Criado por Marissa Alvarez
quase 5 anos atrás
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Questão | Responda |
Follicle Stimulating Hormone (FSH) | -Hydrophilic -a Glycoprotein -produced by gonadotropes -enhances spermatogenesis, needed for remodeling (acts on Sertoli cells) -FSH & Testosterone (T) = synergistic -FSH stimulates the granulosa cells in the ovarian follicle. -Local estrogen, along with FSH, stimulates proliferation of the granulosa cells -FSH & LH stimulate secretion of estrogen |
Luteinizing Hormone (LH) | -Hydrophilic -a Glycoprotein -produced by gonadotropes -stimulates testosterone production from Leydig cells -LH stimulates the thecal cells in the ovarian follicle. Luteinizing Hormone Surge: 1. Halts estrogen synthesis 2. Reinitiates meiosis 3. Triggers prostaglandin release leading to rupture of cell wall 4. Conversion of follicular cells to luteal cell -Maintains Corpus Luteum -FSH & LH stimulate secretion of estrogen |
Growth Hormone (GH) | -Hydrophilic -Peptide w/long chain of amino acids -produced by somatotropes -NOT involved in fetal growth -Exerts actions by binding directly to target tissues (metabolism), BUT INDIRECT effect on growth Under influence of growth hormone: •Net synthesis of proteins •↑Length of the long bones •↑ size and number of cells in soft tissues -Stimulates IGF-1 -GH is the MOST abundant ANTERIOR pituitary hormone secreted -GH (acting through IGF-I) stimulates growth in soft tissues and skeleton -If ↑ protein meal -> ↑ GH secretion -If ↓ [fatty acid]blood -> ↑ GH secretion |
Thyroid hormone (TH) | -lipophilic Made from tyrosine: ->has 2 tyrosine amino acids ->T4 = has 4 iodines ->T3 = has 3 iodines *–T3 more potent than T4 -Inhibits anterior pituitary -a growth-influencing hormone (It is Permissive = Not directly responsible for promoting growth) i.e. Stunted growth in hypothyroid children (but not opposite effect if hyperthyroid) TH does not have any discrete target organs • Affects virtually every tissue in the body through binding to TRE -Effects very long lasting -most important regulator of O2 & energy utilization at rest ->Sympathomimetic Effect (an effect produced that is similar to that of the SNS) ->TH increases sensitivity to catecholamines (NE and Epi) by increasing CA receptors. ->Stressors such as physical stress, starvation, and infection INHIBIT TH ->stimulated by cold |
Thyroid Stimulating hormone (TSH) | -stimulates thyroid gland -produced by thyrotropes ->acts via GPCR (cAMP) in thyrotropes of the anterior pituitary • Maintains structural integrity of the gland |
Progesterone (P) | -Secreted by ovaries -Progesterone and estrogen = antagonistic -Progesterone BLOCKS any positive effects of estrogen on GnRH secretion (lots of P produced during luteal phase) -powerful inhibitor of GnRH/LH release -Progesterone released by cells around the ovum also serve as a chemoattractant. 3. Prevent miscarriage by suppressing myometrial contractions 4. Promotes plug formation in cervix 5. Stimulates the development of milk glands -the drop in E and P initiate lactation. |
Estrogen (E) (sex hormone) | -Secreted by ovaries -Progesterone and estrogen = antagonistic -A growth-influencing hormone (Promotes epiphyseal plate closure -> stops growth) -Local estrogen, along with FSH, stimulates proliferation of the granulosa cells -Some estrogen remains within the follicle and contributes to antral formation -High E levels -> GnRH surge -Estrogen acts upon the anterior pituitary to increase luteinizing hormone during surge secretion 1. Grows the myometrium 2. Promotes development of ducts in mammary glands -the drop in E and P initiate lactation. |
Testosterone (T) (sex hormone) | -Secreted by Leydig cells in the testis -FSH & Testosterone (T) = synergistic -Both T and E2 = halt bone growth at end of puberty (a growth-influencing hormone) -Causes descent of the testes into scrotum -Masculinizes the Reproductive tract and external genitalia -ALL Secondary Sexual Characteristics depend on testosterone -important in spermatogenesis (sustains sperm production) ->necessary for mitosis and meiosis -Negative feedback control of GnRH/LH/FSH -Bone homeostasis (growth & termination) -Testosterone acts on (stim./inhibit) Kiss-peptin neurons to inhibit GnRH secretion |
