Chapter 21: Endocrine Organs

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Welcome back to the Deep Dive.

Today we are strapping in for a really comprehensive look at the body's second communication network.

The one that runs on a chemical clock.

Exactly, the endocrine system.

Our mission today is to take you step by step through the entire microscopic landscape of these glands.

We're using our histology chapter as a map.

And we're going sequentially, gland by gland, concept by concept.

From how a single hormone works all the way to, say, the complex layers of the adrenal cortex.

It's a huge topic.

I mean, this system dictates growth, development, homeostasis, basically the terms of life itself.

If the nervous system is a high speed fiber optic cable.

Right, instantaneous and electrical.

Then the endocrine system is more like the body's broadcast system.

It's chemical, a bit slower, but the effects are often much more widespread and prolonged.

And what's so fascinating is how they overlap.

You have nerve cells literally secreting the hormones.

It's this beautiful neurochemical interface.

So our goal is full mastery.

We'll start with the fundamentals,

then move to the control tower, the hypothalamus and pituitary, before hitting all the peripheral glands.

We'll pull out every key detail and clinical link.

By the end, you'll see this not as a list of organs, but as this masterpiece of biological coordination.

Okay, so let's start at the very beginning.

The word hormone.

Where does that even come from?

It's from the Greek hormane, which means to excite or to set in motion.

And that's exactly what they do.

Precisely.

They are secretions that travel out to regulate activities in other cells and tissues.

And the key difference from an exocrine gland is how they travel.

They're carried through connective tissue and the vascular system.

No ducts.

Absolutely no ducts, which tells you a lot about the glands themselves.

Right.

So what are the defining features we'd see under a microscope?

Well, first, as you said, they are ductless.

Their cells are what we call epithelioid cells.

Which is a fancy way of saying they're epithelial cells, but without a free surface to secrete into.

Exactly.

Their entire job is to dump their secretions into the extracellular matrix, or where they can get picked up.

Which leads right to the second feature, the blood supply.

It has to be incredibly rich.

These glands are some of the most highly vascularized tissues in the body.

They're packed with capillaries to ensure those signals get distributed everywhere and fast.

What I find so amazing is where these glands come from embryologically.

It's not one single origin.

They're cobbled together from all over.

It's incredible.

The chapter lists four completely distinct origins.

You've got the CNS and neuroectoderm, which gives us the posterior pituitary and the pineal gland.

Okay.

So brain tissue.

Then you have the neural crest.

These cells migrate down to form the adrenal medulla.

And most of the others.

They come from the epithelial lining of the gut tube.

So that's your anterior pituitary, your thyroid, your parathyroids.

And then finally, you have some that are mesenchymal, like the adrenal cortex.

The body really did just pull this crucial system together from every available developmental toolkit.

It really speaks to its fundamental importance.

And we need to remember it's not just the big glands on a chart, like in figure 21 .1.

No, not at all.

You also have the diffuse neuroendocrine system or DNS.

These are individual hormone secreting cells scattered all through the gut and respiratory system.

And even fat tissue.

Yes.

Adipose tissue is now considered a major endocrine organ, secreting these things called adipokines.

The body is just constantly talking to itself chemically.

So when we think about how these hormones work, the classic definition is endocrine control.

But it's more localized than that.

Much more.

So you have endocrine control, which is the classic model.

Hormone enters the blood, travels a long distance.

It's a broadcast signal.

Right.

But then you have paracrine control.

This is like a neighborhood announcement.

The cell secretes a signal that only acts on its immediate neighbors.

Very localized.

And then there's the cell that talks to itself.

That's autocrine control.

A cell releases a hormone that binds to receptors on its own surface to regulate itself.

So figure 21 .2 lays this out perfectly.

Systemic, local and self -regulating.

But now there's this whole new layer of communication that's way more complex.

Exosomal signaling.

It's a game changer.

So instead of just a loose hormone molecule, the cell packages up a whole message.

Exactly.

It creates these tiny membrane bound vesicles called exosomes, which you can see in figure 21 .3.

They're like little cargo containers.

And what's inside?

Everything.

Proteins, lipids, different types of DNA and RNA.

They travel through the blood or lymph and deliver these complex packages to distant cells.

And the clinical side of this is huge.

Massive.

The text points out that viruses like SARS -CoV -2 or HIV -1 can use them to transmit viral parts between cells.

