Biomedical subjects

J Meites

Publications and source records attributed to J Meites.

At least 55 records · Page 3Linked to original sources

PubMed1984

Endogenous opiate involvement in acute and chronic stress-induced changes in plasma LH concentrations in the male rat.

The present study was carried out to examine the possible role of the endogenous opioid peptides ( EOP 's) on the pituitary luteinizing hormone (LH) response to both acute and chronic stress and to food deprivation. Thirty minutes after acute (2 min.) exposure to ether, plasma LH levels were elevated compared to controls; morphine (MOR) treatment prior to stress prevented this response. More prolonged etherization (15 minutes) significantly depressed circulating LH, whereas naltrexone ( NALT ), a specific opiate antagonist, reversed this decline. Immobilization for 8 hours resulted in a significant initial increase in LH release, followed by a decline toward baseline levels. Naltrexone treatment increased the magnitude of the acute LH rise, and attenuated the subsequent decrease in plasma LH. The effect of chronic stress on circulating LH was also examined. Plasma LH levels were depressed for 3 consecutive days following subcutaneous gauze pad implantation, whereas 3 daily NALT injections returned LH to control levels. Complete food deprivation for 5 days also resulted in a significant decline in circulating LH. Injection of NALT 3 times daily reversed this decline on days 2, 3 and 4 of treatment. These results support the hypothesis of a mediatory role for the EOP 's in the effect of both chronic stress and food deprivation on LH release in the rat.

Animals↗

PubMed1984

Inhibition by estrogen of autofeedback regulation of prolactin secretion.

The effect of estradiol-17 beta (E2) on autofeedback regulation of prolactin (PRL) secretion was tested in ovariectomized rats after s.c. implantation of an (E2)-containing or empty silastic capsule, followed by i.v. injection of bovine PRL (b-PRL) or bovine serum albumin (BSA; 500 micrograms/100 g B.W.). Implantation of an E2 capsule (day 0), 2.5 mm or 5.0 mm in length, produced plasma E2 concentrations of 79 +/- 6 (9) and 140 +/- 8 pg/ml (8), respectively. Assay of PRL in plasma samples collected at 1 h intervals between 1100-1800 h on days 3, 4 and 5, after E2 capsule implantation showed a daily afternoon PRL surge. Empty capsule-treated rats did not show any afternoon PRL surge. Injection of b-PRL, but not BSA, at 1200 h on day 3 reduced basal PRL release both on days 3 and 4 in empty capsule-treated rats. In ovariectomized rats treated with a smaller E2 capsule (2.5 mm), b-PRL injection at 1200 h on day 3 reduced the amplitude of the afternoon surge of PRL and the total amount of PRL released on day 4. b-PRL, however, was ineffective in reducing PRL release in rats bearing the large E2 capsule (5.0 mm). These results suggest that high E2 levels in the blood can block the negative feedback action of PRL on PRL release.

Animals↗

PubMed1984

Effect of adrenalectomy and 5-hydroxytryptophan on phasic release of luteinizing hormone.

The effect of 5-hydroxytryptophan (5-HTP) on serum progesterone and the possible role of adrenal progesterone in mediating stimulation by 5-HTP of phasic release of luteinizing. hormone (LH) were investigated in estradiol benzoate (EB)-treated ovariectomized rats. LH surges were induced in long-term (at least two weeks) ovariectomized rats by two injections of EB (20 micrograms/rat, s.c.) with an interval of 72 hrs. Administration of 5-HTP (50 mg/kg, i.p.) at 1000 hr in EB-treated ovariectomized rats resulted in a four-fold increase in serum progesterone within 30 mins, and significantly stimulated the LH surge at 1600 hr. This facilitative effect of 5-HTP on serum LH, but not progesterone, was further potentiated in rats pretreated with P-chlorophenylalanine (PCPA) 72 hrs earlier. Adrenalectomy shortly before 5-HTP administration attenuated the LH surge in saline treated controls, and completely blocked the facilitative effect of 5-HTP on the afternoon surge of LH in rats pretreated with PCPA 72 hrs earlier. On the other hand, chronic adrenalectomy (for 6 days) followed by hydrocortisone (0.2 mg/rat/day) replacement not only had no effect on the LH surge in saline treated controls, but also failed to prevent 5-HTP from facilitating the LH surge in PCPA pretreated rats. On the first day of bleeding, the basal LH value at 1000 hr in sham operated controls was significantly suppressed by PCPA pretreatment 48 hrs earlier. The second dose of 5-HTP administered on the next day failed to potentiate LH surges in either sham operated or adrenalectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗

PubMed1984

Reduced tuberoinfundibular dopaminergic neuronal function in rats with in situ prolactin-secreting pituitary tumors.

