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At least 307 records · Page 17Linked to original sources
PubMed1975

Electrical stimulation of the median eminence in ovariectomized and estradiol-treated sheep. Increased LH release and evidence for neural regulation of spontaneous LH rhythms.

Plasma LH was significantly increased by electrical stimulation of the median eminence (ME) in ovariectomized and in estradiol-treated sheep. In untreated castrates, spontaneous discharges of LH occurred at regular intervals of approximately one hour (LH rhythm). When ME stimulations were initiated as early as 5-15 min following a spontaneous discharge, they increased LH as much as either ME stimulations initiated at other times or spontaneous discharges. These data failed to demonstrate any pituitary refractoriness to ME stimulation, and presumably to endogenous LH-releasing factor (LRF). Therefore, neural mechanisms involving rhythmic release of LRF were indicated. The chronic administration of estradiol inhibited the spontaneous discharges of LH, and subsequent ME stimulation increased plasma LH even more markedly than in untreated castrates.

Animals↗
PubMed1976

Induction of LH surges by continuous infusion of LH-RH1.

Preovulatory LH surges were measured in cannulated proestrous rats. Such LH peaks were also obtained by infusing pentobarbital-blocked animals with LH-RH for periods of up to 20 h; this suggested that the pituitary LH stores were exhausted. However, the total amount of LH secreted appeared more or less determined by the LH-RH dose, indicating that the size of the releasable LH pool is not fixed.

Animals↗
PubMed1984

Secretion of luteinizing hormone (LH) and pituitary receptors for LH-releasing hormone as modified by the proestrous surge of progesterone.

Pituitary glands of proestrous (PRO) rats display enhanced LH secretory response to LHRH when compared to pituitary glands of estrous (EST) rats. In addition proestrous pituitary glands display a self-potentiating (priming) response to LHRH, whereas estrous pituitary glands do not. This study addresses the role of the proestrous surge of progesterone in converting the proestrous-like LH secretory responses of the pituitary gland to those of estrus. Anterior pituitary glands were obtained from PRO and EST rats. In addition, Pro rats were treated with pentobarbital alone (PRO/PB) or with pentobarbital plus progesterone (PRO/PB-P4). Pentobarbital was given to prevent proestrous surges of LH and progesterone. Pentobarbital-treated animals were killed the day after treatment, estrus. Pituitary glands from each group were tested for LH secretory response in a superfusion chamber with exposure of two 15-min pulses of 10 nM LHRH separated by 90 min, or assayed for LHRH receptor content using iodinated D-Ala6-LHRH. Anterior pituitary glands from PRO rats secreted higher levels of LH than EST rats in response to an LHRH pulse. Only PRO anterior pituitary glands secreted priming responses to LHRH. Though anterior pituitary glands obtained from pentobarbital-treated rats showed LH responses of similar magnitude to anterior pituitary glands of PRO rats after initial LHRH challenge, they did not display priming responses. Progesterone replacement (PRO/PB-P4) led to depressed secretory responses when compared to PRO pituitary glands similar to EST rats. LHRH receptor concentrations in pituitary glands of EST rats was lower than those in pituitary glands of PRO rats. Depression of pituitary LHRH receptor concentration from proestrus to estrus was prevented by pentobarbital-treatment on proestrus. Estrus-like depression of receptor concentration was restored after progesterone treatment (PRO/PB-P4). These data suggest the LHRH receptor depression on estrus is a consequence of the secretion of progesterone on proestrus. Further, the declining magnitude of the in vitro LH-secretory response to LHRH follows a declining LHRH receptor concentration; however no correlation exists between receptor number and ability to prime.

Animals↗
PubMed1987

Effects of luteinizing hormone (LH)-releasing hormone pulse amplitude and frequency on LH secretion by perifused rat anterior pituitary cells.

Recent studies have shown that LH secretion in vivo is pulsatile. In the present study, a cell perifusion system was employed to characterize the pituitary response to changes in LHRH pulse amplitude and frequency. Increases in pulse amplitude consistently elevated both mean LH levels and the amount of LH released in response to individual LHRH pulses. The EC50 for LHRH was approximately 3 nM. Increases in pulse frequency also increased mean LH levels, but frequencies of three or more pulses per h were associated with a decrease in the amount of LH released per pulse. Alterations in LHRH pulse characteristics changed qualitative as well as quantitative aspects of LH secretion, with high frequency, high amplitude pulses producing a biphasic response to LHRH. Initially a self-priming response was seen during the second and third hours of stimulation; this was followed by increasing desensitization of the cultures to LHRH. These results, by defining the pituitary response to specific conditions of stimulation, will help to clarify the relationship of LHRH stimulation to LH secretion in vivo.

