can anyone help me with a few of these please
1) when histamine is release from WBC's, how does dilation of the aterioles/arteries help injured or infected cells?
It allows the white blood cells (mostly macrophages) to travel to the site of infection and ingest the pathogens.
2)does the breakdown of the pigment in rod/cone cells cause the production of a generator potential?
Pigment in rod cells = rhodopsin = breaks down into retinal and opsin. Opsin binds to sodium ions channels in the upper part of the rod cell, causing it to close. This decreases the membrane potential in the rod cell (hyperpolarisation). It stops secreting neurotransmitter. The neurotransmitter, glutamate, is an inhibitory neurotransmitter. As soon as glutamate secretion stops, the bipolar cell becomes depolarised (generator potential) and sends an impulse down the optic nerve.
None of this is required for the AQA syllabus.
3) what is the second messenger model of adrenaline and glucagon action?
Adrenaline (first messenger) binds to its receptor on the cell memberane forming a receptor-substrate complex. This activates enzymes located on the inside of the membrane, which result in ATP being converted to cyclic AMP (cAMP). cAMP is the second messenger, and activates enzymes responsible for converting glycogen to glucose. *It also stimulates the production of glucagon by the alpha-cells in the pancreas (*info not in AQA textbook)
Adrenaline is produced during times of stress, when the muscles need a quick burst of energy.
Glucagon is not an enzyme, it is an hormone that binds to the receptors on liver cells and results in the activation of enzymes that convert glycogen to glucose.