Tuberoinfundibular dopaminergic (TIDA) neuronal function in rats with spontaneous or estrogen-induced prolactin- (PRL-)secreting pituitary tumors (prolactinomas) was studied by assaying dopamine (DA) concentration in pituitary stalk blood and electrically induced release of 3H-DA from the median eminence in vitro. Old rats with spontaneous prolactinomas showed enlarged and hemorrhagic pituitaries and elevated serum PRL levels. These rats had reduced DA in pituitary stalk blood, showed significantly lower response to the DA-releasing drug, nomifensine, and exhibited reduced electrically induced 3H-DA release from the median eminence in vitro, when compared to corresponding values in young and old rats without prolactinomas. The dopamine agonist piribedil failed to reduce electrically induced 3H-DA release by the superfused median eminence from old rats with prolactinomas, but not from old and young rats without prolactinomas. Old rats without prolactinomas also showed higher serum PRL values and pituitary weight than young rats without prolactinomas. However, stalk blood DA values before and after nomifensine, electrically induced 3H-DA release by the median eminence in vitro, and inhibition by piribedil of 3H-DA release in vitro were significantly lower in old rats without prolactinomas than in young rats without prolactinomas. Estrogen treatment of young ovariectomized rats for 5 months produced enlarged and hemorrhagic pituitaries and elevated serum PRL values, but reduced the content of stalk blood DA and electrically induced release of 3H-DA by the median eminence in vitro as compared with values in untreated young ovariectomized control rats. Estrogen-treated rats also showed no response to piribedil on in vitro 3H-DA release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Decreased ability of old male rats to secrete luteinizing hormone (LH) is not due to alterations in pituitary LH-releasing hormone receptors.

The present study was undertaken to determine if the diminished release of LH in male rats with age in response to castration or LHRH injection is due to alternations in the number or affinity of LHRH receptors in the pituitary. Young (3-4 months old) and old (18-20 months) male Sprague-Dawley rats were killed 0, 2, 4, and 8 days after castration. Serum was collected for determination of LH concentrations, and anterior pituitaries were removed for analysis of LHRH receptors. The numbers and affinity constants of receptors were determined by Scatchard analysis using iodinated des-Gly10-[D-Ala6]LHRH ethylamide (LHRH-a) as ligand. Plasma LH in young rats increased from 54 ng/ml in intact animals to 319 ng/ml 8 days after castration, but in old animals, LH increased only from 47 to 119 ng/ml during the same period (P less than 0.01). However, there were no age-related differences in LHRH receptors in intact animals, and both young and old animals showed similar increases in pituitary LHRH receptors after castration when expressed either as receptors per pituitary (young, 132 +/- 27 to 262 +/- 43 fmol/pituitary; old, 175 +/- 27 to 299 +/- 19 fmol/pituitary) or as receptors per mg protein (young, 420 +/- 48 to 847 +/- 172 fmol/mg protein; old, 432 +/- 38 to 866 +/- 62 fmol/mg protein). Receptor affinity was not statistically different in intact young or old animals (4.51 +/- 0.41 X 10(9) and 4.51 +/- 1.23 X 10(9) M1, respectively), and receptor affinity increased in both groups in response to castration. The capacity of young and old male rats to produce LHRH receptors in response to exogenous LHRH was tested in a second experiment. Animals were castrated and given daily injections of testosterone propionate (500 micrograms/kg, im) for 13 days. Beginning on day 9, LHRH-a (250 micrograms/kg, sc) was injected for 5 days. The rises in serum LH after a single injection of LHRH-a were similar in young and old animals on the first and fifth days of LHRH-a treatment. LHRH receptors at the cessation of hormone therapy also increased similarly in both young and old animals in response to LHRH-a (715 +/- 135 and 811 +/- 203 fmol/mg protein, respectively). Receptor affinity was not statistically different in young (6.27 +/- 0.40 X 10(9) M-1) or old (6.67 +/- 0.79 X 10(9) M-1) animals. In a third experiment, male rats were castrated and given injections of LHRH (166 ng/kg) at 30-min intervals for 4.5 h.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗

PubMed1984

Decline of tuberoinfundibular dopaminergic function resulting from chronic hyperprolactinemia in rats.