Animals↗
PubMed1988

Simultaneous measurement of luteinizing hormone (LH)-releasing hormone, LH, and follicle-stimulating hormone release in intact and short-term castrate rats.

The temporal relationship between LHRH release and gonadotropin secretion as well as the effects of castration on LHRH release were investigated in conscious, freely moving male rats. LHRH release was measured in hypothalamic/median eminence perfusates, while levels of pituitary gonadotropins (LH, FSH) were determined in sequential blood samples obtained via atrial catheters. Twenty-four to 26 h before experiments, rats underwent sham surgery or castration. LHRH release in push-pull perfusates from both groups was pulsatile, and nearly all identified LH pulses (83.3%) were temporally associated with LHRH pulses. Of the fewer irregular FSH pulses that were observed, only 43.7% were temporally associated with LHRH pulses. Mean LHRH pulse amplitude and mean LHRH levels were not different in intact and castrate animals. The frequency of LHRH pulses was moderately increased in castrate rats (1.30 pulses/h) compared to that in intact animals (0.83 pulses/h), and this acceleration was accompanied by a significant increase in LH pulse frequency, pulse amplitude, and mean level. It was also noted that the number of silent LHRH pulses (those not associated with LH pulses) was dramatically reduced in castrate animals. Characteristics of gonadotropin release (pulse frequency, pulse amplitude, and mean level) were not significantly different in animals undergoing push-pull perfusion/bleeding procedures from those in rats not receiving push-pull cannula implants. We conclude from these studies that 1) LH pulses show a high concordance with LHRH pulses, providing evidence that the LHRH pulse generator operates as the neural determinant of LH pulses in male rats, 2) FSH secretion is not associated with LHRH release in an obvious and consistent manner, suggesting that LHRH/FSH relationships are not easily discerned in these animals or that a FSH-releasing factor distinct from the LHRH decapeptide may regulate FSH secretion, 3) a modest increase in LHRH pulse frequency occurs 24-30 h after castration, and 4) silent LHRH pulses occur with much greater regularity in intact than in castrate rats. The latter two observations suggest that both hypothalamic and intrapituitary sequelae of castration may be critically important in the development of postcastration increases in LH secretion and the negative feedback of gonadal steroids.

Animals↗
PubMed1989

Luteinizing hormone (LH)-releasing hormone: effects of induction of LH, follicle-stimulating hormone, and prolactin cell differentiation.

We investigated the influence of LHRH on the differentiation of gonadotrophs and lactotrophs in fetal pituitary glands transplanted beneath the renal capsules of adult hypophysectomized-orchidectomized hamsters (hosts). Hypophyses were removed from hamster fetuses at a gestational age of 14 days. Some of these were immediately fixed in Bouin's solution, and others were transplanted into the hosts. The hosts were injected sc twice daily with 1 microgram LHRH or vehicle for 16 days. Six hosts in each group were killed by decapitation 16 h after the last injection. Six 14-day-old normal male hamsters (age-matched to correspond to the age of the allografts at the time of the hosts' decapitation) also were decapitated. Sections of hypophyses in situ from fetal hamsters, from 14-day-old controls, and from allografts in each group were stained for LH, FSH, or PRL and with hematoxylin. No PRL-containing cells and very few LH or FSH cells (less than 0.025% of the adenohypophysial cell population) were observed in fetal pituitary glands. In allografts from the vehicle-treated hosts, 21.1% of adenohypophysial cells contained LH, but only 1.8% contained FSH. In allografts from LHRH-treated hosts, 28.0% and 22.9% of the adenohypophysial cells contained LH and FSH, respectively. Adenohypophyses that developed for the same length of time in situ had smaller percentages of adenohypophysial cells containing LH (23.8%) and FSH (15.5%) than the LHRH-treated group. LH-containing cells in allografts in the vehicle-treated hamsters, but not in the LHRH-treated animals, were reduced in size compared to those measured in situ. The number of lactotrophs in all allografted tissue was markedly reduced compared to that of lactotrophs in situ, and injection of LHRH into hamsters with allografts did not alter the percentage of adenohypophysial cells that were lactotrophs. These results suggest that in the hamster LHRH 1) plays an important role in stimulating the formation of immunoreactive FSH in the pituitary gland, 2) can increase the number of gonadotrophs that develop during the neonatal period, and 3) plays a role in controlling the size of gonadotrophs during development. The results also suggest that the development of lactotroph cell number requires close proximity to the hypothalamus and/or exposure to a neonatal environment. We found no evidence to support the view that LHRH, LH, or FSH stimulates immunoreactive lactotroph differentiation.