And in cancer, it's a major mechanism for promoting things like chemoresistance.

Wow.

So they can deliver for survival or destruction.

It's a powerful communication tool for good or ill.

Okay.

Let's get back to the classic hormones.

The chemistry dictates everything.

There are three main classes.

The biggest group by far is the peptide hormones.

This is everything from tiny peptides to full proteins.

Hypothalamus, pituitary, pancreas.

They all make these.

And they're water soluble.

Right.

So they travel pretty easily in the blood, though many still use carrier proteins to stay stable.

Then you have the steroids, which are the complete opposite.

They're fat soluble.

Yep.

All derived from cholesterol made in places like the gonads and the adrenal cortex.

And because they don't dissolve in blood, they absolutely need carrier proteins to get around.

And only the tiny bit that's free is actually active.

Correct.

And the third class is a bit of a mix.

The amino acid and arachidonic acid analogs.

This includes things like epinephrine, right?

Exactly.

The catecholamines like epinephrine and norepinephrine are water soluble.

But this group also includes the thyroid hormones, which are tyrosine derivatives, but act more like steroids.

They're mostly bound to carrier proteins.

So that chemistry directly leads to how they signal where the receptor is.

Figure 21 .4 shows this divide really well.

It's a fundamental split.

If you're water soluble, you can't get through the cell membrane.

So you have to use a cell surface receptor.

You knock on the door.

You knock on the door.

And that triggers a G protein cascade inside, which generates second messengers.

Things like campy, IP3, calcium ions.

And the second messengers amplify the signal.

Massively.

One hormone binding can create thousands of second messenger molecules.

It's a very fast way to change cell metabolism.

Okay.

So that's strategy one.

What about the steroids and thyroid hormones?

They're lipid soluble.

So they just walk right through the door.

They use intracellular receptors.

Found in the cytoplasm or the nucleus.

Right.

And when the hormone binds, that whole complex becomes a transcription factor.

It goes to the DNA and literally turns genes on or off.

That sounds slow.

It is.

This is called nuclear initiated steroid signaling.

And because you're making new proteins, it can take hours or days.

But steroids can also act fast, right?

They can.

And this was a huge discovery.

It's called membrane initiated steroid signaling.

It turns out some steroid receptors are also on the cell surface.

So they can knock on the door too.

Exactly.

They can trigger a rapid G protein cascade, just like a peptide hormone.

The full response to a steroid is often this combination of a fast membrane effect and a slow long -term genetic effect.

Now, none of this works without tight control.

That's where feedback comes in.

Feedback is everything.

The system constantly monitors its own output and overwhelmingly it uses negative feedback.

The thermostat analogy.

The thermostat analogy.

The response diminishes the original stimulus.

When hormone levels get high enough, it tells the gland to stop making more.

But sometimes you need the opposite.

You need to amplify a signal.

That's positive feedback.

It's much rarer because it's inherently unstable.

The response enhances the stimulus.

Like oxytocin in childbirth.

The classic example.

Contractions trigger more oxytocin, which triggers stronger contractions, creating a loop that only ends when the baby's delivered.

And we see this control in its most complex form with the pituitary gland, which folder 21 .1 describes as a three tiered system.

Right.

Tier one is the hypothalamus secreting its regulating hormones.

They get sent directly to the pituitary through that special portal system.

Tier two is local chatter within the gland itself.

Yes.

Paracrine and autocrane secretions.

The pituitary cells release growth factors and cytokines that influence their neighbors.

Just fine tuning the response locally.

And tier three is the classic feedback loop.

That's the negative feedback from the circulating hormones produced by the target glands.

So thyroid hormone or cortisol travels all the way back to the pituitary and the hypothalamus and says, okay, we have enough.

Shut it down.

That dual level feedback is what gives the system such exquisite control.

All right.

Let's talk about the master regulators themselves,

the pituitary and the hypothalamus.

The absolute command center.

They're linked physically by the infundibulum or pituitary stock and functionally they are inseparable.

The pituitary itself is tiny, right?

Sits in the cell at tersica at the base of the brain.

It is only about half a gram, though the text mentions it can swell up to one and a half grams in women who had multiple pregnancies.

That's a huge increase.

It is due to the growth of the lactin producing cells.

But the key to understanding its function is its bizarre dual origin, which is shown in figure 21 .6.

It's everything.

The anterior lobe, the adnohypophysis is glandular tissue.

