal bone growth using mikro-knemometry, during normal feeding, severe food restriction (starvation), and refeeding of 14 intact and 28 GH-deficient male rats. Starvation induced rapid weight loss (P < 0.001), and stunted leg growth (P < 0.001). Refeeding led to rapid catch-up in weight of up to 4 times above normal daily weight gain, both in intact and GH-deficient animals, whereas an equivalent compensation of lower leg growth remained undetectable. Intact and GH-deficient animals show a circaseptan spontaneous variation of growth velocity (mini growth spurts). During starvation, mini growth spurts disappear, and return to normal after refeeding with no evidence of catch-up. In GH-deficient animals, GH (1 IU/rat, administered twice daily s.c. at 10:00 hand 16:00 h) was capable of augmenting catch-up in weight and, to a lesser extent, in leg length increment.

Animal Nutritional Physiological Phenomena↗
PubMed1995

Recombinant-human luteinizing hormone (r-hLH) as ovulatory stimulus in superovulated does.

PURPOSE: To study the effects of r-hLH as ovulatory stimulus in does. METHOD: New Zealand does, 18 wk old, in estrus, received 25 IU of pregnant mare serum gonadotropin (PMSG) followed at 48 h either by 50 IU of r-hLH (n = 20) or hCG (n = 20) to induce follicular growth and ovulation. All does were previously artificially inseminated to avoid endogenous LH surge. Half of the animals receiving r-hLH (n = 10) or hCG (n = 10) were killed at 72 h after the hormone administration, and the remaining half were killed at 14 days. At 72 h the number of corpora lutea and preovulatory follicles was determined, and fertilization rate, embryo quality, degree of embryonic development, and oviductal transit were all assessed. On day 14 the number corpora lutea and implanted embryos were counted, and implantation rate was determined. Median and interquartile ranges were calculated for each parameter. RESULTS: At 72 h the median for corpora lutea was 8 (7-10) in the r-hLH group vs 13 (10-14) in the hCG group (P = 0.009); preopvulatory follicles were 7 (6-10) vs 0 (0-0) (P = 0.0007); the percentage of good-quality embryos was 71.4% (54.5-75) vs 33.3% (25-37.5) (P = 0.001), for intermediate-quality embryos it was 25% (14.3-36.4) vs 33.3% (25-38.5), and the percentage of degenerated embryos was 0% (0-12.5) vs 33.3% (25-37.5) (P = 0.015), respectively. Fertilization rates were similar in both groups. Embryonic development was more homogeneous in the animals receiving r-hLH (8 to > or = 16 cells) compared to those receiving hCG (2 to > or = 16 cells). The median of embryos still in oviducts at 72 h was significantly higher in the hCG group [6 (4-13)] than in the r-hLH group [0 (0-4)] (P = 0.41). At 14 days the median of corpora lutea was higher in the hCG [12 (11-16)] than in the r-hLH group [10 (7-13)] (P = 0.008), but no differences were noted in the number of implanted embryos. Implantation rate was higher in the r-hLH group [100 (92.3-100)] than in the hCG group [87.5 (83.3-94.1)] (P = 0.056). CONCLUSIONS: At the studied dose an ovulatory stimulus with r-hLH induced fewer follicles to ovulate than hCG. Recombinant-hLH produced superior embryo morphological quality, a more homogeneous degree of embryo development, and more synchronous embryo transit than hCG. In spite of the larger number of ovulations following hCG, subsequent events essential for pregnancy were higher with r-hLH, offsetting differences in terms of implanted embryos at 14 days of pregnancy.

Animals↗
PubMed1995

Regulation of hypothalamic somatostatin by glucocorticoids.