The effect of hyperprolactinemia on tuberoinfundibular dopaminergic (TIDA) neurons was studied after sc transplantation of a PRL-secreting pituitary tumor (MtT.W15) to young female rats. TIDA activity was determined by measuring the concentration of dopamine (DA) in pituitary stalk portal blood, the uptake and release of [3H]DA by the median eminence in vitro, and the presynaptic DA receptor activity. Eight weeks after transplantation of the tumor, serum PRL increased to approximately 100 times higher values than those in nontumor-bearing animals. Both the DA concentration and the content in pituitary stalk blood collected from rats bearing tumors for 6 weeks were significantly lower than those in nontumor-bearing rats. Injection of a DA uptake blocker, nomifensine, significantly increased stalk blood DA in nontumor-bearing rats, but did not increase DA release in tumor-bearing rats. The uptake of [3H]DA in vitro by the median eminence of rats bearing pituitary tumors for 8 weeks was lower than that in control rats. Basal and electrically induced release of [3H]DA from the median eminence in vitro from rats with tumors for 8 weeks were also significantly lower than in rats without tumors. Piribedil, a DA receptor agonist, reduced stimulated release of [3H]DA in vitro from the median eminence of rats without tumors, presumably by activating presynaptic DA receptors. However, piribedil had no effect on release of [3H]DA from the median eminence of rats with tumors. These results indicate that chronic elevation of PRL can produce a decline in TIDA function.

Animals↗

PubMed1984

Reduced ability of old male rats to release ACTH and corticosterone in response to CRF administration.

A single injection of oCRF at either 2 or 15 micrograms/kg BW was given to old (19-21 mo) and young (4 mo) male rats, and plasma ACTH and corticosterone (CORT) were measured. Both doses of CRF caused a significant increase in plasma ACTH by 5 min in both age groups (p less than 0.01), but young rats had significantly greater ACTH levels by 25 min after injection (p less than 0.05) compared with old. Plasma CORT in both age groups was significantly elevated (p less than 0.01) above preinjection values by 5 min after either dose of CRF. However at 5, 15, and 25 min, young animals had significantly greater levels of CORT (p less than 0.05) compared with old. These results indicate that old male rats have a diminished capacity to secrete ACTH in response to oCRF; this decreased sensitivity may be responsible for decreased release of ACTH and CORT observed in old rats in response to stress.

Adrenocorticotropic Hormone↗

PubMed1984

Failure of high dietary fat to influence serum prolactin levels during the estrous cycle in female Sprague-Dawley rats.

The influence of a 20% high-fat and a 4.5% control fat diet on circulating prolactin levels was determined during the estrous cycle of intact female rats, and during a progesterone-induced surge of prolactin in ovariectomized, estrogen-primed rats. An indwelling right atrial cannula was implanted into each rat to facilitate repeated blood sampling in conscious, undisturbed animals. No differences in serum prolactin levels were observed at any time during the estrous cycle or in the progesterone-induced surge of prolactin in rats fed either the high-fat or control fat diet. There also were no differences in the estrous cycles of rats on high- or low-fat diets. It is concluded that high dietary fat promotes mammary tumor development by a mechanism that does not involve alterations in circulating prolactin levels or of estrous cycles.

Animals↗

PubMed1984

Counteraction by morphine of stress-induced inhibition of growth hormone release in the rat.

The purpose of this study was to determine the effect of morphine (MOR) administration on pituitary growth hormone (GH) release during stress in the male rat. Circulating GH levels were significantly decreased following a brief (2 min) exposure to either, during repetitive etherization coupled with blood withdrawal, and during continuous immobilization. Under all three stress conditions, systemic administration of MOR resulted in a significant increase in plasma GH levels compared to the vehicle-treated group. These results indicate that the pathway for opiate-induced stimulation of GH release is functional during stress, and suggest that the suppressive effect of stress does not involve a blockade of opiate receptor stimulation of GH. Thus, the present findings, taken together with reports that the overall activity of central opioid neurons is enhanced during stress, support the view that the decline in GH is due to the overriding inhibitory influence of an independent nonopioid mechanism. However, MOR can apparently increase opiate receptor stimulation sufficiently to counteract this inhibitory signal, implying that stress and the opiates may influence GH release via separate mechanisms.

Animals↗

PubMed1984

Counteraction by naltrexone of stress-induced inhibition of TSH release: role of noradrenergic system.

