Signaling by any of these hormones involves three key events:
Cell-Surface Receptors for Water-Soluble Hormones
The receptors for most water-soluble hormones are embedded in the plasma membrane, projecting outward from the cell surface
Animation: Water-Soluble Hormone
LE 45-3 SECRETORY CELL Hormone molecule Signal receptor VIA BLOOD VIA BLOOD TARGET CELL TARGET CELL Signal transduction pathway OR Cytoplasmic response DNA NUCLEUS Nuclear response Receptor in plasma membrane Receptor in cell nucleus DNA NUCLEUS mRNA Synthesis of specific proteins Signal transduction and response Signal receptor Hormone molecule SECRETORY CELL
The hormone epinephrine has multiple effects in mediating the body’s response to short-term stress
LE 45-4 Different receptors different cell responses Epinephrine receptor Epinephrine receptor Epinephrine receptor Vessel constricts Vessel dilates Intestinal blood vessel Skeletal muscle blood vessel Liver cell Different intracellular proteins different cell responses Glycogen deposits Glycogen breaks down and glucose is released from cell
Intracellular Receptors for Lipid-Soluble Hormones
Steroids, thyroid hormones, and the hormonal form of vitamin D enter target cells and bind to protein receptors in the cytoplasm or nucleus
Protein-receptor complexes then act as transcription factors in the nucleus, regulating transcription of specific genes
Aspirin (known chemically as acetyl salicylic acid and often abbreviated as ASA) belongs to a class of medications called nonsteroidal anti-inflammatory drugs or NSAIDs. Aspirin and other NSAIDs, for example, ibuprofen (Motrin, Advil) and naproxen (Aleve), are widely used to treat fever, pain, and inflammatory conditions such as arthritis , tendonitis, and bursitis . In addition to its effects on fever, pain, and inflammation , aspirin also has an important inhibitory effect on platelets in the blood. This antiplatelet effect is used to prevent the platelets from initiating the formation of blood clots inside arteries, particularly in individuals who have atherosclerosis or are otherwise prone to develop blood clots in their arteries.
Aspirin prevents blood from clotting by blocking the production of thromboxane A-2, a chemical that platelets produce that causes them to clump. Aspirin accomplishes this by inhibiting the enzyme cyclo-oxygenase-1 ( COX-1 ) that produces thromboxane A-2. While other NSAIDs also inhibit the COX-1 enzyme, aspirin is the preferred NSAID for use as an antiplatelet agent because its inhibition of the COX-1 enzyme lasts much longer than the other NSAIDs. Thus, aspirin ﾕ s antiplatelet effect lasts for days while the other NSAIDs ﾕ antiplatelet effects last for only hours.
Aspirin will inhibit the enzyme cyclo-oxygenase and will inhibit the prostaglandin-like substance, thromboxane A2 which in turn will increase the adhesion of platelets and cause a vascular blood clot, especially in a coronary artery.
aspirin inhibits the formation of chemicals called "prostaglandins" by blocking an essential enzyme needed for their formation. Among the many properties of prostaglandins is their ability to promote blood cells to stick together. Thus, by blocking the formation of prostaglandins, aspirin decreases the likelihood of blood clots forming in your blood vessels.Since a large number of heart attacks and strokes are directly caused by small, spontaneously forming blood clots, the ability of aspirin to prevent the formation of these small clots means that heart attacks and strokes become less likely.
LE 45-11 STIMULUS: Rising blood Ca 2+ level Thyroid gland releases calcitonin. Calcitonin Stimulates Ca 2+ deposition in bones Reduces Ca 2+ uptake in kidneys Blood Ca 2+ level declines to set point Homoeostasis: Blood Ca 2+ level (about 10 mg/100 mL) STIMULUS: Falling blood Ca 2+ level Blood Ca 2+ level rises to set point Stimulates Ca 2+ release from bones PTH Parathyroid gland Stimulates Ca 2+ uptake in kidneys Active vitamin D Increases Ca 2+ uptake in intestines
LE 45-12 Beta cells of pancreas release insulin into the blood. Insulin Liver takes up glucose and stores it as glycogen. STIMULUS: Rising blood glucose level (for instance, after eating a carbohydrate- rich meal) Blood glucose level declines to set point; stimulus for insulin release diminishes. Homeostasis: Blood glucose level (about 90 mg/100 mL) STIMULUS: Dropping blood glucose level (for instance, after skipping a meal) Blood glucose level rises to set point; stimulus for glucagon release diminishes. Liver breaks down glycogen and releases glucose into the blood. Body cells take up more glucose. Alpha cells of pancreas release glucagon into the blood. Glucagon
Hormones from the adrenal cortex also function in response to stress
They fall into three classes of steroid hormones:
Glucocorticoids, such as cortisol , i nfluence glucose metabolism and the immune system
Mineralocorticoids, such as aldosterone , a ffect salt and water balance
Sex hormones a re produced in small amounts
LE 45-13 Stress Hypothalamus Anterior pituitary Blood vessel ACTH ACTH Releasing hormone Nerve cell Nerve cell Long-term stress response Effects of mineralocorticoids: 1. Retention of sodium ions and water by kidneys 2. Increased blood volume and blood pressure Effects of glucocorticoids: 1. Proteins and fats broken down and converted to glucose, leading to increased blood glucose 2. Immune system may be suppressed Short-term stress response Effects of epinephrine and norepinephrine: 1. Glycogen broken down to glucose; increased blood glucose 2. Increased blood pressure 3. Increased breathing rate 4. Increased metabolic rate 5. Change in blood flow patterns, leading to increased alertness and decreased digestive and kidney activity Nerve signals Spinal cord (cross section) Adrenal gland Kidney