Response of superfused goldfish pituitary fragments to mammalian and salmon gonadotropin-releasing hormones

MacKenzie, Duncan S.; Gould, David R.; Peter, Richard; Rivier, Jean; Vale, Wylie

doi:10.1016/0024-3205(84)90558-7

Cited by 46 publications

(12 citation statements)

References 11 publications

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“…Similar results have been reported for the goldfish (Chang et al, 1984;MacKenzie et al, 1984 (Rubin, 1982 (Limor et al, 1987 (Conn et al, , 1980Harris et al, 1985 (Reuter, 1983;Ovichinnikov, 1985 (Hopkins and Walker, 1978;Stern and Conn, 1981;Gorospe and Conn, 1987) and in fish (Jamaluddin et al, 1989 (Jamaluddin et al, 1989) Alberta, Canada, 1988 (abstract 49).…”

Section: Gth Determination and Statisticssupporting

confidence: 76%

Calcium ions as a mediator in GnRH action on gonadotropin release in the common carp (Cyprinus carpio L)

Mikołajczyk¹,

Weil²,

Epler³

et al. 1990

Reprod. Nutr. Dévelop.

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Section: Gth Determination and Statisticssupporting

confidence: 76%

Calcium ions as a mediator in GnRH action on gonadotropin release in the common carp (Cyprinus carpio L)

Mikołajczyk¹,

Weil²,

Epler³

et al. 1990

Reprod. Nutr. Dévelop.

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“…The present results conflict with the finding of Grill et al (1972) (Mackenzie et al, 1984), LHRH is 10 fold more potent than sLHRH in elevating amphibian blood pressure (present experiments), and LHRH is about 50 fold more potent than sLHRH in releasing luteinizing hormone from rat pituitary cells (Sherwood et al, 1983). Elevation of blood pressure by LHRH and sLHRH was accompanied by bradycardia.…”

Section: Discussioncontrasting

confidence: 57%

Conjugated catecholamines and pressor responses to angiotensin, luteinizing hormone‐releasing hormone and prazosin in conscious toads

Wilson

1985

British J Pharmacology

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1 Synthetic angiotensin II (Ang II), mammalian luteinizing hormone-releasing hormone (LHRH) and salmon LHRH (sLHRH) were injected intravenously into conscious, adult toads (Bufo marinus) to elucidate the cardiovascular actions of the hormones. The maximal increases in pulse pressure elicited by the three peptides did not differ from each other but only Ang II increased cardiac frequency. The maximal increases in mean arterial blood pressure (MAP) caused by LHRH and sLHRH were identical, while Ang II caused a 100% greater maximal effect. The median effective doses (ED50) for both Ang II and LHRH were approximately 0.1 nmol kg-' whereas the potency of sLHRH was 10 fold less. Pressor responses to LHRH and sLHRH were blocked completely by (D-pGlu', DPhe2, D-Trp3 6)-LHRH but this antagonist did not inhibit Ang II. 2 Significant proportions of circulating, endogenous dopamine, noradrenaline (NA) and adrenaline (Ad) were found to be sulphoconjugated. Arterial plasma concentration of free NA increased simultaneously with the rise in blood pressure following Ang II injection. The magnitude of the free NA response increased with increasing Ang II dose but even a high dose failed to augment the plasma level of conjugated NA. Ang II did not alter concentrations of free or conjugated dopamine and Ad. 3 Intraarterial injection of an a-adrenoceptor antagonist, prazosin, caused sustained elevation of arterial pressure and free Ad. Subsequently Ang II lowered plasma Ad concentration. Prazosin inhibited the NA response to Ang II yet the pressor effects ofthe x-adrenoceptor antagonist and Ang II were additive. Administration of a P-adrenoceptor antagonist, propranolol, largely reversed the cardiovascular sequelae of x-adrenoceptor blockade. 4 It is concluded, firstly, that the cardiovascular actions of Ang II and LHRH are mediated through different receptors. Secondly, although it had been shown that a-and P-adrenoceptor mechanisms mediate the pressor effect of LHRH, the present experiments showed that mobilization of catecholamines cannot account for the pressor response to Ang II. Thirdly, both free and conjugated catecholamines circulate in toads; however the extent of conjugation can be dissociated from the changes in free NA and Ad induced by Ang II and prazosin.

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“…Experiments were conducted using a column perifusion system for pituitary fragments of common carp, similar to that used for goldfish pituitary fragments (Mackenzie et al 1984;Habibi et al 1989), with minor modifications. Briefly, the pituitaries were removed and fragments were prepared (< 1 mm 3 ).…”

Section: Methodsmentioning

confidence: 99%

The regulatory effects of thyrotropin-releasing hormone on growth hormone secretion from the pituitary of common carp in vitro

Lin

Peter

1993

Fish Physiol Biochem

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The effects of thyrotropin-releasing hormone (TRH) on growth hormone (GH) and gonadotropin (GtH) release, and the influences of somatostatin (SRIF), the dopamine agonist apomorphine (APO) and extracellular calcium on basal and TRH-induced GH release were examined using an in vitro perifusion system for pituitary fragments of common carp (Cyprinus carpio). Five minute pulses of different dosages of TRH stimulated a rapid and dose-dependent increase in GH release from the perifused pituitary fragments with an ED50 of 9.7 ± 2.3 nM. TRH was ineffective on GtH release. SRIF significantly inhibited basal and TRH-induced GH release from the perifused pituitary fragments, and the effects of SRIF were dose-dependent. APO induced a dose-dependent increase in basal and TRH-stimulated GH release from the perifused pituitary fragments. Increasing the concentrations of extracellular calcium from 0 mM to 1.25 mM resulted in an increase in basal and TRH-induced GH release. The high dose of calcium (6.25 mM) caused a slight decrease in basal and TRH-induced GH release compared with those at a concentration of 1.25 mM.

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Response of superfused goldfish pituitary fragments to mammalian and salmon gonadotropin-releasing hormones

Cited by 46 publications

References 11 publications

Calcium ions as a mediator in GnRH action on gonadotropin release in the common carp (Cyprinus carpio L)

Calcium ions as a mediator in GnRH action on gonadotropin release in the common carp (Cyprinus carpio L)

Conjugated catecholamines and pressor responses to angiotensin, luteinizing hormone‐releasing hormone and prazosin in conscious toads

The regulatory effects of thyrotropin-releasing hormone on growth hormone secretion from the pituitary of common carp in vitro

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