The purpose of the present study was to examine the effect of administering an opiate receptor antagonist, naltrexone (NALT) on the decline in pituitary thyrotropin (TSH) release induced by both acute and chronic stress, and to determine whether norepinephrine (NE) is involved in the mechanism by which opiate receptor blockade counteracts inhibition of TSH release during stress. Administration of NALT, a specific opiate receptor antagonist, significantly attenuated the decrease in plasma TSH observed after acute exposure to ether or restraint stress. The ability of NALT to prevent suppression of circulating TSH in ether-stressed rats was blocked by pharmacological suppression of NE activity induced by pretreatment with diethyldithiocarbamate (DDC) or phenoxybenzamine (PB), both NE antagonists. In chronically stressed rats, thrice daily injections of NALT attenuated the sustained decline in circulating TSH, and resulted in a significant elevation in plasma TSH when compared with stressed, saline-treated animals. Pretreatment with DDC prior to NALT injection abolished this stimulatory effect of NALT. These observations indicate that opiate/receptor interaction is prerequisite for the decrease in circulating TSH release during both acute and chronic stress, and support the hypothesis that endogenous opioid peptides (EOPs) mediate the suppressive effect of stress on TSH release. The finding that uninterrupted NE function is necessary for NALT's action on TSH release during stress suggests that the suppressive effect of stress on TSH and its reversal by opiate antagonists involves alterations in hypothalamic NE activity.

Animals↗

PubMed1984

Promotion of 7,12-dimethylbenz[a]anthracene-induced mammary tumorigenesis by high dietary fat in the rat: possible role of intercellular communication.

The effect of high levels of dietary fat on the promotion phase of rat mammary tumorigenesis and the effect of unsaturated and saturated fatty acids on metabolic cooperation in hamster cells were examined. Female Sprague-Dawley rats were given iv injections of 5 mg 7,12-dimethylbenz[a]anthracene (DMBA) and subsequently placed on 20% high-fat (HF) and 4.5% corn oil control (CF) diets. Rats treated with DMBA and fed HF diet for the entire duration of the experiment developed more tumors with shorter latency than rats fed CF diet for the entire experiment. Rats fed HF diet for 3 weeks at different times after DMBA treatment showed similar, enhanced mammary tumor development. Lengthening the duration of HF diet treatment (0, 3, 6, 16 wk) increased mammary tumor development, suggesting a time dose-response relationship. Removal of the HF diet treatment partially reversed its stimulatory effects on tumor development. These results indicate that dietary fat acts as a classical tumor promoter to enhance mammary tumorigenesis. The influence of unsaturated and saturated fatty acids on metabolic cooperation between 6-thioguanine-sensitive (6-TGS) and 6-thioguanine-resistant (6-TGr) Chinese hamster V79 cells was examined. Linoleic acid, palmitoleic acid, and arachidonic acid significantly increased the recovery of 6-TGr cells at noncytotoxic concentrations. Stearic acid, palmitic acid, and arachadic acid had no effect on the recovery of 6-TGr cells at either cytotoxic or noncytotoxic concentrations. These results demonstrate that unsaturated fatty acids but not saturated fatty acids can inhibit metabolic cooperation between Chinese hamster V79 cells, and suggest, mechanistically, that high dietary levels of polyunsaturated fat could promote tumorigenesis by inhibition of intercellular communication.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1984

Role of estrogen and prolactin in stimulation of carcinogen-induced mammary tumor development by a high-fat diet.

