Effect of vagotomy on postcastration gonadotropin secretion in male rats

The postcastration increase in gonadotropins was studied in intact and vagotomized male rats. Rats underwent vagotomy or sham surgery immediately prior to castration. In the first experiment, rats were bled before castration and at 1, 2, 4, and 7 days after castration. Serum LH and FSH were significantly lower in vagotomized rats 1 day after castration. On days 2, 4, and 7 postcastration, serum gonadotropin levels were generally not different among experimental groups. In a second experiment, rats were decapitated at 12 or 24 hr after surgery and castration. Trunk blood was collected for assay of LH. Vagotomy had no effect on LH levels at 12 hr postcastration, but, at 24 hr postcastration, vagotomized rats had significantly lower serum LH than did sham-operated rats. These experiments indicate that vagotomy has a transient suppressive effect on gonadotropin release following castration. Such observations support the hypothesis that the vagus nerve may play a modulatory role in gonadotropin secretion.     

Basal and LH-RH-stimulated gonadotropin release after transport stress in male rats

A total of 120 male rats of the Sprague-Dawley-strain (6 weeks old) were used in this experiment. 5 groups of 12 animals each were treated intraperitoneally with 200 ng gonadotropin releasing hormone (LH-RH) per animal. 30 minutes later blood was sampled by heart puncture. Group I were animals without transport, group II immediately after, group III one day, group IV one week and group V six weeks after a standardised transport. Another 5 groups were subjected to the same protocol but received saline i.p. instead of LH-RH. Serum levels of LH and FSH were estimated by radioimmunoassay. LH and FSH serum levels could be stimulated by LH-RH in all groups. A significant rise of basal and LH-RH stimulated LH levels was observed until the first day after transport. Thereafter a drop was registered. No consistent patterns of basal as well LH-RH stimulated FSH-levels were noted. These data combine to suggest an elevation of LH-RH secretion as response to the stress. This results in a sensibilisation of the pituitary to exogenous LH-RH.     

Effect of CRF in the median eminence on gonadotropin levels in conscious female rats

To evaluate whether the median eminence (ME) is the site of action of CRF (corticotropin releasing factor) in inhibiting LH levels in female rats, we have injected CRF (1 nmol) directly into the ME and then measured plasma LH and FSH concentrations in conscious ovariectomized (OVX) rats in the absence or presence of a single dose of estradiol benzoate (EB). CRF caused a significant decrease in plasma LH levels in both OVX and OVX + EB rats at 30 min postinjection, in comparison to the values obtained in animals injected with water only. Injection into the ME of water had no effect on plasma LH levels in either OVX or OVX + EB animals. The results suggest that CRF probably inhibits LH secretion, at least in part by a central action on GnRH release in ME.     

The effect of beta-endorphin on basal and TRH-stimulated TSH release in conscious male rats

The inhibitory effect of beta-endorphin (EP) or other opioids on TSH secretion is, in contrast to their stimulating properties on PRL release, still a matter of debate. In the present study a dose of 1 microgram beta-EP injected intracerebroventricularly (IVT) in unstressed conscious male rats, though highly effective on PRL release, did not affect basal TSH levels, nor the TRH-induced TSH secretion. The previously reported inhibition of TSH release by opioids may therefore be an effect only seen when pharmacological doses are used.     

Effect of chorionic gonadotropin on the content of prostaglandins (E + A) in pathologically altered liver tissue and blood of rats

Twenty-four and 48 hours after injection of chorionic gonadotropin (CG) the content of prostaglandins E + A in the liver and blood plasma of white random-bred rats with chronic hepatitis increases (both after and without castration). This accounts for some aspects of the mechanism of the CG-induced stimulation of liver regeneration, which results in structural and functional normalization of the organ.     

Reduced gonadotropin release in response to progesterone or gonadotropin releasing hormone (GnRH) in old female rats

Ovariectomized rats that were 3–4, 12 or 22 months old were injected s.c. with 4 mg, of testosterone propionate and 3 days later were injected s.c. with 2.8 mg. progesterone or the oil vehicle. Blood samples were collected by heart puncture 5 hrs. later. Serum levels of LH and FSH decreased significantly as age increased. Progesterone significantly increased serum LH and FSH levels regardless of age. The increase in serum LH concentration attributed to progesterone was greatest in the young and least in the old rats. To determine if age effects were due to differences in pituitary response to GnRH, ovariectomized rats that were 2.5 to 23 months old were injected i.v. with GnRH at doses of 100 ng or 40 ng/100 g body weight or were primed with 25 mg progesterone and 50 μg estradiol-benzoate 3 days before an injection of 2 ng GnRH/100 g body weight. Blood was obtained by heart puncture before and 20 min. after GnRH. In each experiment serum LH levels significantly decreased with increasing age but were significantly elevated by GnRH. This increase in serum LH level in response to GnRH declined with increasing age. The data suggest that the elevation in serum LH level in response to GnRH declines as a result of aging in female rats and that this effect is independent of circulating ovarian steroid levels.     