It forms from an upward pouching from the roof of the primitive mouth called Rathke's pouch.

And the posterior lobe.

That's the neurohypophysis.

It's pure neural tissue.

It grows downward from the brain.

So you have a glandular part and a neural part fused together.

One makes hormones, the other just stores them.

Precisely.

And the text breaks them down further.

The anterior lobe has the large pars distalis, the pars intermediate, and the pars tuberalis that wraps the stock.

And the posterior lobe is the pars nervosa and the infundibulum itself.

Right.

The blood supply here is so important.

It's the whole secret to how the hypothalamus maintains control.

It really is the anatomical key.

The text points out that the main part of the anterior lobe, the pars distalis, has no direct arterial supply.

So how does it get its instructions?

Through the hypothalamus -hypophysial portal system.

It's brilliant.

It's shown really well in figure 21 .7.

Walk us through it.

The superior arteries form a primary capillary plexus in the median eminence.

Hypothalamic neurons dump their regulating hormones right there.

Those capillaries then drain into the hypophysial portal veins, which travel down the stock and immediately open up into a secondary capillary plexus in the pars distalis.

So it's like a private subway line.

That's a perfect analogy.

A private subway that delivers a super concentrated dose of hycothalamic hormones directly to the target cells without being diluted in the general circulation.

And it's in that secondary plexus that the anterior pituitary cells do their work, releasing six key hormones.

The text splits them into two groups.

They have the tropic hormones, ACTH, TSH, FSH, and LH.

They're tropic because their target is another endocrine gland.

And then the non -tropic hormones.

GH and prolactin.

They act directly on non -endocrine tissues like bone or the mammary glands.

Table 21 .1 has a great summary of what each one does.

Histologically, the early stains gave us a rough idea of cell types.

Figure 21 .8 shows the classic acidophils, basophils, and chromophobes.

Right.

Acidophils stain red, basophils stain blue, and chromophobes don't stain well at all.

But modern immunocytochemistry gives us the real functional breakdown into five cell types.

Let's run through them.

Let's do it.

The most numerous, at 50%, are the somatotropes.

They're acidophils.

And they make growth hormone.

Yes.

Stimulated by GHRH, inhibited by somatostatin, and, get this, powerfully stimulated by ghrelin, the hunger hormone.

Linking growth directly to feeding.

Makes sense.

It does.

Next, at about 15 to 20%, are the lactotropes, another acidophil population.

They make prolactin.

And their control is weirdly backward, right?

It is.

The main control is inhibitory.

Dopamine from the hypothalamus constantly tells them not to release prolactin.

They only get going when that break is removed.

Okay, now for the basophils.

First, the corticotropes, another 15 to 20%.

They make a huge precursor molecule called POMC, which gets chopped up to make ACTH and other things.

They're controlled by CRH.

The gonadotropes, about 10%.

They make both LH and FSH, and they're regulated by GNRH.

And finally, the smallest group.

The thyrotropes, only about 5%.

They make TSH and are controlled by TRH.

And what about the cells that don't make hormones, the support cells?

Ah, the folliculostalate cells.

They're star -shaped cells that are all interconnected by gap junctions.

They don't secrete hormones, but the theory is that they form a communication network to coordinate the activity of the whole gland.

Briefly, what about the other parts of the anterior lobe, the pars intermedia and tuberalis?

The pars intermedia, which you can see in figure 21 .9, is mostly a remnant in humans.

It surrounds these little cystic leftovers from Rathke's pouch.

Its function isn't really clear.

And the pars tuberalis?

It's the collar that wraps around the infundibulum.

It's highly vascular because it's where those crucial portal veins run.

Okay, let's shift gears to the posterior lobe.

If the anterior is the factory, the posterior is, what, the warehouse?

The warehouse is a perfect description.

It's not a gland, doesn't make anything.

It's just a storage and release site for two hormones made way up in the hypothalamus.

Specifically, oxytocin and ADH.

Right.

They're made in the cell bodies of neurons in the paraventricular and supraoptic nuclei of the hypothalamus.

They're packaged up and then shipped all the way down the axons to the terminals in the pars nervosa.

So, when we look at the histology, what are we actually seeing?

Figures 21 .10 and 21 .1 show some distinct features.

You're seeing a ton of unmyelinated axons, and the key feature to look for are the herring bodies.

The large pink blobs.