Animals↗
PubMed1990

Luteinizing hormone (LH)-releasing hormone: chronic effects on LH and follicle-stimulating hormone cells and secretion in adult male rats.

We investigated whether chronic administration of LHRH to normal adult rats could increase the percentages of anterior pituitary gland (APG) cells that contain immunoreactive LH and/or FSH and gonadotropin secretion. Vehicle or 1 microgram LHRH was injected sc twice daily for 6 days, and rats were decapitated 16 h after the last injection. Treatment with LHRH caused nearly a doubling in the numerical density of LH and FSH cells and in the percentage of APG cells that contained LH or FSH. It also caused a shift in the gonadotroph population from LH and LH/FSH cells to LH/FSH cells. It did not change the mean size of gonadotrophs or APG weight. These changes at the light microscopic level were not accompanied by any apparent changes in LH cells at the ultrastructural level. However, they were accompanied by an approximate doubling of the basal serum LH and FSH concentrations, an increase in the APG FSH concentration, and an increase in the basal FSH release rate (measured in vitro). The results indicate that exogenous LHRH can be administered to increase numbers of gonadotrophs in the APG, synthesis of FSH in gonadotrophs, and basal serum LH and FSH concentrations.

Animals↗
PubMed1994

Changes in pulsatile release of neuropeptide-Y and luteinizing hormone (LH)-releasing hormone during the progesterone-induced LH surge in rhesus monkeys.

In previous studies we have shown that the pulsatility of LH-releasing hormone (LHRH) release in gonadectomized monkeys is modulated by input from neuropeptide-Y (NPY) neurons: 1) the endogenous release of NPY in the stalk-median eminence (S-ME) was pulsatile; 2) NPY pulses were temporally correlated with LHRH pulses, with NPY pulses preceding LHRH pulses by approximately 5 min; and 3) infusion of NPY into the S-ME stimulated LHRH release, whereas 4) infusion of antiserum to NPY suppressed endogenous LHRH pulses. It is not known, however, whether ovarian steroid hormones alter the pulsatility of NPY and LHRH release or whether the temporal correlation of NPY and LHRH pulses is maintained during the LH surge. In the present study we examined the changes in pulsatile release of NPY and LHRH in ovariectomized monkeys treated with estradiol benzoate (EB) followed by progesterone or oil. Using push-pull perfusion, perfusate samples from S-ME were collected at 10-min intervals for 15 h. NPY and LHRH concentrations in the perfusates were measured by RIA. Circulating LH levels were also monitored by periodic blood sampling and RIA. Injection of progesterone (sc) after EB induced an LH surge with a peak latency of 7.3 +/- 1.3 h (mean +/- SE) in seven of seven monkeys, whereas oil injection after EB elicited an LH surge in none of seven monkeys. The progesterone-induced LH surge was associated with an increase in LHRH release; the mean, pulse amplitude, and pulse frequency increased significantly (for all, P < 0.05) 4-8 h after progesterone. NPY pulse frequency also increased significantly (P < 0.05) 4-8 h after progesterone treatment, whereas mean release and pulse amplitude did not change in response to progesterone. Oil treatment after EB administration did not alter any parameter of LHRH and NPY pulses. Interestingly, the NPY and LHRH pulses were highly correlated (P < 0.001) in monkeys treated with either EB-progesterone or EB-oil, and NPY pulses preceded LHRH pulses by 4.8 +/- 0.7 and 5.1 +/- 0.6 min, respectively. In summary, 1) an episode of increased LHRH release occurs before and during the progesterone-induced LH surge; 2) acceleration of LHRH pulse frequency and the increase in LHRH pulse amplitude after progesterone are accompanied by acceleration of NPY pulse frequency; and 3) ovarian steroids do not affect the temporal correlation between NPY and LHRH pulses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1978

Dose-response study with a new LH-RH analogue, D-Ser (TBU)6 LH-RH 1-9 (EA)10 during the follicular phase of the menstrual cycle.

