Angiotensin II acts as a mediator for the Renin-Angiotensin-Aldosterone system, it does this by activating Angiotensin type 1 (AT1) receptor and Angiotensin type 2 (AT2) receptor. The AT1 receptors stimulate the production of aldosterone from the adrenal zona glomerulus. The receptors are found in vasculature,
They receive signals in order to be activated. One of these signals is a cytokine known as interferon gamma (IFN-γ) secreted mainly by T helper cells. When LDL is deposited, macrophages are activated and the number of MHC class II molecules displayed on their surfaces is increased. When they engulf the LDL, it is broken down and presented to the T helper cells along with the MHC class II molecules for destruction and they are now seen as antigen presenting
As Angiotensin I flows through the renal and pulmonary circulations, a second enzyme called Angiotensin Converting Enzyme (ACE) cleaves Angiotensin I into Angiotensin II. Angiotensin II acts in three ways to conserve ECF volume. First, AT-II is a powerful vasoconstrictor. AT-II constricts the renal arteries and arterioles in order to increase perfusion pressure in the renal cortex where most glomeruli are located. Second, AT-II crosses into 2 areas of brain lacking the blood-brain barrier (the SFO- Subfornical Organ and OVLT – Vascular Organ of the Lamina Terminalis) to trigger the sensation of thirst.
The resting potential is generated by the specific changes in membrane permeability for of potassium (K+) and sodium (Na+) ions, which in turn result from concentrated changes in functional activity of ion channels. Cell membranes are made up of a phospholipid bilayer- consisting of two layers of linked fatty molecule. Various specialized proteins, such as ion channels, float in this bilayer. Ion channel are membrane-spanning proteins that allows the passage of certain ions through the membrane. The cell membrane of a neuron is selectively permeable to potassium ions, meaning that ion channels that will only allow potassium ions to exit or enter the cell freely.
There are many theories of emotion: i. James-Lange theory (1890) [cited in Taylor, 1999]: Subjective emotional responses are the result of physiological changes within human bodies. The brain perceives an event and, in turn, sends messages down its neural circuit to other areas of the brain. This action ultimately produces motor, autonomic and endocrine responses. These responses elicit an emotional response, which in turn, is perceived by the brain. Therefore, it is a cyclical process.
Receptors Receptors specifically bind to target molecules and initiate a response in the target cell. In most cases, these receptors are transmembrane proteins on the cell surface. When an extracellular signal molecule binds to them, they release a cascade of intracellular signals that alter the behavior of the cell1. In this experiment, we will be adding compounds, such as eserine and acetylcholine to a muscle cell bath and measuring its effect, in this case being force of contraction. These compounds target muscarinic acetylcholine receptors to produce their response, which will be made into a concentration/effect curve.
The adrenal cortex is responsible for secreting corticosteroids and hormones such as: • Cortisol enables the control the body 's use of fats, proteins, and carbohydrates as well as suppresses inflammatory reactions in the body • Aldosterone which regulates the level of sodium and potassium in the body and helps maintain blood volume and blood pressure. Aldosterone is regulated by complex feedback mechanisms involving sodium and potassium levels as well as blood volume. • Androgenic steroids which are hormones that are converted elsewhere in the body to female hormones (estrogens) and male hormones (androgens) The adrenal medulla is responsible for helping the body cope with emotional and physical stress and secretes hormones such as: • Epinephrine which helps the body to respond to a stressful situation by increasing the heart rate and force of heart contractions, facilitating blood flow to the muscles and brain, causing the relaxation of smooth muscles, helping with conversion of glycogen to glucose in the liver, and other activities.
Acetylcholine travels from the neuromuscular junction and binds to acetylcholine receptors which are activated and generate a muscle contraction. In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle contraction
The brain is the control centre for the nervous system The nervous system is split into two; -central nervous system; *brain *spinal cord -peripheral nervous system; *sensory division- informs the central nervous system of outer changes *somatic division- sends instructions of movement to different muscles *autonomic division- controls the running of inner organs -autonomic nervous system -somatic nervous system
A few cases have been described that have proved resistant to aggressive treatment with surgery, radiotherapy, dopamine agonists, and, occasionally, chemotherapy. In a small proportion, extracranial metastases in liver, lungs, bone, and lymph nodes have been documented. • ACTH-secreting adenomas (or corticotropinomas). ACTH stimulates the adrenal gland to make glucocorticoids (or steroids, which influence metabolism and act as anti-inflammatory and immunosuppressive agents). An oversupply of ACTH, such as that produced by this type of tumor, can cause Cushing's disease (one type of Cushing's