The role of estrogen and prolactin in high-fat (HF) dietary stimulation of carcinogen-induced mammary tumors was examined in female Sprague-Dawley rats. At 55 days of age, the rats were given injections i.v. of 5 mg of dimethylbenz(a)anthracene and, 5 days later, rats were sham- or bilaterally ovariectomized. Ten days after dimethylbenz(a)anthracene administration, the rats were placed on either a 20.0% HF diet or a 4.5% control fat (CF) diet and were then subjected to various drug and endocrine treatments to maintain uniform levels of circulating estrogen and prolactin. Sham-operated intact rats and bilaterally ovariectomized rats were given daily injections of haloperidol to increase prolactin secretion, bromocryptine to decrease prolactin secretion, and/or estradiol benzoate (EB). The intact rats fed the HF diet showed significant stimulation of all parameters of mammary tumor development when compared to similarly treated rats fed the CF diet. In ovariectomized rats fed either the HF or CF diet, there was nearly complete inhibition of mammary tumor development. When the HF diet was given to ovariectomized rats treated daily with either haloperidol or EB, or EB and bromocryptine, some parameters of mammary tumor development were enhanced by the HF diet. However, in all cases, mammary tumorigenesis was reduced when compared to sham-operated control rats. Ovariectomized rats fed the HF diet and given both EB and haloperidol exhibited significantly greater tumor number per rat, increased average tumor size, and reduced tumor latency period when compared to similarly treated rats fed the CF diet. However, these parameters of mammary tumorigenesis were still reduced when compared to those of sham-control rats fed the HF diet. These results indicate that a HF diet requires adequate circulating levels of estrogen and prolactin to maximally promote increased mammary tumorigenesis in dimethylbenz(a)anthracene-treated rats. Moreover, the enhancing effects of a HF diet on mammary tumorigenesis can be achieved in the presence of similar circulating levels of estrogen and/or prolactin, whether decreased or increased. These results suggest, therefore, that mechanisms independent of altered secretion of estrogens and/or prolactin are involved in promotion of mammary tumorigenesis by high levels of dietary fat.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1983

Immunoreactive beta-endorphin in the plasma, pituitary and hypothalamus of young female rats on the day of estrus and intact and chronically castrated old constant estrous female rats.

Immunoreactive beta-endorphin (IR-beta-ENDO) was compared in the plasma, pituitary and hypothalamus of young female rats on the day of estrus and old constant estrous (CE) female rats, and in intact and chronically castrated old CE female rats. The concentration of IR-beta-ENDO in the plasma and the content and concentration of IR-beta-ENDO in the neurointermediate lobe of the pituitary were significantly greater in the old CE female rats than in the young female rats on the day of estrus. The content and concentration of IR-beta-ENDO in the anterior pituitary and hypothalamus were similar in the two age groups. To determine if estrogen contributed to the increase in plasma and pituitary levels of IR-beta-ENDO observed in the old animals, a group of old CE female rats were castrated and compared to sham operated control CE rats. Thirty days after castration, levels of plasma, pituitary and hypothalamic IR-beta-ENDO were comparable in the intact and the chronically castrated old female rats. These data indicate that in old CE female rats, plasma and pituitary IR-beta-ENDO are significantly increased in comparison to young female rats on the day of estrus, and that these increased levels of IR-beta-ENDO observed in old female rats do not appear to be influenced by gonadal estrogen.

Aging↗

PubMed1983

Effects of ovariectomy and steroid replacement on hypothalamic LHRH content in aging female rats.

To examine the role of age on the hypothalamic LHRH response to ovariectomy (ovx) and steroid replacement, young cycling (3-4 months) and old constant estrous (18-20 months) rats were ovariectomized. Two weeks later, rats were treated for 5 days with estradiol benzoate (E, 5 micrograms/kg), progesterone (P, 10 mg/kg), E + P (5 micrograms E + 10 mg/kg) or corn oil, after which time they were killed for determination of hypothalamic LHRH content. The young and old ovx rats had similar levels of LHRH in the medial basal (MBH) and anterior (AH) hypothalamus, but E treatment was only effective in increasing MBH-LHRH content in the young animals. There was no significant effect of P alone or in combination with E. In the second experiment, similar results were seen using a single dose of E (1 microgram/rat) in young and old ovx rats. In addition, the radioimmunoassay of LHRH using two different antibodies binding to different portions of LHRH gave similar results in young and old rats, suggesting that the LHRH peptide was being processed similarly in the two age groups. In conclusion, it appears that hypothalamic LHRH content of young and old ovx rats does not differ with age despite a marked attenuation of serum LH levels with age. The hypothalamus from old rats, however, is less responsive to steroid stimulation of LHRH content.

Aging↗

PubMed1983

Uptake and release of [3H]dopamine by the median eminence: evidence for presynaptic dopaminergic receptors and for dopaminergic feedback inhibition.