D-Ser (TBU)6 LH-RH 1-9 (EA)10 (HOE 766) a highly active LH-RH analogue, was studied with regard to its effects on the release of follicle stimulating hormone (FSH), luteinizing hormone (LH) and oestradiol-17beta (Oe2) during the follicular phase of the menstrual cycle. Forty-two regularly menstruating women were allowed to five different treatment groups with different doses (1.25 microgram; 2.5 microgram; 5.0 microgram; 10.0 microgram; 20.0 microgram) of HOE 766 given as intravenous bolus injections and the plasma concentrations of FSH, LH and Oe2 were measured up to 24 h after injection using specific radioimmunoassays. In the majority of cases, peak values of both FSH and LH occurred 4 h after injection being significantly different from pre-injection levels (P less than 0.02 in the 1.25 microgram treatment group, P less than 0.005 for the other treatment groups). Statistical analysis of maximum values as well as the absolute and relative increase in the different treatment groups revealed a dose-dependent effect of HOE 766. Maximum values of Oe2 occurred 8 h after injection and were found to be significantly different from pre-injection levels (P less than 0.005). However, no dose dependent effect was observed. It was concluded that HOE 766 is a potent and long-acting stimulator of FSH, LH and OE2 release in women. The effect of HOE 766 is dose dependent for FSH and LH but not for Oe2.

Adult↗
PubMed1979

The plasma FSH and LH response to synthetic LH-RH in normal pre-pubertal and early pubertal girls--a re-evaluation.

A standard LH-RH test (50 microgram/m2) given iv was carried out in 65 normal girls, 42 of them pre-pubertal aged from 4 7/12 to 11 years and 23 in the early stage of puberty, aged from 9 to 12 9/12 years. The results indicate that in pre-pubertal girls the basal levels of the plasma gonadotrophins remain steady (LH 0.6 +/- 0.1 mIU/ml; FSH 0.8 +/- 0.1 mIU/ml, m +/- SD) and that there is a small but significant response of LH to LH-RH (1.6 +/- 0.2 mIU/ml). During this period the FSH response to LH-RH is very marked (8.0 +/- 1.0 mIU/ml) with a gradual, significant decrease seen towards the onset of puberty (6.5 +/- 0.9 mIU/ml, P less than 0.001). These results support earlier reports that the LH-RH test is a useful tool to evaluate the secretion of pituitary LH and FSH in early childhood.

Adolescent↗
PubMed1981

Changes in pituitary LH content and LH secretion in the long-term ovariectomized rat during prolonged infusion of LRH.

LH secretion and the depletion of the pituitary LH stores caused by continuous infusion of LRH, were studied in the 5-weeks ovariectomized rat. After 1 day of infusion at the rate of 416 ng/h, pituitary LH content decreased to about 40% of its initial value. Upon continuation of the infusion the LH content increased slowly until, after 7 days, it increased to about 54% of the original value. The plasma LH concentrations, after having reached peak values of 7122 +/- 291 ng/ml after 2 h of infusion, declined to a plateau at about 300 ng/ml but it took 5 days to reach this value. When after either 2 or 8 days of LRH infusion at the rate of 416 ng/h the infusion was changed to a 'supramaximal' rate of 10,400 ng/h for 24 h, a transient secondary rise of LH secretion was induced. The magnitude of the secondary response, was essentially the same after 2 or 8 days of LRH infusion, but these secondary responses were significantly smaller than the LH-response during a similar LRH-infusion in previously untreated ovariectomized rats.

Animals↗
PubMed1981

Inadequate corpus luteum function after the induction of ovulation in anoestrous ewes by LH-RH or an LH-RH agonist.

