1991Journal of NeuroendocrinologyOpen access

Porcine Relaxin Affects the Release of Luteinizing Hormone in Rats

Alastair J. S. Summerlee, Andrew Mumford, M. Susan Smith

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Abstract

Abstract The effects of intravenous injection of porcine relaxin on the pulsatile secretion of luteinizing hormone (LH) were investigated in conscious rats. In untreated, ovariectomized animals, relaxin at doses 2.5 to 10/mug/rat caused a dose-dependent suppression of pulsatile release of LH. At 5mug relaxin, pulses were suppressed for approximately 60 min and there was a significant (P<0.05) fall in mean plasma LH levels. Pulses returned with the same frequency as the pretreatment period but amplitude and nadir of these pulses were significantly (P<0.05) reduced at doses >2.5mug/rat. In ovariectomized rats pretreated with either estradiol or progesterone alone, relaxin did not alter plasma LH levels. In contrast, injection of 5mug relaxin in rats primed with a combination of estradiol and progesterone caused a 90% increase in circulating LH levels. Intracerebroventricular infusion of a specific angiotensin II antagonist blocked the inhibitory effect of relaxin on LH release in untreated, ovariectomized rats and negated the stimulatory effect of relaxin on LH release in estradiol-progesterone-primed, ovariectomized rats. The results demonstrate that acute injections of porcine relaxin in ovariectomized rats suppress the pulsatile release of LH. This effect is blocked when the central angiotensinergic system is compromised suggesting that relaxin might act through the central angiotensin system. The findings are in agreement with other studies that indicate relaxin activates the central angiotensin system. It is also possible that relaxin may act at the level of the adenohypophysis to alter secretion of LH but data in the present study suggest that this may not be a significant site of relaxin action.

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Abstract The effects of intravenous injection of porcine relaxin on the pulsatile secretion of luteinizing hormone (LH) were investigated in conscious rats. In untreated, ovariectomized animals, relaxin at doses 2.5 to 10/mug/rat caused a dose-dependent suppression of pulsatile release of LH. At 5mug relaxin, pulses were suppressed for approximately 60 min and there was a significant (P<0.05) fall in mean plasma LH levels. Pulses returned with the same frequency as the pretreatment period but amplitude and nadir of these pulses were significantly (P<0.05) reduced at doses >2.5mug/rat. In ovariectomized rats pretreated with either estradiol or progesterone alone, relaxin did not alter plasma LH levels. In contrast, injection of 5mug relaxin in rats primed with a combination of estradiol and progesterone caused a 90% increase in circulating LH levels. Intracerebroventricular infusion of a specific angiotensin II antagonist blocked the inhibitory effect of relaxin on LH release in untreated, ovariectomized rats and negated the stimulatory effect of relaxin on LH release in estradiol-progesterone-primed, ovariectomized rats. The results demonstrate that acute injections of porcine relaxin in ovariectomized rats suppress the pulsatile release of LH. This effect is blocked when the central angiotensinergic system is compromised suggesting that relaxin might act through the central angiotensin system. The findings are in agreement with other studies that indicate relaxin activates the central angiotensin system. It is also possible that relaxin may act at the level of the adenohypophysis to alter secretion of LH but data in the present study suggest that this may not be a significant site of relaxin action.

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Available abstract

Abstract The effects of intravenous injection of porcine relaxin on the pulsatile secretion of luteinizing hormone (LH) were investigated in conscious rats. In untreated, ovariectomized animals, relaxin at doses 2.5 to 10/mug/rat caused a dose-dependent suppression of pulsatile release of LH. At 5mug relaxin, pulses were suppressed for approximately 60 min and there was a significant (P<0.05) fall in mean plasma LH levels. Pulses returned with the same frequency as the pretreatment period but amplitude and nadir of these pulses were significantly (P<0.05) reduced at doses >2.5mug/rat. In ovariectomized rats pretreated with either estradiol or progesterone alone, relaxin did not alter plasma LH levels. In contrast, injection of 5mug relaxin in rats primed with a combination of estradiol and progesterone caused a 90% increase in circulating LH levels. Intracerebroventricular infusion of a specific angiotensin II antagonist blocked the inhibitory effect of relaxin on LH release in untreated, ovariectomized rats and negated the stimulatory effect of relaxin on LH release in estradiol-progesterone-primed, ovariectomized rats. The results demonstrate that acute injections of porcine relaxin in ovariectomized rats suppress the pulsatile release of LH. This effect is blocked when the central angiotensinergic system is compromised suggesting that relaxin might act through the central angiotensin system. The findings are in agreement with other studies that indicate relaxin activates the central angiotensin system. It is also possible that relaxin may act at the level of the adenohypophysis to alter secretion of LH but data in the present study suggest that this may not be a significant site of relaxin action.

Key concepts: Relaxin, Endocrinology, Internal medicine, Luteinizing hormone, Hormone, Chemistry, Medicine

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