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These processes are controlled by the size and frequency of GnRH pulses, as well as by feedback from androgens and estrogens. Low-frequency GnRH pulses are required for FSH release, whereas high-frequency GnRH pulses stimulate LH pulses in a one-to-one manner. [10] There are differences in GnRH secretion between females and males.
Approximately 40% of women with PCOS display higher GnRH pulse frequency and tonic hypersecretion of LH due to hypersecretion of androgens from the polycystic ovary. [3] [32] [33] Androgens are readily metabolized to estradiol in the ovaries. [33]
The frequency and amplitude of GnRH pulses are tightly regulated, particularly in women, over the course of the reproductive cycle. For instance, the FSHβ gene exhibits ultrasensitive behavior in response to GnRH pulse frequency, with its expression sharply increasing at lower pulse frequencies and decreasing at higher frequencies.
The shift to high frequency electrical activity in GnRH neurons is the signal that initiates puberty. GnRH neurons receive input from classical neurotransmitters like glutamate and GABA . [ 14 ] These neurotransmitters cause electrical activity that is regulated through development to cause broad changes in calcium ion entry into the cell ...
Progestogen negative feedback decreases the pulse frequency of gonadotropin-releasing hormone (GnRH) release by the hypothalamus, which decreases the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) by the anterior pituitary. Decreased levels of FSH inhibit follicular development, preventing an increase in estradiol ...
LH is released from the pituitary gland along with FSH in response to GnRH release into the hypophyseal portal system. [4] Pulsatile GnRH release causes pulsatile LH and FSH release to occur, which modulates and maintains appropriate levels of bioavailable gonadal hormone—testosterone in males and estradiol in females—subject to the requirements of a superior feedback loop. [3]
Heart Rate (Per min.): 85; Blood Pressure: Unaffected; Cardiac output increases throughout early pregnancy, and peaks in the third trimester, usually to 30-50% above baseline. [6] Estrogen mediates this rise in cardiac output by increasing the pre-load and stroke volume, mainly via a higher overall blood volume (which increases by 40–50%). [22]
GnRH binds to gonadotropin-releasing hormone receptors (GnRHR), which is a G-protein coupled receptor, and signals the oscillation of calcium that hyperpolarizes gonadotropic cell membranes. [6] This oscillation of calcium ions occurs through the resultant signaling cascade of the GnRH binding to the GnRHR in the plasma membrane of the gonadotroph.