Glucocorticoids (GCs) play a key role in the physiology of the hypothalamic-somatotroph axis, since these steroids enhance growth hormone (GH) gene transcription and increase GHRH receptor synthesis. However, GC excess inhibits normal growth in all species studied. This is mainly due to the impaired GH secretion observed during hypercortisolism, a situation in which GH responses to a number of stimuli, including GHRH, are blunted. The inhibitory effect of GCs on GH secretion seems to be dependent on enhanced hypothalamic SS secretion. Since SS release is stimulated by beta-adrenergic agonism we tested the possibility that GC inhibition of GH secretion would depend on increased beta-adrenoceptor activity in SS-producing neurons. The experimental design consisted in evaluating the GH response to GHRH in normal subjects after having induced hypercortisolism, with DEX, and blocking beta-adrenoceptors with propranolol (PRO). Moreover, to investigate the specificity of this mechanism, GHRH-induced GH release was tested after inducing hypercortisolism and enhancing alpha 2-adrenergic or muscarinic cholinergic tone, by giving clonidine (CLO) or pyridostigmine (PD), respectively. As expected, nocturnal DEX administration inhibited the GH response to GHRH. In this situation of hypercortisolism, both PRO and CLO, but not PD, were able to reverse the inhibitory effect of DEX on GHRH-elicited release. However, the potentiating effect of these drugs on the GHRH-induced GH secretion was only observed for PRO. These data confirm that GC excess inhibits GH release by increasing hypothalamic SS secretion, and that the mechanism is mediated by GC-induced enhanced beta-adrenergic responsiveness. Therefore, the defective GHRH secretion observed in chronic hypercortisolism must be a consequence of the continuous blockade that SS excess exerts on GHRH-producing neurons. Our postulate agrees with other data in the literature showing that GCs modulate the secretion of some hypothalamic peptides by changing the responsiveness of the producing neurons from alpha 2-adrenoceptors to that of beta-adrenoceptors.

Clonidine↗
PubMed1995

Effect of recombinant human luteinizing hormone versus human chorionic gonadotrophin: effects on ovulation, embryo quality and transport, steroid balance and implantation in rabbits.

A total of 40 New Zealand female rabbits which had been given follicular stimulation and artificial insemination received 50 IU of either recombinant human luteinizing hormone (rhLH; n = 20) or human chorionic gonadotrophin (HCG; n = 20) to induce ovulation. In each hormone group, 10 animals were killed 72 h later to study the ovulatory process and the number, location, morphological quality and variation in the degree of development of recovered embryos. Pre-ovulatory and post-ovulatory oestradiol and progesterone concentrations were determined in these 10 animals; the remaining 10 animals of each group were killed at 14 days to study implantation up to day 14. At 72 h the number of luteinized follicles and the total number of embryos in the rhLH group were lower than in the HCG group, and the number of pre-ovulatory follicles was higher. The percentage of good quality embryos was higher with rhLH, whereas the percentage of degenerated embryos was lower. Oviductal transit of the embryos was slower and variation in the degree of embryo development greater after HCG. Progesterone concentrations were comparable with pre-ovulatory concentrations at 24 h in the rhLH group, but not in the HCG group where they increased. In the study performed at 14 days, the implantation rate was significantly higher with rhLH versus HCG. These observations suggest that rhLH induces a lower number of follicles to ovulate than does HCG, probably due to its shorter half-life; however, the better embryo quality produced by rhLH may ultimately lead to a better implantation rate; rhLH may mimic the physiological endogenous LH surge more closely than HCG.

Animals↗
PubMed1995

Restraint-induced changes in serum luteinizing hormone, prolactin, growth hormone and corticosterone levels in rats: effect of superior cervical ganglionectomy.

From about 10 to 36 h after superior cervical ganglionectomy (SCGx), peripheral sympathetic nerve terminals in the median eminence degenerate, nerve ending content is released, and a transient period of increased postsynaptic activity ensues. After this time, an irreversible, paralytic phase is established in the denervated territory. The present experiment was undertaken to examine, at single points during the wallerian degeneration phase (24 h after SCGx) and during the paralytic phase (10 days after denervation), the participation of peripheral sympathetic nerves in restraint-stress-induced changes of circulating luteinizing hormone (LH), prolactin (PRL), growth hormone (GH) and corticosterone levels. During the wallerian degeneration phase, serum LH did not augment after stress, as it did in sham-operated controls. In the paralytic phase, the poststress increases in LH attained similar values in sham-operated and SCGx rats. Immobilization stress augmented PRL levels to a similar extent in sham-operated and SCGx rats either 24 h or 10 days after surgery. During the wallerian degeneration phase, a decrease in serum GH levels was found in unrestrained rats. Immobilization stress decreased GH levels to 5-12% of unrestrained values in sham-operated and SCGx rats at both examination time points after surgery. Rats studied 24 h after SCGx exhibited significantly augmented serum corticosterone levels and failed to show restraint-stress-induced stimulation of corticosterone release. In rats subjected to SCGx 10 days earlier, both basal and poststress levels of corticosterone did not differ from sham-operated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Clonidine potentiates the growth hormone response to a growth hormone releasing hormone challenge in hypothalamic growth hormone releasing hormone deficient rats.

