BLOOD SUGAR REGULATION homeostasis

1. Liver Need to maintain 4-6 millimoles/L of sugar in blood Organs involved: Pancreas / adrenal glands (hormones) Liver 1. Liver Liver is connected via hepatic portal vein to: Stomach Spleen Pancreas Intestines

Liver (cont.) Liver has 4 functions for glucose: Removed by liver for energy in Liver Removed by liver or muscles & converted to glycogen (for storage) Circulated in blood to be available for body cells to use (as energy) Excess is converted into fat (long-term storage) Body stores approx 500g glycogen (100g in liver, remainder in muscles) Glycogenesis: glucose glycogen (influenced by insulin – from pancreas) Glycogenolysis: glycogen  glucose (influenced by glucagon – from pancreas) Glycogen in Liver: enough reserves for 6hrs, after that need to start converting fat

2. Pancreas Islets of Langerhans: Alpha cells: glucagon Beta Cells: insulin Insulin: (decrease blood sugar) from Beta cells Accelerates transport of glucose from blood to cells Accelerates ‘glycogenesis’ (glucose glycogen) Stimulates glucose  fat (adipose tissue) Increases protein synthesis in some cells Glucagon: (increase blood sugar) from Alpha Cells Stimulates ‘glycogenolysis’ (glycogen  glucose) Stimulates ‘gluconeogensis’ (fat/amino acid  sugar molecules) Stimulates protein breakdown

3. Adrenal Glands 3 hormones: Cortex: glucocorticoids (eg cortisol) Medulla: adrenaline Noradrenaline Glucocorticoids (increase blood sugar) Stimulated from anterior pituitary (ACTH) Stimulate glycogenolysis (glycogen  glucose) Increases rate by which amino acids are removed by cells & transported to liver for gluconeogenesis (fat/amino acids  glucose) Promotes mobilisation of fatty acids from adipose to allow fat  glucose

Adrenal Glands (cont.)   Adrenalin / Noradrenaline: (increase blood sugar) Stimulates glycogen (in muscle cells)  lactic acid  glucose (in liver) Stimulates glycogenolysis *Note: glucagon’s target organ is the liver Adrenaline/noradrenaline’s target organ is the liver and the muscles.

Gas concentrations homeostasis

Control of Breathing Diaphragm & intercostals require stimulation from nerves to contract. (unlike heart) Phrenic nerve (a spinal/cervical nerve from neck  thorax)  diaphragm Intercostal nerve (a spinal/thoracic nerve from neck  thorax)  Intercostal muscles Controlled by respiratory centre in lower medulla 2 regions: expiration & inspiration Chemoreceptor’s (conc. of chemicals in plasma- specifically CO2, O2 , and H+): Aortic – in aorta Carotid bodies – in carotid (neck) artery Medulla Oblongata

Conc .of O2: Receptors in Medulla, Carotid, and aortic bodies. only a large change will have an effect   Conc. of CO2: small change results in a large response but chemoreceptors are only located in medulla (70-80% of breathing rate changes are a consequence of CO2 change detection) Takes several minutes for response  

Conc. of H+: CO2 + H2O H2CO3  H+ + HCO3- As H+ increase, pH decreases, Aortic & Carotid bodies are stimulated Faster response but not as sensitive as CO2   Stretch Receptors: Stimulated when lungs inflate Send impulses to inspiratory neurons in Resp. Centre of Medulla & inspiration ceases, expiration begins Not very sensitive, only a protective mech. to prevent overstretching

Voluntary Control of Breathing Connectors from Cerebral Cortex to descending tracts in spinal cord Protective device  stops us inhaling water, irritating gases etc. Hyperventilation: Rapid deep breathing, Increases O2, decreased CO2 Dangerous as if done before swimming as: Can hold breath longer but not because of abundance of O2, but lack of CO2 Exercise and Breathing rate: Depth & rate must increase Heavy exercise can cause 10 – 20x more ventilation Due to fluctuations in O2, CO2 & H+ conc.

Blood Pressure/ heart rate homeostasis

Cardiac Output Heart rate: number of times heart beats/min Stroke volume: vol of blood forced from a ventricle/contraction Cardiac Output: vol of blood leaving ventricle / min Cardiac Output = Stroke vol x Heart rate Venus return: return of blood to heart Blood Pressure: Pressure of blood on vessel walls Influenced by: cardiac output & diameter of blood vessels

Regulation of heart rate Specialised cells which initiate impulse in heart: Sinoatria node (SA node) – in right atrium Causes both atria to contract Can be influenced by sympathetic (noradrenaline) and parasympathetic NS (acetylcholine) Atrioventricular node (AV node) -in septum between two atria (near AV valves) After being stimulated by Av node, conducting fibres from Av node pass impulse to both ventricles May be stimulated by sympathetic NS (noradrenaline)

Regulation of heart rate (cont.) Heart can be influenced by brain/CNS (Cardiovascular Regulating Centre) in Medulla Oblongata  to SA node or AV node Detected by pressoreceptors: (baroreceptors) detect blood pressure

Factors influencing stroke Volume Length of diastole: period of relaxation between contractions. (time to fill up) Venus return: contraction of the muscle fibres of the heart is more forceful when fibres are stretched (elasticity) influenced by activity of skeletal muscles, respiratory movements, tone of vein walls, reduced friction in vessels Autonomic nervous system Other factors: Age: Highest at birth, slows down towards old age Ave (70-80 bmp) Sex: females faster Emotional state: strong emotions (anger, fear, anxiety) increase & depression, grief decrease.

Blood Flow Amount of blood flowing through an organ or vessel (mL/min) Determined by: Cardiac output Diameter of arterioles. Determined by: CNS Hormones (adrenaline – vasodilator in muscle, vasoconstrictor everywhere else) CO2, lactic acid: Vasodilator, O2: Vasoconstrictor e.g Exercise Output of heart may rise from 5L/min to 30L/min