Decrease in blood pressure induces ADH secretion by reducing input from pressure receptors.
The reduced neural input to baroreceptors relieves the source of tonic inhibition on hypothalamic cells that secrete ADH.
12 Hypothalamus posterior pituitary and ADH secretion connection with baroreceptors 13 Secretion of ADH
Hypovolemia also stimulates the generation of renin and angiotensin directly within the brain.
This local angiotensin II enhances ADH release in addition to stimulating thirst.
Volume regulation is also reinforced by atrial naturetic peptide (ANP).
When circulating volume is increased ANP is released by cardiac myocytes this ANP along with the ANP produced locally in the brain acts to inhibit ADH release.
14 Secretion of ADH
The two major stimuli of ADH secretion interact.
Changes in volume reinforce osmolar changes.
Hypovolemia sensitizes the ADH response to hyperosmolarity.
15 Osmotic and hemodynamic control of ADH secretion changes in osmolality changes in blood volume or pressure interactions between osmolar and volume/pressure stimuli on ADH secretion. 16 Actions of ADH
The major action of ADH is on renal cells that are responsible for reabsorbing free (osmotically unencumbered) water from the glomerular filtrate.
ADH responsive cells line the distal convoluted tubules and collecting ducts of the renal medulla.
ADH increases the permeability of these cells to water.
The increase in membrane permeability to water permits back diffusion of water along an osmotic gradient.
ADH significantly reduces free-water clearance by the kidney
17 Actions of ADH
ADH action in the kidney is mediated by its binding to V2 receptors coupled to adenylate cyclase and cAMP production.
cAMP activates protein kinase A which prompts the insertion of water channels into the apical membrane of the cell.
When ADH is removed the water channels withdraw from the membrane and the apical surface of the cell becomes impermeable to water once again. .
18 Actions of ADH
This mechanism of shuttling water channels into and out of the apical membrane provides a very rapid means to control water permeability
The basolateral membrane of the ductal cells are freely permeable to water so any water that enters via the apical membrane exits the cell across the basolateral membrane resulting in the net absorption of water from the tubule lumen into the peritubular blood.
19 Actions of ADH
Water deprivation stimulates ADH secretion decreases free-water clearance and enhances water conservation. ADH and water form a negative feedback loop.
20 Inputs reflexly controlling thirst. 21 Actions of ADH
ADH deficiency is caused by destruction or dysfunction of the supraoptic and parventricular nuclei of the hypothalamus. Inability to produce concentrated urine is a hallmark of ADH deficiency and is referred to as diabetes insipidus.
ADH also acts on the anterior pituitary to stimulate the secretion of ACTH.
22 Pathways by which sodium and water excretion are decreased in response to severe sweating. 23 Aldosterone and the mineralocorticoids
The mineralocorticoid aldosterone is vital to maintaining sodium and potassium balance and extracellular fluid volume.
Aldosterone is an adrenal corticosteroid synthesized and secreted by the adrenal cortex.
24 Cross section through the adrenal gland cortex and medulla salt sugar sex 25 Aldosterone
The adrenal cortex is composed of three major zones differentiated by the histological appearance and type of corticosteroid they produce.
The outermost is the zona glomerulosa is very thin and consists of small cells with elongated mitochondria.
26 Adrenal zones
The middle zona fasiculata is the widest zone and consists of columnar cells that are highly vacuolated with numerous lipid droplets.
These lipid droplets are composed of cholesterol esters the substrate for adrenal steroid hormone biosynthesis.
27 Adrenal zones
The innermost zona reticularis contains fewer lipid droplets than fasiculata cells but have similar mitochondria.
ACTH has trophic effects on the zona fasiculata and reticularis.
28 Aldosterone synthesis
Aldosterone is synthesized and secreted by the zona glomerulosa .
The synthesis of aldosterone from cholesterol to corticosterone is identical to the synthesis of glucocorticoids in the zona fasiculata.
The C18 methyl group of corticosterone is hydroxylated and converted to an aldehyde yielding aldosterone.