This study was designed to further investigate our postulate regarding the inhibitory role played by central alpha 2-adrenergic pathways on hypothalamic somatostatin (SS) release in rats. The growth hormone (GH) responses to exogenous GH-releasing factor (GRF; 3 micrograms/kg i.v.) or clonidine (CLO; 100 micrograms/kg i.v.), either given alone or in combination, were tested in 3-month-old male rats made GH-releasing hormone (GH-RH) deficient neonatally by administration of monosodium glutamate (MSG; 4 mg/g body weight s.c.). To prevent the presumable decrease in the pituitary GH content in these animals from leading to an erroneous interpretation of the results obtained, half of these rats were given GRF (MSG-GRF rats; 30 micrograms/kg s.c.) for 3 days immediately prior to GH testing. The other half of MSG-treated and non MSG-treated rats received saline during these days (MSG-S and controls, respectively). To establish the efficiency of GRF priming, the pituitary GH content was measured in other MSG-GRF, MSG-S, and control animals. The mean (+/- SEM) GH peaks in response to GRF challenge were significantly higher in controls than in MSG-GRF rats (125.2 +/- 28.5 vs. 67.5 +/- 19.4 micrograms/l; p < 0.05), while no significant GRF-induced GH release was observed in the MSG-S group. Most likely these results are related to the different pituitary GH content, significantly (p < 0.01) higher in controls than in MSG-GRF rats, and in the latter higher than in MSG-S animals (p < 0.05). CLO administration did not evoke a significant GH release in MSG rats, whether primed with GRF or not.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Changes in serum growth hormone and prolactin levels, and in hypothalamic growth hormone-releasing hormone, thyrotropin-releasing hormone and somatostatin content, after superior cervical sympathectomy in rats.

After bilateral superior cervical ganglionectomy (SCGx) of adult male rats, norepinephrine (NE) content of the medial basal hypothalamus (MBH) decreased significantly by 39-47% from 16 h to 7 days after surgery. During this time the levels of serum growth hormone (GH) and prolactin (PRL) and of MBH GH-releasing hormone (GRH), thyrotropin-releasing hormone (TRH) and somatostatin were measured by RIA. In sham-operated controls, serum PRL increased and serum GH decreased 16-24 h after surgery, attaining pre-surgical levels later on. In SCGx rats, significantly lower serum GH and PRL and higher MBH GRH and TRH content as compared to controls was observed 16-24 h after surgery, during the wallerian degeneration phase after SCGx. MBH somatostatin concentration decreased in SCGx rats 20 h after surgery. Two injections of the alpha 1-adrenoceptor blocker prazosin 45 and 90 min before sacrifice, alone or together with the beta-blocker propranolol, prevented the changes in MBH hypophysiotropic hormone content, as well as in serum GH and PRL levels, found in SCGx rats 20 h after surgery. Propranolol treatment did not affect hormone levels. Neither drug modified the decrease in MBH NE content observed after SCGx. The results argue in favor of the existence of physiologically relevant projections from superior cervical ganglion neurons to the MBH controlling hypophysiotropic hormone release.

Animals↗
PubMed1993

Studies on alpha 2-adrenergic modulation of hypothalamic somatostatin secretion in rats.

This study was undertaken to investigate whether or not alpha 2-adrenergic pathways would negatively modulate the hypothalamic somatostatin release in rats. To induce pharmacological changes in SS release, three groups of male Sprague-Dawley rats (n = 30/group) were separately anesthetized by ip administration of urethan (which increases SS tone; 1.2 g/kg), pentothal (which impairs SS release; 30 mg/kg), or ketamine (which does not affect spontaneous SS secretion; 40 mg/kg). Ten rats from each group were challenged with GRF (2 micrograms/kg iv), clonidine (40 micrograms/kg iv), or GRF plus clonidine. Administration of clonidine markedly increased the GH responsiveness to GRF in rats anesthetized with urethane or ketamine. In contrast, the GH response to GRF was not modified by clonidine in rats anesthetized with pentothal. These results show that alpha 2-adrenergic stimulation only modifies the GRF-induced GH rise when SS release is high. Therefore, in rats, central alpha 2-adrenergic pathways appear to play a main inhibitory effect on hypothalamic SS secretion.

Animals↗