Exactly.

Those are massive accumulations of neurosecretory vesicles, basically visible storage depots of ADH and oxytocin, waiting for a nerve signal to be released.

And the main cell type here isn't a neuron, it's a glial cell.

Yes, the pituitcite.

It's a specialized astrocyte -like cell that provides structural support for all those axons and terminals.

So, let's quickly summarize the two hormones released here, as shown in table 21 .4.

First, oxytocin.

Oxytocin is all about smooth muscle contraction.

It targets the uterus during labor and the myoepithelial cells in the breast for milk ejection.

Classic positive feedback.

And second, antidiuretic hormone or ADH.

Also called vasopressin.

Its main job is water balance.

It acts on the collecting ducts in the kidney.

How?

It triggers the insertion of water channels, called aquaporins, into the cell membranes.

This makes the ducts permeable to water, allowing the body to reabsorb water and concentrate the urine.

And its release is triggered by what?

High plasma osmolality.

Basically, when your blood gets too salty, the hypothalamus senses it and releases ADH to conserve water.

Since ADH is so critical for water balance, when it goes wrong, the effects are dramatic.

Folder 21 .3 covers this.

Absolutely.

If you don't have enough ADH, you get diabetes insipidus.

This is a state of extreme thirst and polyuria, where a person can produce up to 20 liters of very dilute urine a day.

And that can be a problem with the hypothalamus or the kidney itself.

Right.

If the brain can't make or release ADH, it's hypothalamic DI.

If the kidney receptors are broken and can't respond to it, it's nephrogenic DI.

And the opposite problem.

Too much ADH.

That's SIADH, the syndrome of inappropriate ADH secretion.

Often caused by certain tumors or brain injuries.

And what happens then?

You retain way too much water.

This dilutes your blood sodium to dangerously low levels, a condition called hyponatremia, which can cause the brain to swell.

So to wrap up this section, let's revisit the hypothalamus.

It's the ultimate translator.

It really is.

It coordinates the autonomic nervous system, it maintains homeostasis, and as we've seen, it directly controls the pituitary gland.

It translates neural signals, emotions, stress, temperature, into physiological hormonal responses.

And tail 21 .5 is a great cheat sheet for those hypothalamic releasing and inhibiting hormones.

GHRH, CRH, GNRH, TRH are the big stimulators.

Somatostatin and dopamine are the key inhibitors of this beautiful push and pull system.

Before we move on, folder 21 .2 summarizes how this can all break down.

Right.

Endocrine diseases generally boil down to one of four things.

Hormone overproduction, like from a tumor.

Hormone underproduction, from something like autoimmune destruction, altered tissue response like insulin resistance, or simply tumors themselves.

Okay, let's move on to two smaller but fascinating glands, starting with the pineal gland.

The epiphysis cerebre.

Figure 21 .12 shows it tucked away near the third ventricle.

Like the posterior pituitary, it develops from neuroectoderm.

And its main job is all about rhythm.

It's the body's timekeeper.

The Chi cells here are the pinealocytes, and they secrete melatonin.

The other cells are just supportive interstitial cells, which are basically glial cells.

And as we age, a very strange feature appears here.

The corpora erinacea, or brain sand.

You can see it in figure 21 .13.

It's basically calcified concretions that build up over time.

Do they do anything?

Not that we know of, but they're very dense, so they show up on x -rays, and are a great landmark for radiologists to find the brain's midline.

So how does the pineal gland know when to make melatonin?

It's photosensitive, but indirectly.

It gets information about the light -dark cycle from the retina.

And melatonin secretion goes up in the dark.

Dramatically.

This is what regulates our circadian rhythms.

It also has an antigenatal effect, inhibiting GnRH, which helps time puberty.

This is why it's so linked to jet lag and seasonal affective disorder.

Okay, now to the neck and the largest pure endocrine gland, the thyroid.

Located right in the anterior neck, as you can see in figure 21 .14, its functional unit is completely unique in the endocrine system.

Not cords of cells.

No, it's the thyroid follicle,

which figure 21 .15 shows is basically a sphere of epithelial cells surrounding a central lumen filled with a gel -like substance called colloid.

And the wall of that sphere has two different cell types.

The main ones are the follicular cells.

They form the wall and they produce the thyroid hormones, T4 and T3, which are critical for metabolism.

And tucked in between them.

You find the paraphilicular cells, or C cells.

