Endocrine vs Nervous Systems Overview

Comparison of Endocrine and Nervous Systems

• Endocrine system uses hormonal signaling via bloodstream, while the nervous system uses electrical signals through neurons.
• Endocrine responses are slow (seconds to days), while nervous system responses are fast (milliseconds).
• Endocrine effects are long-lasting (hours to weeks), while nervous system effects are short-term.
• Endocrine Target Range is widespread (systemic), while the nervous system target is specific and localized.
• Examples of endocrine function include regulating growth (GH, insulin), while examples of nervous system function are reflex actions (pain withdrawal).

Hormone Action Based on Chemical Structure

• Peptide Hormones: Examples include insulin and glucagon. These hormones bind to surface receptors and use second messengers like cAMP. Their target is the plasma membrane.
• Steroid Hormones: Examples include cortisol and estrogen. These hormones cross cell membranes and bind to intracellular receptors. Their target is inside the cell, either the membrane or nucleus.
• Amine Hormones: Examples like thyroxine (T4) and epinephrine. These hormones act like peptide or steroid hormones depending on their solubility, meaning their target site can be either the membrane or the nucleus.

Key Determinants of Hormone-Target Cell Interactions

• Hormone Concentration: Availability of the hormone in the bloodstream (controlled by secretion rate or degradation).
• Receptor Availability: Specificity and density of receptors on the target cell.
• Affinity: The strength of bonding between hormone and receptor.

Hypocalcemia Effects and Bodily Response

• Hypocalcemia Effects: Include muscle spasms/tetany, tingling/numbness in extremities, and cardiac arrhythmias.
• Bodily Response: Increased parathyroid hormone (PTH) secretion to elevate calcium levels. Vitamin D activation enhances calcium absorption from the gut. Bone resorption releases calcium into circulation.

Fluticasone for Asthma

• Fluticasone reduces inflammation, preventing asthma exacerbations in the long term.
• Stopping fluticasone abruptly can cause rebound symptoms or loss of control over inflammation.
• Fluticasone requires continued use to maintain anti-inflammatory effects.

Adipose Tissue Hormones

• Leptin: A peptide hormone, proportional to fat stores, suppresses appetite and increases energy expenditure. The target is the brain.
• Resistin: A peptide hormone proportional to fat stores, increases insulin resistance. The target is primarily the liver, fat, and muscle.
• Adiponectin: A peptide hormone inversely proportional to fat stores, enhances insulin sensitivity. The target is the same as resistin target.

Short-Term Stress Response (Adrenal Cortex)

• Glucocorticoids (Zona fasciculata): Maintain blood glucose levels, energy metabolism.
• Mineralocorticoids (Zona glomerulosa): Regulate sodium (Na+), potassium (K+) balance, blood volume, and blood pressure.
• Catecholamines (Adrenal medulla): Cause a fight-or-flight response (e.g., epinephrine release).

Thyroid and Parathyroid Glands

• Thyroid (T3, T4): Regulate metabolic rate, growth, and development. Location is anterior neck, below the larynx.
• Parathyroid (PTH): Regulates calcium and phosphate levels. Location is posterior to the thyroid gland.

Renin-Angiotensin-Aldosterone System (RAAS)

• RAAS is a system involving the kidneys, lungs, and adrenal cortex that regulates blood pressure.
• The steps in RAAS include renin release, Angiotensin conversion in the lungs, then aldosterone release from the adrenal cortex.
• Outcomes include converting angiotensinogen to angiotensin I, vasoconstriction, stimulating aldosterone, and increasing blood pressure.

cAMP in Cellular Signaling

• cAMP is ubiquitous (present in every tissue and cell), has brief but powerful activation effects, and is quickly degraded via phosphodiesterase (PDE).
• Hormones bind to receptors, activating G-proteins, which trigger cAMP synthesis by activating adenylate cyclase.
• cAMP activates protein kinase A (PKA) and the resulting phosphorylations lead to cellular effects.
• Terminating the signal is done via PDE degrading cAMP.

Hormone Classes and Mechanisms

• Water-soluble hormones bind to plasma membrane receptors, using second messengers. Examples include insulin and epinephrine.
• Lipid-soluble hormones cross plasma membranes, bind to intracellular receptors and directly affect gene transcription. Examples include cortisol and thyroid hormones.

Water-Soluble Hormones: Second Messenger Mechanism

• Hormones bind to extracellular GPCRs. G-protein subunits (α, β, γ) are involved, with GDP exchanged for GTP. Beta-gamma subunits detach.
• This leads to second messenger production (cAMP, DAG, IP3).
• Signal termination happens when cAMP is degraded, or Ca2+ levels are reduced.

Lipid-Soluble Hormones: Intracellular Mechanism

• Lipid-soluble hormones pass through the plasma membrane due to their hydrophobic nature. Receptor binding happens inside the cell, in cytoplasm or nucleus.
• Receptor-hormone complexes bind to DNA and mediate protein synthesis to produce specific effects.

G-Protein Coupled Receptor (GPCR) Signaling

• Gs stimulates adenylate cyclase to increase cAMP levels.
• Gi inhibits adenylate cyclase, reducing cAMP levels.
• Gq activates phospholipase C to initiate PIP2 signaling via DAG and IP3.

PIP2-Calcium Signaling Pathway

• Hormone binding to a GPCR activates Gq. Gq activates phospholipase C (PLC), which cleaves PIP2 into DAG and IP3.
• IP3 releases calcium from the endoplasmic reticulum. Calcium activates calmodulin which activates other target proteins. DAG activates protein kinase C (PKC) and phosphorylates target proteins.

Overview of Endocrine Glands

• Endocrine glands produce and release hormones directly into the bloodstream.
• Endocrine glands lack ducts and act systemically, impacting distant targets in the body.

Types of Endocrine Glands

• Examples of dedicated endocrine glands include the pituitary, thyroid, parathyroid, adrenal, and pineal glands.
• Examples of dual-function organs include the pancreas (insulin, glucagon, digestive enzyme production), gonads (sex hormones, gamete production), and placenta (placental hormones, nutrient/waste exchange).

Nervous vs. Endocrine System Comparison

• Nervous system responses are fast and short-lived, using action potentials and neurotransmitters.
• Endocrine responses are slow and long-lasting, using hormones in the blood.
• Nervous system action is specific to defined pathways, while endocrine actions are broad, touching all areas where the blood goes.

Examples of Hormone-Producing Glands and Their Hormones

• Pituitary: Growth hormone (GH), adrenocorticotropic hormone (ACTH)
• Thyroid: T3, T4
• Adrenal: Cortisol, aldosterone
• Pineal: Melatonin
• Pancreas: Insulin, glucagon
• Gonads: Testosterone, estrogen

Hormones and Their Broad Mechanisms

• Water-soluble hormones bind to plasma membrane receptors, triggering second messenger pathways. Examples include insulin and epinephrine.
• Lipid-soluble hormones cross cell membranes, bind to intracellular receptors, and directly affect gene transcription. Examples include cortisol and thyroid hormones.

Highlights from Table 16.1: Systems Comparison

• Nervous system initiates responses rapidly and has short-duration effects, using action potentials and neurotransmitters. It operates in specific locations.
• Endocrine system initiates responses slowly and has long-duration effects, using hormones in the blood. It has diffuse effects throughout the body.