A self-calibrating telemetry system for measurement of ventricular pressure-volume relations in conscious, freely moving rats

Using Bluetooth wireless technology, we developed an implantable telemetry system for measurement of the left ventricular pressure-volume relation in conscious, freely moving rats. The telemetry system consisted of a pressure-conductance catheter (1.8-Fr) connected to a small (14-g) fully implantable signal transmitter. To make the system fully telemetric, calibrations such as blood resistivity and parallel conductance were also conducted telemetrically. To estimate blood resistivity, we used four electrodes arranged 0.2 mm apart on the pressure-conductance catheter. To estimate parallel conductance, we used a dual-frequency method. We examined the accuracy of calibrations, stroke volume (SV) measurements, and the reproducibility of the telemetry. The blood resistivity estimated telemetrically agreed with that measured using an ex vivo cuvette method (y=1.09x - 11.9, r2= 0.88, n=10). Parallel conductance estimated by the dual-frequency (2 and 20 kHz) method correlated well with that measured by a conventional saline injection method (y=1.59x - 1.77, r2= 0.87, n=13). The telemetric SV closely correlated with the flowmetric SV during inferior vena cava occlusions (y=0.96x + 7.5, r2=0.96, n=4). In six conscious rats, differences between the repeated telemetries on different days (3 days apart on average) were reasonably small: 13% for end-diastolic volume, 20% for end-systolic volume, 28% for end-diastolic pressure, and 6% for end-systolic pressure. We conclude that the developed telemetry system enables us to estimate the pressure-volume relation with reasonable accuracy and reproducibility in conscious, untethered rats.     

Pulsatile release of immunoreactive luteinizing hormone (irLH) in hypophysectomized male rats

The concentration of plasma luteinizing hormone (LH) was monitored every minute by radioimmunoassay in male rats that were either hypophysectomized, or castrated and hypophysectomized. Castrated rats showed a pulsatile fluctuation of plasma immunoreactive LH (irLH) concentration with an elevated basal level, confirming previous work. The hypophysectomized and castrated hypophysectomized rats also showed pulsatile changes in plasma irLH concentration. This unexpected result indicates that ectopic irLH is not only actively released after hypophysectomy, but is released in pulses. The pulse interval was approximately 20 minutes for all 3 groups. The slope of the rate of decline of plasma irLH in the castrated rats is parallel to a theoretical disappearance rate of 5 min, while these slopes in the hypophysectomized and castrated hypophysectomized rats correspond to a 1 to 2-min disappearance rate. The difference in these slopes implies that the two irLH molecules may not be identical.     

Effect of gonadotropin (FSH-LH) and thyrotropin (TSH) treatment in adolescence on TSH-sensitivity in adult rats

Hormonal imprinting is characteristic of the neonatal age, in which the receptor of the target cell matures, i.e. acquires its adult binding capacity, and cellular response becomes established in presence of the adequate hormone. The normal course of imprinting may be altered by certain molecules (related hormones, hormone analogons) which are able to bind to the receptor of the adequate hormone. The chemically related gonadotropic and thyrotropic hormones may overlap on each other's receptors not only in the perinatal age, but also in the early adulthood, and this overlap of the binding may give rise to an imprinting-like effect. An example of this phenomenon was observed in the present study, in which rats of seven weeks of age treated with gonadotropin showed a significant decrease in thyroidic response to TSH, and exposure to TSH failed to increase their basic thyroxine concentration to the normal (control) level. This depressive effect of gonadotropin was slightly reduced in the presence of LPS (endotoxin), causing membrane perturbation, while pretreatment with LPS and TSH accounted for an increased sensitivity to TSH in later phases of the rat's life. These experimental observations support the possibility of a special form of imprinting in adolescence.     

Effect of thyroidectomy on rhythmic gonadotropin release.