They're shown in figure 21 .1c.

They don't touch the colloid.

Their job is to make calcitonin, which lowers blood calcium.

So what exactly is that colloid in the middle?

Colloid is almost entirely a massive glycoprotein called thyroglobulin, or T.

The thyroid is the only endocrine gland that stores a huge three -month supply of its hormone precursor extracellularly.

The synthesis of thyroid hormone is famously complex.

Figure 21 .18 lays out the six steps.

Let's walk through them.

Okay.

Step one is simple.

The follicular cells make thyroglobulin and secrete it into the colloid.

Step two, you need iodide.

Right.

The cell actively pumps iodide from the blood using a transporter called NIS.

It concentrates it massively.

Then another transporter, pendrin, moves it into the colloid where an enzyme, thyroid peroxidase, TPO, immediately oxidizes it.

So steps three and four happen out in the colloid.

Correct.

TPO then attaches that active iodine to the tyrosine residues on the thyroglobulin molecule.

This forms MIT and DIT.

And then TPO couples them together.

Exactly.

MIT plus DIT makes T3.

DIT plus DIT makes T4.

And these hormones are still attached to the huge TTU molecule in storage.

Step five is getting it back, and this is triggered by TSH.

Right.

The cell reaches out and engulfs some of the colloid.

The main pathway involves fusing that vesicle with a lysosome, which digests the TG and frees the T4 and T3.

And finally, step six is release.

The free T4 and T3 diffuse out of the cell and into the blood.

Most of it immediately binds to carrier proteins like TVG.

Only about 1 % remains free and active.

And T3 is the much more potent form.

How does the body activate the T4 it produces?

Through diadenase enzymes in the target tissues, they locally convert the storage form T4 into the active form T3.

It's a way of fine -tuning the metabolic effect right where it's needed.

And this whole process is under tight negative feedback control, as shown in figure 21 .19.

A classic loop.

High levels of free T4 and T3 in the blood feed back to the pituitary and hypothalamus and shut down the production of TSH and TRH.

When this system goes wrong, it's very common.

A major sign is often a goiter.

Right, which is just an enlargement of the gland.

And it can happen in both hypothyroidism and hyperthyroidism.

Let's talk about hyperthyroidism.

This is an underactive gland.

Maybe due to iodine deficiency or an autoimmune attack like Hashimoto's thyroiditis.

Low T4 and T3 levels mean TSH is constantly high, which makes the gland grow.

And the opposite, an overactive gland.

That's hyperthyroidism.

And the classic cause is Graves' disease.

This is an autoimmune disease where the body makes antibodies that mimic TSH.

So they're constantly stimulating the gland.

Constantly.

It leads to high metabolic rate, weight loss, and the characteristic bulging eyes or exophthalmos, which you can see in figure F21 .4 .1a.

And under the microscope.

The follicular cells become tall and columnar instead of cuboidal, and the colloid looks depleted and scalloped at the edges because it's being eaten up so quickly.

All right.

Let's move on to the four tiny but vital parathyroid glands.

Usually found on the back of the thyroid as figure 21 .1 tune shows, they are absolutely essential for life.

Two cell types here, as seen in figure 21 .20.

The most numerous are the principal or chief cells.

They're small and pale, and they're the ones that make parathyroid hormone or PTH.

And those big pink cells.

Those are the oxyfil cells.

They show up around puberty and are packed with mitochondria, which is why they stain so brightly.

But weirdly, we have no idea what they do.

So PTH is the star here, its main job.

It is the single most important regulator of blood calcium.

Its job is to raise blood calcium levels.

If you remove these glands, calcium plummets, and you get fatal muscle tetany.

How does it raise calcium?

It has three targets.

First, on bone.

It doesn't act on osteoclasts directly.

It stimulates osteoblasts to release factors that then activate the osteoclasts to break down bone and release calcium.

Second, the kidney.

In the kidney, it increases calcium reabsorption and increases phosphate excretion.

And third, it involves vitamin D.

It tells the kidney to convert vitamin D into its most active form, which then dramatically increases calcium absorption from the gut.

So PTH and calcitonin are a pair.

An antagonistic pair.

PTH is for slow, long -term control.

Calcitonin is for rapid, short -term adjustments if calcium gets too high.

Okay, on to our final stop, the adrenal glands.

The suprenal glands, sitting on top of the kidneys, as shown in figure 21 .21.