Scottish Blackface ewes were given LH-RH (3 x 30 micrograms i.v., at 90 min intervals) or D-Ser-(But)6-des Gly10 LH-Rh ethylamide (LH-RH agonist) as a single injection (8 or 40 micrograms) during anoestrus. Ovulation as judged by laparoscopy occurred in 8 of the 27 animals. Despite the fact that the LH-RH agonist induced a greater release of LH and FSH the different treatments had no effect on the number of ewes ovulating and within each treatment group there was no apparent difference in the amounts of gonadotrophins released between the ewes that did or did not ovulate. All ovulations resulted in the formation of CL associated with plasma progesterone concentrations of less than 1 ng/ml (1--5 ng/ml in the normal luteal phase). In comparison with CL of the normal cycle the induced CL were of lower weight and had reduced progesterone content and ability to secrete progesterone in vitro. However, the binding of hCG was equivalent to that of normal CL. These results suggest that the inadequate CL formed in anoestrous ewes after a single LH-RH injection have not developed the ability to synthesize and secrete progesterone in spite of the presence of normal amounts of LH receptors.

Animals↗
PubMed1983

Differential effects of LH-RH immunoneutralization on LH and FSH secretion in the ewe.

Neutralization of LH-RH by injection of an ovine antiserum to LH-RH in ewes during the late follicular phase of the oestrous cycle resulted in an immediate blockade of pulsatile secretion of LH. Plasma concentrations of FSH gradually rose in the antiserum-treated ewes during the 36-h study period but levels declined in control ewes. These results show that, in the ewe, pulsatile LH secretion is dependent on LH-RH from the hypothalamus, while FSH is largely unresponsive to short-term reduction of LH-RH stimulation. Since reduction in LH secretion is likely to reduce ovarian function, the changes in FSH secretion may be attributed to the removal of a negative feedback influence of an ovarian factor, perhaps oestradiol, on FSH secretion.

Animals↗
PubMed1994

Acute changes in pulsatile LH and FSH secretion after ovariectomy in rats: treatment with oestradiol for 24 h suppresses LH, but not FSH, for at least 48 h.

Concentrations of LH in female rats do not increase to concentrations seen in the male at 24 h after castration until up to one week after ovariectomy, while FSH concentrations increase rapidly in both sexes. We hypothesized that the lag in LH rise is due to the imposition of a prolonged suppression by the high concentrations of oestradiol seen during each cycle at pro-oestrus, which prevents a rapid response to the removal of negative feedback. This hypothesis was tested by studying the effect of exposure to pro-oestrus oestradiol concentrations, administered in Silastic capsules, for 24 h on the pulsatile release of LH and FSH. In the first experiment, treatment with oestradiol for 24 h began on day 3 after ovariectomy and resulted in a significant suppression of LH pulse frequency, which appeared to persist for up to 4 days after removal of the implant. In the second experiment, exposure for 24 h to high, pro-oestrous oestradiol concentrations beginning on day 3 or 7 after ovariectomy significantly suppressed mean LH concentrations and LH pulse amplitude compared with vehicle-treated controls, while FSH secretion did not differ between the two treatments. These results suggest that the acute lag in the rate of LH rise after ovariectomy depends on a prolonged suppressive effect of oestradiol and that the rise in oestradiol during the cycle, which exerts a positive feedback to trigger the preovulatory gonadotrophin surges, also exerts a negative feedback for 3-4 days, and this contributes to the relative stability of cycle duration in female rats.

Animals↗
PubMed1976

LH- and FSH-releasing activities of synthetic tetrapeptide and synthetic LH-RH in rats.

Changes in serum LH and FSH were measured following injection of synthetic tetrapeptide (Glu-Tyr-Arg-Trp-NH2) or synthetic LH-RH into the femoral vein of oophorectomized rats. A considerable secretion of LH occurred after injection of synthetic tetrapeptide although its LH-releasing activity was less prominent than that observed after injection of LH-RH. No appreciable FSH-releasing activity was noted following injection of the tetrapeptide. A significant rise of LH and an observable, but extremely modest, rise of FSH with an indistinct peak were noted after single injection of synthetic LH-RH.

Animals↗
PubMed1984

Effect of immunoneutralization of LH releasing hormone on LH, FSH and ovarian steroid secretion in the preovulatory phase of the oestrous cycle in the ewe.