The accumulation and release of [3H]dopamine by the median eminence in vitro was studied after treatments with different pharmacological agents, to determine whether such a procedure would be useful for measuring neuronal activity in the tuberoinfundibular dopaminergic system. The accumulation of [3H]dopamine was temperature, time, and sodium dependent, and reduced by unlabelled dopamine and by a potent dopamine uptake blocker, nomifensine. The outflow of tritium was studied after blocking the oxidative deamination of dopamine by nialamide. The outflow of tritium was elicited consistently by biphasic square wave electrical pulses and by high molarity potassium ions. The response to electrical stimulation was dependent largely on calcium and partially on sodium. The response to high molarity potassium ions was reduced in the absence of calcium ions. The response to electrical stimulation was increased by nomifensine and by a dopaminergic antagonist, haloperidol, and was reduced by dopamine and by a dopaminergic agonist, piribedil. The inhibitory action of dopamine was antagonized by haloperidol. These results indicate the existence of uptake and release mechanisms in the tuberoinfundibular dopamine neurons, and suggest that dopamine may inhibit its own release via dopaminergic receptors. This in vitro method may be useful for measuring dopamine uptake and release by tuberoinfundibular dopaminergic neurons.

Animals↗

PubMed1983

Failure of prolactin short loop feedback mechanism to operate in old as compared to young female rats.

The short loop feedback effect of PRL was studied in young (4-5 months of age) and old (24-26 months of age) ovariectomized rats after a single iv injection of bovine PRL (bPRL, 500 micrograms/100 g BW) or BSA (500 micrograms/100 g BW). Blood samples were collected via intraatrial cannula every 20 min for assay of PRL. Plasma PRL levels in both young and old ovariectomized rats were pulsatile in nature, and showed approximately one PRL pulse per hour. The magnitude of the PRL peaks and concentrations of plasma PRL, but not the number of PRL peaks, were significantly greater in the old than in the young rats. The effect of bPRL on in situ PRL release was studied after verifying that bPRL does not cross-react with rat PRL RIA, but does significantly increase the release of [3H] dopamine from the median eminence in vitro. This latter effect was dose dependent. In young rats, a single injection of bPRL minimally reduced the concentration of plasma PRL between 100 min and 5 h, but by 22-25 h it decreased plasma PRL to approximately one third of preinjection levels. The magnitude of the PRL pulses, but not the pulse frequency was significantly reduced after administration of bPRL treatment to young rats. Treatment with BSA did not alter the concentration of plasma PRL or the magnitude and frequency of the PRL pulses in young rats. In old rats, plasma PRL concentrations and the frequency and magnitude of the PRL pulses were not significantly decreased after injection of either bPRL or BSA. Thus, the feedback inhibition of PRL on PRL release may not be operative in old rats. The loss of the short loop feedback inhibition of PRL is believed to be due to the reduction in hypothalamic dopaminergic activity previously reported by our and other laboratories in old rats.

Aging↗

PubMed1983

Impaired ability of old male rats to secrete growth hormone in vivo but not in vitro in response to hpGRF(1-44).

The capacity of hpGRF (1-44) to induce release of GH in young (3-4 month old) versus old (19-21 month old) male rats was compared in vivo and in vitro. Injection of 1 ug/kg hpGRF to rats anesthetized with sodium pentobarbital increased plasma GH concentrations in young animals to greater than 1600 ng/ml within 5 min, and a dose of 10 ug/kg hpGRF increased GH levels to approximately 1900 ng/ml at 10 min. In old rats, plasma GH concentrations were increased after hpGRF but the increases were significantly lower than in the young rats at 5, 10, and 20 min after injection (P less than 0.01). The total GH released in old animals was calculated to be approximately 50% of that in young animals. In vitro release of GH from anterior pituitary slices incubated with hpGRF was also compared between young and old animals. After 20 min incubation with hpGRF (10(-9) or 10(-7) M) or vehicle, both young and old animals demonstrated a dose related and equivalent increase in GH release. These results indicate a reduced capacity of hpGRF to stimulate GH release in vivo in aged as compared to young male rats. This decline is believed to be due to a hypothalamic influence on the anterior pituitary since the in vitro response of anterior pituitary tissue to hpGRF was similar in young and old rats. The reduced response to hpGRF in old male rats in vivo may be due to increased release of or enhanced sensitivity to somatostatin.

Aging↗

PubMed1983

Elevation of plasma LH in response to systemic injection of beta-endorphin antiserum in adult male rats.

A single injection of beta-endorphin antiserum into mature male rats produced approximately a 3-fold rise in plasma LH levels by 10 to 50 min, and declined by 90 min, but remained significantly elevated above pre-injection values. Control rats injected with normal rabbit serum showed no elevation in plasma LH values. These results indicate that beta-endorphin is one of the endogenous opiates that tonically depresses basal release of LH in mature male rats.

Animals↗