Structurally, these are two glands in one.

An outer cortex and an inner medulla.

And again, a dual embryological origin.

Which is key.

The cortex is mesodermal and makes steroids.

The medulla is from the neural crest, so it's basically a modified sympathetic ganglion.

And the blood supply is designed to make them work together.

Brilliantly designed.

The medulla gets a dual supply.

It gets fresh arterial blood, but also gets venous blood that has already flowed through the cortex.

So it's getting a blood supply that's full of cortical steroids.

Exactly.

And those steroids are what tell the medullary cells to become hormone -secreting cells instead of regular neurons.

It's a beautiful local control mechanism.

And the vein that drains it all is pretty special, too.

The central adrenal medullary vein.

You can see in figure 21 .25 that it has these thick longitudinal bundles of smooth muscle.

When they contract, they squeeze the hormones out of the gland for a rapid release.

Let's talk about the medulla first.

Its cells are called chromothin cells.

And as we said, they're modified neurons.

They're innervated by sympathetic nerves.

And when stimulated, they dump catecholamines, epinephrine, and norepinephrine into the blood.

And the cortical steroids actually determine which one they make?

Yes.

The glucocorticoids induce the enzyme that converts norepinephrine to epinephrine.

And this release is the classic fight -or -flight response.

The body's instant mobilization.

Increase heart rate, blood pressure, release glucose, shuttle blood to the muscles.

Table 21 .9 summarizes it all.

And tumors of these cells?

That's a pheochromocytoma, as described in folder 21 .5, a rare tumor that causes massive uncontrolled release of catecholamines, leading to severe hypertension and anxiety.

Now for the cortex.

It's divided into three distinct zones.

The classic mnemonic, salt, sugar, sex.

Let's start from the outside in.

The zona glomerulosa, about 15 % of the cortex.

It makes mineralocorticoids, mainly aldosterone.

The salt hormone.

Exactly.

It regulates sodium and potassium balance.

And it's controlled by the renin -angiotensin system, not the pituitary.

Next, the biggest zone.

The zona fasciculata, 80 % of the cortex.

The cells are arranged in long cords and look foamy, which is why they're called spongiocytes.

All the lipid droplets.

Full of cholesterol.

This zone makes the glucocorticoids, mainly cortisol.

The sugar and stress hormone.

Right.

It manages long -term metabolism and suppresses inflammation.

And this zone is controlled by ACTH from the pituitary.

And the innermost layer.

The zona retricularis.

Smaller cells in a net -like arrangement.

It makes the gonadocorticoids, or adrenal androgens.

The sex precursors, also controlled by ACTH.

And all of these steroids start from one molecule.

Cholesterol.

Folder 21 .6 explains that the first rate -limiting step for all of them is an enzyme called P450SCC, which is located in the mitochondria.

And the rest of the synthesis is this complex back and forth.

It is.

The steroid precursors have to be shuttled between the mitochondria and the smooth ER, where the different enzymes are located, until you get the final product.

Finally, we have to mention the unique fetal adrenal gland.

It's huge, proportionally.

And as figure 21 .29 shows, it has a thin outer permanent cortex and a massive inner fetal cortex.

And this fetal cortex works with the placenta.

It forms the fetal placental unit.

Neither organ has all the enzymes for steroid synthesis, so they pass precursors back and forth to get the job done.

And after birth.

The fetal cortex just disappears almost completely.

It undergoes rapid involution.

And the permanent cortex slowly matures into the three adult zones.

A failure in any of those enzymes leads to conditions like congenital adrenal hyperplasia.

What an incredible journey, from paracrine signaling all the way to these complex, multilayered glands.

The key takeaway is the hierarchy.

You have the master regulators, the metabolic regulators, and this constant, beautiful feedback that keeps it all in balance.

It's just exquisite chemical engineering.

So as we wrap up, here's a final thought to leave you with.

The nervous system evolved for pure speed using electricity.

The endocrine system, built from so many different parts and reliant on physical transport in the blood, seems to have prioritized something else.

So the question is, considering things like that portal system in the pituitary, or how the adrenal cortex has to chemically prepare the medulla, how might evolution have prioritized redundancy and metabolic fine tuning over raw speed in our chemical communication systems?

Thank you for joining us on the Deep Dive.

We hope this tour has given you the knowledge you need to really master this fascinating system.