29 Aldosterone synthesis in the adrenal zona glomerulosa 30 Aldosterones function
The principal function of aldosterone is to sustain extracellular fluid volume by conserving body sodium.
Aldosterone is largely secreted in response to signals that arise from the kidney when a reduction in circulating fluid volume is sensed.
When body sodium is depleted the fall in extracellular fluid and plasma volume decreases renal arterial blood flow and pressure.
31 Regulation of aldosterone secretion Activation of renin-angiotensin system in response to hypovolemia is predominant stimulus for aldosterone synthesis. 32 Aldosterone and renin-angII
The justaglomerular cells of the kidney respond to this change by secreting renin. Renin acts on angiotensinogen (which is secreted by the liver) to form angiotensin I which is further cleaved by angiotensin converting enzyme (which is secreted by the lungs) to angiotensin II.
Angiotensin II acts on the zona glomerulosa to stimulate aldosterone synthesis.
Angiotensin II acts via increased intracellular cAMP to stimulate aldosterone synthesis.
34 Components of renin-angiotensin-aldosterone system 35 Aldosterone
ANP reinforces the effects of the renin-angiotensin system on aldosterone secretion.
In response to volume expansion artrial myocytes secrete ANP which binds to receptors in the zona glomerulosa to inhibit aldosterone synthesis.
ANP acts via increased intracellular cGMP which opposes cAMP and inhibits aldosterone synthesis.
ANP also reduces aldosterone indirectly by inhibiting renin release.
36 Aldosterone clears potassium
Aldosterone facilitates the clearance of potassium from the extracellular fluid and potassium stimulates aldosterone synthesisthus providing a feedback control mechanism to control potassium levels.
However the ACTH stimulation is more transient than the other stimuli and is diminished within several days.
ACTH provides a tonic control of aldosterone synthesis.
In the absence of ACTH sodium depletion still activates renin-angiotensin system to stimulate aldosterone synthesis.
Aldosterone levels fluctuate diurnallyhighest concentration being at 8 AM lowest at 11 PM in parallel to cortisol rhythms.
39 Aldosterone action
Aldosterone binds to the mineralocorticoid receptor in target cells and affects transcriptional changes typical of steroid hormone action.
The kidney is the major site of mineralocorticoid activity.
40 Model for basic renal handling of potassium. Net absorption occurs in the proximal portions of the nephron and net secretion in the more distal portions of the nephron. 41 Action of aldosterone on the renal tubule. Sodium reabsorption from tubular urine into the tubular cells is stimulated. At the same time potassium secretion from the tubular cell into urine is increased. Na/K-ATPase and Na channels work together to increase volume and pressure and decrease K. 42 Aldosterone action
Aldosterone stimulates the active reaborsption of sodium from the tubular urine back into the nearby capillaries in the distal tubule.
Water is passively reabsorbed with sodium which maintains sodium concentrations at a constant level.
Hence extracellular fluid volume expands in a virtually isotonic fashion
43 Aldosterone action
Aldosterone stimulates the active secretion of potassium from the tubular cell into the urine.
Most potassium that is excreted daily results from distal tubular secretion.
Hence aldosterone is critical for disposal of daily dietary potassium load at normal plasma potassium concentrations.
44 Pathway by which an increased potassium intake induces greater potassium excretion mediated by aldosterone 45 Pathway by which aldosterone sercretion and tubular sodium reabsorption is increased when plasma volume is decreased 46 Aldosterone action
Increased blood pressure results from excess aldosterone.
Hypertension is an indirect consequence of sodium retention and expansion of extracellular fluid volume.
47 Cortisol is at 1000 fold higher concentrations than aldosterone 48 Aldosterone action
Cortisol binds well to the mineralocorticoid receptor and plasma cortisol levels are orders of magnitude higher than aldosterone.
Target tissues for aldosterone are protected from glucocorticoid excess via the action of 11b-hydroxysteroid dehydrogenase the enzyme that converts cortisol to cortisone a biological inactive metabolite.
Aldosterone is not a substrate for 11b-HSD and thus only it can bind to its receptor.
49 Summary of aldosterone system
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