Immunoneutralization of LH releasing hormone (LHRH) by the i.v. administration of LHRH antiserum in the preovulatory period in the ewe resulted in a prompt abolition of the pulsatile secretion of LH without alteration of basal plasma levels of LH. This resulted in an immediate cessation of the pulsatile secretion of ovarian oestradiol, with no change in the secretion rate of androstenedione or plasma levels of FSH. The ovarian secretion rate of testosterone increased significantly. Twenty to 22h after the injection of LHRH antiserum, pulsatile secretion of LH and ovarian oestradiol and androgen secretion remained suppressed while plasma levels of FSH had increased significantly. The bolus injection of ovine LH (10 micrograms, i.v.) at this time caused a significant increase in oestradiol, androstenedione and testosterone, these responses being inversely related to the titre of LHRH antiserum in the plasma at this time. These results show that (1) the secretion of oestradiol from the preovulatory sheep follicle is entirely dependent on the pulsatile secretion of LH and (2) since the secretion of ovarian androgens was not inhibited, LH may exert a short-term control over the aromatase enzyme system controlling the conversion of androgen to oestrogen in the granulosa cell of the preovulatory sheep follicle.

Androstenedione↗
PubMed1986

Influence of acute intracerebroventricular (i.c.v.) administration of adrenocorticotrophin (ACTH) on LH secretion in male rats: effect of pretreatment (i.c.v.) with ACTH antiserum on the serum LH response to an acute ether stress.

Adult male rats with chronic indwelling intracerebroventricular (i.c.v.) and jugular catheters were given an i.c.v. injection (over 1 min) of 1, 10, 100 ng or 1 microgram ACTH(1-24), or 300 ng ACTH(4-10) or saline, and blood samples were taken 0, 5, 15, 30 and 60 min later. Increasing dosages of ACTH(1-24) caused a dose-related rise in serum LH levels. Peak levels of serum LH (ranging from 157 to 473% of pretreatment levels) were reached 5-15 min after treatment, and then serum LH values returned to pretreatment levels by 60 min. The serum LH response to 1 microgram ACTH(1-24) did not differ from the response to 100 ng ACTH(1-24). Administration (i.c.v.) of 300 ng ACTH(4-10) was also effective in increasing serum LH values. Repeated withdrawal of blood during the experiment increased serum corticosterone values in all groups (including saline-treated), but i.c.v. administration of ACTH(1-24) or ACTH(4-10) did not further increase serum corticosterone levels. Two additional groups of rats were injected i.p. with either saline or pentobarbital (30 mg/kg body weight) 1 h before i.c.v. administration of 10 ng ACTH(1-24) and blood samples were taken as in the other groups. The animals in these groups did not show a rise in serum LH concentrations in response to ACTH(1-24). In a third experiment, rats were pretreated (i.c.v.) with either ACTH antiserum (ACTH-Ab) or normal rabbit serum 15 min before a 2-min ether stress. The ether stress evoked a significant rise in serum LH concentrations within 15 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1986

Effects of LH and an LH-releasing hormone agonist on different second messenger systems in the regulation of steroidogenesis in isolated rat Leydig cells.

The stimulation of steroid production in Leydig cells by LH is accompanied by increased cyclic AMP levels, activation of protein kinase A, increased phosphorylation of at least six phosphoproteins and requires protein synthesis. However, an LH-releasing hormone agonist (LHRH-A) can stimulate steroid production without stimulation of cyclic AMP levels. In the present study we have shown that LH action involves calcium fluxes through the plasma membrane, in addition to activation of protein kinase A. The action of LHRH-A, in contrast, does not require calcium fluxes and is not potentiated by 1-methyl-3-isobutylxanthine, indicating that cyclic AMP is not involved. Extracellular calcium is required for the action of both LH and LHRH-A. An increase in intracellular calcium concentration due to the effect of ionophore A23187 did not stimulate steroidogenesis and had deleterious effects on intracellular adenosinetriphosphate levels. LH and 4 beta-phorbol-12-myristate-13-acetate (PMA), an activator of protein kinase C, both stimulated phosphorylation of proteins of 17 000 and 33 000 mol. wt, whereas LHRH-A had no effect. However, compared with the effect of LH, PMA had a much smaller effect on steroid production, indicating that even if protein kinase C may be activated by LH its role in the regulation of steroid production may be less important than the role of protein kinase A. Action of LHRH-A does not appear to be mediated by calcium fluxes, protein kinase C activation or active protein phosphorylation.

Animals↗