Lecture 34

Estrogens

-actions

1. facilitate the growth of the ovarian follicle

2. thickens the endometrium in the first half of the menstrual cycle, growth of decidua due to estrogen

3. causes duct growth in breasts

4. increase libido (need for sexual activity, males seek sexual activity on a fairly stable basis)

5. secondary sex characteristics including enlargement of the breasts

-places a small role in the enhancement of other minor sex characteristics that you find in a castrate male (have same characteristics)

1. high voice

2. broad hips

3. more head hair

4. narrower shoulders

5. flat top pattern of pubic hair

6. decrease LHRH

-estrogen is a group, secreted as estradiol (secreted form of estrogen, most powerful form of estrogen), in bloodstream this goes back to estrone in a reversible reaction

-estrone is a weaker form of estradiol, can get taken up by the liver and change it to estriol (the weakest estrogen)

-Progesterone

-stimulates the growth of the lobules and asoni in the breasts

-increases the rate of estradiol release to the lesser active forms, increase conversion to lesser active forms

-maintains the endometrium during secretory phase of the mensutral cycle and also during pregnancy

-thermogenic, just prior to ovulation there is a spike in progesterone and that can give a little spike ot the women's temperature, this is how certain monitor when ovulation will occur (monitor their basal temperature)

-Follicle stimulating hormone releasing factor

-released in a pulsatile fashion and will cause the release of FSH (will be turned off by inhibin – sole function is to turn off FSH)

-in male FSH causes sertoli cells of the seminiferous tubule to produce androgen binding protein (binds to testosterone to hold it in the seminiferous tubules to increase spermatogenesis, testosterone causes spermatogenesis and ABP enhances it), causes sertoli cells to secrete inhibin to turn off flow, only cells in male with FSH receptors are sertoli cells

-in female causes:

-early maturation of ovarian follicles and shares the responsibility of the final maturation of the follicles to the graffian stage

-stimulate granulosa cells to change androstendione to estradiol

-causes granulosa cells to secrete inhibin

-only cells in female that have FSH receptors are the granulosa cells

-Corticotropic Releasing Hormone (CRH)

-released constantly however it is increased by

1. fever

2. hypoglycemia

3. stress

-secretion of CRH is decreased by

1. glucocorticoids

-action of CRH causes the release of ACTH

-CRH has a variable pattern of secretion

-we can monitor the variable pattern of CRH by minotring the levels of ACTH (ACTH is irregular bursts)

-75% of ACTH release in the morning is between 4 and 10am

-CRH exhibits a similar pattern of release

-Actions of ACTH

1. stimulate release of glucocorticoids from the adrenal cortex

2. stimulates the release of some gonadocorticoids from the zona reticularis (much lesser effect)

3. stimulates the release of mineralcorticoids from the zona glomerulosa

-Glucocorticoids:

1. cortisol

-circulates in the blood attached to an alpha globulin called transcortin (carrying protein) and cortisol is inactive when it is bound

-day/night rhythm of cortisol release will be interrupted by stress which increases CRH and thus increases cortisol

-actions of cortisol:

1. stimulate gluconeogenesis

2. mobilize fat stores, cause cells to use more free fatty acids and less glucose

3. increase blood a.a. level by causing protein breakdown by the cells, this is both a catabolic and an anabolic system, causes protein breakdown in cells which increase blood a.a which are then taken up by the liver and the liver is stimulated to increase the production of blood plasma proteins

4. acts as a permissive action for other hormones, a co-factor

-glucagon and catecholamines have a calorigenic affect can't this effect in the absence of cortisol

-catecholamines exert a lipolitic affect which doesn't work in the absence of cortisol

-smooth muscle unresponsive to circulating catecholamines in the absence of cortisol

5. changes the WBC count in favor of neutrophils

6. increases the number of platelets and RBCs

7. cortisol acts as an anti-inflammatory and anti-allergen

2. corticosterone

-ratio of cortisol to corticosterone is 7:1

-Gonadocorticoids

-released as androgens including DHEA and androstenodione

-both DHEA and androstenodione will quickly change to testosterone and estradiol in the blood, this is the source of opposite sex hormones for both males and females (source of estrogen in the male, testosterone in the female, unsure of why this happens)

-proposed gonadocorticoid stimulating hormone but have not yet found it

-ACTH causes a small release but cannot account for all of it

-Mineralcorticoids – release caused by ACTH

1. Renin = produced by the kidney

-change the blood protein angiotensinogen to angiotensin I

-angiotension I's only role is to change to angiotensin II via the enzyme ACE which is found at the surface of endothelial cells

-after converted to angiotensin II (most happens it the lungs, first chance have to touch an endothelial cell is in the lung)

-role of angiotensin II

1. vasoconstricts arterioles

2. increases aldosterone release

3. major regulator of aldosterone release

4. contract mesengeal cells in the kidney (mesengeal cells on the glomerular capillaries)

5. increase ADH secretions and thirst sensations

6. increase ACTH secretion

-mineralcorticoids made by the zona glomerulosa of the adrenal cortex

2. aldosterone (angiotensin II is the main regulator of aldosterone)

-95% of mineralcorticoid activity is due to aldosterone release

-aldosterone released in response to angiotensin II, increase in plasma K

-if drop level of Na this will stimulate aldosterone release (FALSE)

-actions of aldoesterone

1. increase Na uptake by kidney and colon

2. decrease the amount of Na we put into tears and sweat

3. increase excretion of hydrogen (follows K out, kick potassium ion out and hydrogen ion follows) and potassium ions (running pump faster)

3. Atrial natriuretic factor

-produced by the atria of the heart

-secretion is due to an increase of NaCl in the plasma or an increase in extracellular fluid (blood volume)

-actions:

1. relax the mesengeal cells of the glomerulus increase the surface area for filtrate, cause to lose more filtrate

2. decrease aldosterone release

3. inhibits ADH secretion, inhibits ADH water induced reabsorption in the iMCDt cells, no effect on ADH induced urea reabsorption

4. inhibits rennin secretion which results in a decrease in BP

5. causes vasodilation – NOT TRUE

Vessels have dialated but this is b/c the atrial natriuretic factor is an inhibitor of vasconstrictors