Physiology & Anatomy II: Posterior Pituitary Hormones

Antidiuretic Hormone (ADH) is primarily synthesized in the supraoptic nucleus (SON) of the hypothalamus and transported through the hypothalamic-hypophysial tract for storage in the posterior pituitary. It is a peptide hormone composed of 9 amino acids.

ADH's primary function is to increase water reabsorption in the late distal tubules and collecting ducts of the kidneys. This occurs by inserting water channels (aquaporins) into the luminal membrane, making the tubules permeable to water. Without ADH, these tubules are impermeable, leading to increased water loss in urine.

In addition to its water reabsorption role, ADH also causes vasoconstriction of vascular smooth muscle. This helps to regulate blood pressure.

ADH secretion is primarily regulated by changes in extracellular fluid volume and osmolarity. Increased osmolarity (concentrated fluids) and decreased volume trigger increased ADH release. Pain, exercise, and stress can also stimulate ADH secretion.

Diabetes insipidus is characterized by the production of large volumes of diluted urine due to a deficiency in ADH. This leads to excessive fluid loss, dehydration, and potential electrolyte imbalances.

Excess ADH secretion can lead to water retention and increased extracellular fluid volume. This can result in hyponatremia (low sodium levels) and possibly edema.

Oxytocin, a polypeptide hormone composed of 9 amino acids, is synthesized in the paraventricular nucleus (PVN) of the hypothalamus and transported to the posterior pituitary for storage.

Oxytocin's primary action is to stimulate contraction of the myoepithelial cells surrounding mammary alveoli, forcing milk from the alveoli into ducts and delivering it to the baby. This is known as milk ejection.

A hormone released during childbirth that stimulates uterine contractions, leading to the expulsion of the baby. It also plays a role in breast milk production.

The process where a substance, like oxytocin, stimulates its own production, leading to a rapid increase in its levels.

The outer layer of the adrenal gland, responsible for producing steroid hormones like cortisol and aldosterone.

A type of steroid hormone produced by the adrenal cortex, primarily responsible for regulating blood sugar levels.

The main glucocorticoid hormone, responsible for regulating blood sugar, immune responses, and stress responses.

The process of converting non-carbohydrate sources, like amino acids, into glucose.

The breakdown of proteins into smaller units, amino acids.

The process of building proteins from smaller units, amino acids.

Glucocorticoids boost gluconeogenesis by stimulating the synthesis of enzymes required for glucose production from non-carbohydrate sources.

Glucocorticoids oppose insulin's effects, decreasing glucose uptake and oxidation by muscles and adipose tissue.

Glucocorticoids promote protein breakdown and inhibit protein synthesis, mainly in skeletal muscles.

Glucocorticoids increase the release of free fatty acids from adipose tissue, boosting their levels in the bloodstream.

Glucocorticoids suppress inflammation by inhibiting the release of arachidonic acid, a precursor to inflammatory mediators.

Glucocorticoids suppress the immune response by inhibiting the production of crucial immune cells and signaling molecules.

Glucocorticoids are essential for the full effect of hormones like glucagon and catecholamines.

Glucocorticoids increase blood pressure by enhancing the vasoconstriction effect of norepinephrine.

Glucocorticoids mediate stress responses, increasing blood glucose levels through gluconeogenesis and enhancing the effects of glucagon and catecholamines. They also maintain vascular reactivity and contribute to the mobilization of fatty acids for emergency energy.

Cortisol, the main glucocorticoid, increases blood glucose by promoting gluconeogenesis and enhancing the effects of glucagon and catecholamines.

Glucocorticoids are essential for catecholamines, like adrenaline, to exert their full effects on blood vessels and fat mobilization. This is called a permissive effect.

The hypothalamus, anterior pituitary, and adrenal cortex form a feedback loop to regulate cortisol secretion.

Stressful stimuli trigger the hypothalamus to release corticotropin-releasing hormone (CRH), which stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH). ACTH then acts on the adrenal cortex, leading to cortisol production.

High levels of cortisol inhibit the release of CRH and ACTH, reducing further cortisol production and creating a negative feedback loop.

Cortisol levels naturally rise in the early morning and decline throughout the day, following a cyclical pattern.

The hypothalamus contains a biological clock that regulates the release of ACTH and, consequently, cortisol.