Secretion of catecholamines by the adrenal medulla
Chromaffin cells located in the adrenal medulla are responsible for the production of catecholamines. The primary hormone they store in their secretory granules is epinephrine (adrenaline). Norepinephrine (noradrenaline) is synthesized in smaller amounts. Interestingly, along with these hormones, ATP molecules and enkephalins are released into the bloodstream.
At physiological rest, secretion is low, with blood norepinephrine levels slightly exceeding epinephrine concentrations. The situation changes radically upon activation of the sympathetic nervous system: hormone release increases sharply. During short-term excitation, epinephrine dominates, but with prolonged stimulation, its proportion drops, giving way to norepinephrine.
This process is controlled by the hypothalamus. Nerve impulses travel via sympathetic preganglionic fibers of the celiac nerve. Their endings release the neurotransmitter acetylcholine, which binds to nicotinic cholinergic receptors, triggering the release of catecholamines into the blood. Inactivation of spent hormones occurs with the participation of monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) enzymes, after which the metabolites are excreted by the kidneys.
Adrenoreceptors and systemic effects
The action of catecholamines is mediated through specific G protein-coupled membrane receptors. They are divided into alpha- and beta-adrenoreceptors. Stimulation of $\alpha_1$-receptors leads to an increase in intracellular calcium concentration, whereas activation of $\alpha_2$-receptors decreases cAMP levels. Interaction with $\beta$-receptors, conversely, activates adenylate cyclase and increases intracellular cAMP.
Epinephrine has the highest affinity for $\beta$-receptors, while norepinephrine has the highest affinity for $\alpha$-receptors. The number and sensitivity of these structures can change: they lose sensitivity upon prolonged contact with agonists (desensitization via phosphorylation) and increase it under the influence of glucocorticoids and thyroid hormones.
Main physiological effects of epinephrine:
- Metabolism: causes hyperglycemia (enhances glycogenolysis, activates gluconeogenesis, decreases glucose uptake by tissues), stimulates lipolysis, and increases basal metabolic rate.
- Cardiovascular system: via $\beta_1$-receptors, increases the force and rate of heart contractions. In physiological doses, it dilates blood vessels in muscles and the liver, but constricts abdominal blood vessels. It is important to note that skin blood vessels constrict at any concentration.
- Nervous system: stimulates the reticular formation, enhances attention, and decreases pain sensitivity (antinociceptive effect).
Norepinephrine differs in that it causes total vasospasm, increasing both systolic and diastolic blood pressure (epinephrine increases only systolic). In addition, its effects on metabolism and the heart are less pronounced.
Endocrine function of the pancreas
The islets of Langerhans in the pancreas synthesize the most important regulators of carbohydrate metabolism—insulin and glucagon. The main factor governing their release is the blood glucose level. Secretion is also modulated by the autonomic nervous system and the paracrine influence of somatostatin, which is produced in neighboring islet cells.
Insulin is a peptide hormone synthesized by $\beta$-cells. Its key task is to stimulate nutrient deposition processes and lower plasma glucose levels. Interacting with tyrosine kinase receptors, insulin activates glucose transporters in muscle and adipose tissue, as well as in the myocardium.
Tissue effects of insulin:
- In the liver: inhibits gluconeogenesis and glycogenolysis while stimulating glycogen synthesis.
- In adipose tissue: blocks lipolysis and activates the formation of triglycerides from fatty acids (pronounced lipogenic effect).
- In muscles: promotes glycogen accumulation, enhances amino acid uptake and protein synthesis, exerting a potent anabolic effect.
Briefly: answers to topical questions
What hormones are secreted by the corpus luteum of the ovary?
The corpus luteum of the ovary secretes progesterone and estrogens.
- Progesterone is the dominant hormone of the corpus luteum; it regulates the cycle, controls the secretory phase, prepares the endometrium for implantation, and maintains pregnancy.
- Estrogens are secreted by the corpus luteum together with progesterone.
What are the main physiological effects of testosterone?
Testosterone has a wide range of effects on various tissues:
- During embryogenesis, it ensures male fetal development.
- It promotes the establishment of male sex characteristics and the ossification of epiphyseal cartilages.
- It maintains secondary sex characteristics and shapes sexual behavior.
- It stimulates spermatogenesis, regulates the prostate gland and seminal vesicles.
- It exerts an anabolic effect on muscles and bones, increasing protein accumulation.
- It stimulates erythropoietin production.
- It has an atherogenic effect (increases LDL, decreases HDL).
What phases are distinguished in the endometrial (uterine) cycle?
The endometrial cycle of the uterine mucosa has three phases:
- Menstrual phase (desquamation) — shedding of the necrotic functional layer of the endometrium (5±2 days).
- Proliferative phase — occurs before ovulation (days 4–14), characterized by proliferation of basal layer cells and regeneration of the functional layer under the influence of estrogens.
- Secretory phase — lasts from ovulation to menstruation (days 15–28), during which, under the action of progesterone, mucosal swelling and stimulation of uterine gland secretion occur.
Where is somatostatin produced in the pancreas and what are its exact functions?
Somatostatin is synthesized in D-cells ($\delta$-cells) of the pancreatic islets of Langerhans, which make up 5–10% of the cell population and are located predominantly at the periphery of the islets.
Its main function is the paracrine inhibition of secretion. The mechanism of action involves the activation of the inhibitory cAMP G-protein system. Somatostatin locally suppresses the secretion of insulin (by B-cells), glucagon (by A-cells), as well as the secretion of pancreatocytes in the exocrine part of the gland.
Class and exam questions
What stimulates insulin release?
The main stimulus is an increase in blood glucose concentration. Additionally, secretion is enhanced by gastrointestinal hormones such as gastrin and secretin.
What effect does insulin have on protein metabolism?
Insulin exhibits an anabolic effect: it enhances the entry of amino acids into cells, stimulates protein synthesis, and blocks its breakdown.
What else to study on this topic
- Mechanisms of intracellular signal transduction from adrenoceptors via G-proteins
- The role of somatostatin in the paracrine regulation of the islets of Langerhans
- Detailed effects of glucagon as an insulin antagonist
- Functioning of the sympathoadrenal system during stress and adaptation
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