Vasopressin | -Antidiuretic hormone -triggered by: •Hypothalamic osmoreceptors (dominantly) ↑ vasopressin = ↑ permeability of distal and collecting tubules (of kidney) -> ↑ H20 reabsorption -> ↓ urine ouptut & ↑ plasma volume **Vasopressin release triggered by increased plasma osmolarity or decreased ECF volume or blood pressure -Detected by hypothalamic osmoreceptors and left atrium volume receptors -Targets the kidney (distal and collecting tubules), causes insertion of aquaporins and enhances the retention of water -Targets the arteriolar smooth muscle to cause pressor effect |
Oxytocin | Release triggered by: •Stimulation of cervical & nipple mechanoreceptors -↑ oxytocin = ↑ contraction of myoepithelial cells around alveoli = milk ejection from nipple -↓ oxytocin (low levels) = ↑ uterine contractions = fetus pushed against cervix (neuroendocrine reflex) = ↑ oxytocin (+ feedback loop) -causes corpus luteum (CL) termination **Oxytocin release triggered by mechanoreceptors in cervix or nipple -Acts at uterus (increase contractions) -Acts at breast (milk ejection) -Act at corpus luteum to aid in termination of CL function |
Prolactin (PRL) | -protein similar to GH -produced by lactotropes |
Adrenocorticotropic Hormone (ACTH) | -produced by corticotropes -ACTH triggers cortisol secretion, which, in turn, limits its own secretion -ACTH also = ↑ growth zona fasciculata and reticularis ACTH stimulates secretion: Cortisol and DHEA output is parallel **Exception: DHEA rises prior to puberty (cortisol not changed) & declines with aging **DHEA negative feedback directly affects GnRH secretion (not CRH) |
Insulin | -A growth-influencing hormone: ->Insulin–Deficiency = blocks growth –>Excess = excessive growth –Promotes protein synthesis –Structurally resembles IGFs (so interaction with IGF-I receptor is possible Insulin effects that lower blood glucose and promote storage: -Stimulates glycogenesis (In liver and muscle) -Inhibits glycogenolysis -Favors storage -Inhibits gluconeogenesis (By ↓ amino acid in blood) -Inhibition of enzymes -Facilitates transport into cells |
Estradiol (E2) | -Both T and E2 = halt bone growth at end of puberty -Rising estradiol stimulates the thickening of the endometrium. |
Parathyroid Hormone (PTH) | -controls osteocytes (entombed osteoblasts) Parathyroid Glands: 4 individual glands -Posterior surface of thyroid gland -Secrete PTH -Essential to life IF no PTH = ↓Ca2+ leads to spasm of respiratory muscles = asphyxiation ->Prevents hypocalcemia Acts on bone, kidneys, and GI tract ↑ plasma Ca2+ when low Ca2+ “detected” ↓ plasma PO43 Actions at the kidney: ->reduces urinary excretion of Ca2+ ->promotes urinary excretion of PO43- ->Acts at kidney to increase activation of Vit D ->No direct actions at GI, mediated via increased Vit D ->Control of secretion regulated by calcium levels ->PTH increases activation of Vit D in kidney |
Gonadotropin-Releasing Hormone (GnRH) | **Increases at the time of puberty •Do NOT have receptors for androgens or estrogens •Increases to cause puberty: ->Nocturnal increase initially ->Involves Kiss1 neurons ->Likely involves other neuron types as well -GnRH surge = stimulated by HIGH E levels -GnRH only inhibited by Kiss-1 neurons |
Aldosterone | 1. Influence electrolyte and water balance Conserves Na+ by increasing renal absorption of Na+ and promotes urinary excretion of excess K+ through actions at the distal and collecting ducts Promotes insertion of additional Na+ leak channels into the luminal membrane and additional Na+/K+ pumps into the basolateral membranes of principal cells. This leads to greater passive movement of Na+ into cell and increased active pumping out of cell into plasma About 8% of filtered Na+ depends on aldosterone for REABSORPTION Water is reabsorbed osmotically secondary to Na+ reabsorption (important for maintaining extracellular fluid volume and hence blood pressure) |
Cortisol | -Glucocorticoid ↑ blood glucose concentrations, at expense of protein and fat stores ↑ gluconeogenesis (liver) ↑ blood amino acids ↑ blood fatty acids ↓ muscle and liver response to insulin ->STRESS overrides negative feedback control (If ↑ stress = ↑ cortisol) |
Adrenal Cortex: Sex Steroids DHEA | DHEA - most predominant adrenal androgen In females: Growth of pubic and axillary hair Enhancement of pubertal growth spurt Sex Drive In males: Not much effect, overpowered by T |
Calcitonin | Acts on bone to prevent Ca2+ mobilization and reduces osteoclast activity Reduces Ca2+ and PO43- uptake in kidney |
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