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Arsenals of Pharmacotherapeutically Active Proteins and Peptides: Old Wine in a New Bottle
Published in Debarshi Kar Mahapatra, Swati Gokul Talele, Tatiana G. Volova, A. K. Haghi, Biologically Active Natural Products, 2020
GnRH agonists (GnRHa) are those molecules which mimic the function of GnRH and stimulate release of LH and FSH. A continuous treatment with GnRHa results in down-regulation of LH and FSH production [130]. The continued use of GnRH superagonists results in drop of the levels of steroid hormones giving rise to no fertility conditions in males and females. The continuous use of GnRHa is therefore beneficial in cases like precocious puberty, endometriosis, and advanced metastatic breast and prostrates cancers [126]. The GnRH antagonists (GnRHag) function by acting as competitive inhibitors for the GnRH receptors. The GnRHag can be used to prevent surge of LH and thus ovarian hyperstimulation syndrome [130]. The list of GnRH agonist and antagonist is given in Table 2.13.
Fluid and electrolyte balance considerations for female athletes
Published in European Journal of Sport Science, 2022
Paola Rodriguez-Giustiniani, Nidia Rodriguez-Sanchez, Stuart D.R. Galloway
To better isolate oestradiol effects from those of progesterone or progestins, Stachenfeld et al. performed a series of studies using a gonadotropin releasing hormone (GnRH) agonist to supress both oestradiol and progesterone. The suppression of endogenous hormone release was followed by controlled administration of oestradiol and progesterone in order to mimic the concentrations attained during the mid to late follicular and mid-luteal phases of a normal menstrual cycle. This ultimately enabled examination of hormone combinations on fluid balance (Stachenfeld, 2008). It was observed that oestradiol alone shifted the osmotic threshold for the release of AVP to a lower plasma osmolality. The authors interpreted the oestrogen-associated lowering of the osmotic threshold for AVP release as a lowering of the osmoregulatory set-point, rather than a change in fluid regulation, because the greater plasma levels of AVP did not seem to contribute to greater water retention (Stachenfeld, 2008). It is important to note that these studies used hypertonic saline (3% NaCl) infusion rather than exercise-dehydration protocols. Hypertonic saline infusion elevates plasma osmolality in a more dramatic fashion than observed during exercise-dehydration and is quite a different state than dehydration. Despite significant increases in thirst and AVP with hypertonic saline infusion there is also large intravascular fluid volume expansion, under resting conditions at least, as water is drawn from the extravascular space in response to the increased osmotic pressure (Stachenfeld, 2008).