Nonstress blood samples were obtained from intact and thyroidectomized (TE) male rats at 3-hr intervals over a 24-hr period via rapid decapitation. The animals were thyroidectomized when 40 days old and used 6 weeks later. Intact animals showed periodicity in serum LH (P less than 0.01) and prolactin (P less than 0.01). Both gonadotropins began increasing after 8 PM and peak levels occurred at 11 PM. In contrast, 24-hr periodicity was not observed in serum FSH. Corticosterone levels in these same serum samples showed the expected circadian periodicity. After TE, the 24-hr pattern in all gonadotropins was altered significantly. Serum LH increased (P less than 0.01) and circadian periodicity appeared to be absent. FSH and prolactin levels were increased and decreased, respectively (P less than 0.01), with serum prolactin showing a 9-hr phase shift. Prolactin began increasing at 2 AM and reached a peak at 8 AM. Corticosterone in TE animals showed a 24-hr rhythm similar to that of intact rats. These findings confirm our previous observations that nonstress serum LH and prolactin levels fluctuate with a 24-hr periodicity and suggest that the level of, and the phase angle betweeen, these rhythms is markedly influenced by pituitary-thyroid activity.     

Central injections of noradrenaline and adrenaline differentially affect plasma free fatty acid and glucose in conscious pigeons (Columba livia)

The possible involvement of central noradrenergic and/or adrenergic circuits in central mechanisms controlling free fatty acids and glucose levels was investigated in conscious pigeons. The effects of intracerebroventricular injections of noradrenaline (80 nmol) or adrenaline (80 nmol) on plasma free fatty acids and glucose concentrations were examined. The possible role of the autonomic nervous system, of sympathetic terminals and of pituitary hormone release in the metabolic responses induced by intracerebroventricular injections of adrenaline and noradrenaline was investigated by systemic pretreatment with a ganglionic blocker (hexamethonium, 1 mg/100 g), guanethidine (5 mg/100 g), and somatostatin (15 μg/100 g), respectively, 15 min before intracerebroventricular administration of adrenaline, noradrenaline or vehicle. Intracerebroventricular noradrenaline injections strongly increased plasma free fatty acid concentration but evoked no change in blood glucose levels, while adrenaline treatment increased glycemia without affecting free fatty acid levels. Hexamethonium did not block the increase in plasma free fatty acids induced by noradrenaline, while somatostatin pretreatment abolished noradrenaline-induced lipolysis during the experimental period. Adrenaline-induced hyperglycemia was blocked by systemic injections of somatostatin, hexamethonium and guanethidine. The present results suggest that: (1) adrenergic and noradrenergic mechanisms may participate in central control of blood glucose and free fatty acids, respectively, as observed in mammals, (2) noradrenaline-induced lipolysis may be mediated by pituitary mechanisms, and (3) postganglionic sympathetic fibers, possibly innervating the endocrine pancreas, may be involved in adrenaline-induced hyperglycemia. Accepted: 14 April 2000     

Stimulatory effects of islet amyloid polypeptide (amylin) on exocrine pancreas and gastrin release in conscious rats.

A rat islet amyloid polypeptide (amylin), 37-residue peptide amide was synthesized by the Fmoc-based solid phase method and the biological activity of synthetic rat amylin on exocrine pancreas was evaluated for the first time in conscious rat. Amylin (1, 10 nmol/kg/h) stimulated pancreatic exocrine secretion and plasma gastrin concentration. CR-1409, a CCK receptor antagonist, did not change amylin-stimulated pancreatic secretion. However, omeprazole (proton pump inhibitor) and atropine inhibited amylin-stimulated pancreatic secretion. This study suggests that amylin may play a role in biological action in the exocrine pancreas possibly mediated by gastric acid hypersecretion.     

The role of circulating ghrelin in growth hormone (GH) secretion in freely moving male rats

To examine the physiological significance of plasma ghrelin in generating pulsatile growth hormone (GH) secretion in rats, plasma GH and ghrelin levels were determined in freely moving male rats. Plasma GH was pulsatilely secreted as reported previously. Plasma ghrelin levels were measured by both N-RIA recognizing the active form of ghrelin and C-RIA determining total amount of ghrelin. Mean +/- SE plasma ghrelin levels determined by N-RIA and C-RIA were 21.6 +/- 8.5 and 315.5 +/- 67.5 pM, respectively, during peak periods when plasma GH levels were greater than 100 ng / ml. During trough periods when plasma GH levels were less than 10 ng / ml, they were 16.5 +/- 4.5 and 342.1 +/- 29.8 pM, respectively. There were no significant differences in plasma ghrelin levels between two periods. Next, effect of a GH secretagogue antagonist, [D-Lys-3]-GHRP-6, on plasma GH profiles was examined. There were no significant differences in both peak GH levels and area under the curves of GH (AUCs) between [D-Lys-3]-GHRP-6-treated and control rats. These findings suggest circulating ghrelin in peripheral blood does not play a role in generating pulsatile GH secretion in freely moving male rats.