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  • Title: Plasma norepinephrine during the rat estrous cycle and after progesterone treatment to the ovariectomized estrogen-primed rat.
    Author: Nagle CA, Rosner JM.
    Journal: Neuroendocrinology; 1976; 22(1):89-96. PubMed ID: 1035969.
    Abstract:
    In four-day cycling rats studied during the estrous cycle, the levels of circulating norepinephrine (NE) showed a sharp rise concomitant with the LH surge in the afternoon of proestrus. Following the peak, plasma NE fell rapidly to the minimum value by the morning of estrus. The administration of progesterone to ovariectomized estrogen-primed rats resulted in a surge in plasma NE levels 4 h after progesterone treatment. The maximal levels attained were 3-fold greater than baseline values, falling rapidly to reach basal values 8 h after the administration of progesterone. The amine levels remained unaffected 12-20 h later. The LH values attained a maximum 8 h after the injection of progesterone. In rats treated with estradiol benzoate (EB) followed by 0.1 ml of oil instead of progesterone, neither the NE nor the LH peak were observed. These findings are discussed with respect to the significance of increased amounts of plasma NE related to the LH surge. The relationship between plasma norepinephrine (NE) and luteinizing hormone (LH) in the normal estrous cycle of rats was investigated and the effect of progesterone (P) treatment during the estrus cycle or after the induction of LH secretion in ovariectomixed (OVX) estrogen-primed rates on NE levels was determined. Levels of NE rose concomitantly with the surge in LH the afternoon of proestrus. OVX rats were primed with 5 mg estradiol benzoate (EB) and 48 hours later given 1.5 mg P or control substances. OVX estrogen-primed rates had a surge of NE 4 hours after treatment. The maximum levels reached were 30 fold greater than baseline values. Values fell to the baseline level 8 hours after administration of p. Amine levels remained unaffected 12-20 hours later. LH values peaked at 8 hours after P injection. The source of the NE rise is discussed and it is suggested that general adrenergic activation is involved.
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