Control of Vasculature and Pressure

• influences on blood flow are neural and hormonal means of regulation • these central mechanisms are critical for maintaining constant blood pressure and regulating distribution of blood flow to organs and tissues

• refer to local effectors which exert local influences - these local mechanisms are important in regulating the distribution at the organ and tissue level

PNS - release of acetylcholine, binds muscarinic receptors on pacemaker cells, rate of depolarisation decreases, decrease SNS - release of noradrenaline, binds to beta adrenergic receptors, this increases the rate of depolarisation of pacemaker cells increasing heart rate and also affects the myocardium by increasing sarcomere length and increasing contractile force

Noradrenaline release from SNS helps to maintain myogenic tone. It is released from post-ganglionic neurons and binds to alpha1 receptors leading to vasoconstriction.

Release of adrenaline from the adrenal medulla Binds to alpha1 receptors and causes vasoconstriction

Adrenaline = alpha1, beta1, beta2 Noradrenaline = alpha 1, beta1 Alpha1 - vasoconstriction of vascular beds Beta1 - cardiac contractility and HR Beta2 - vasodilation in the heart, liver and skeletal muscle arterioles

It causes vasodilation in select vascular beds: salivary glands, pancreas, intestines

Local hormones Nitric oxide Sympathetic nerves releasing noradrenaline

It increases vascular permeability. Leads to NO release which causes vasodilation.

Metabolic - (increase in blood flow to a particular tissue) important in cardiac and skeletal muscle increased metabolism enhances production of substances which cause vasodilation of arteries Reactive - (reduced blood flow to a tissue) if local blood flow is cut off, metabolites accumulate and cause vasodilation. When blood flow is resumed, it is enhanced until the metabolites wash out.

Thermoregulation • Arteriovenous anatomises are muscular vessels found in skin extremities. • Blood flow is regulated by thermoreceptors and the SNS • Cold temperature causes increase in vasocontriction to shunt blood away from the venule (increase in sympathetic discharge) • Hot temperature causes a decrease in sympathetic discharge and allows blood to enter the dermal venous plexus

• Stroke Volume and Heart Rate • Total Peripheral Resistance • Central venous pressure and blood volume

Baroreceptors contain fine nerve ending sensitive to stretch - located in the aortic arch and carotid sinus The thin wall of the carotid sinus allows small changes in pressure to be detected. A decrease in pressure causes a decrease in firing of nerve endings.

Gravity causes pooling pf blood in lower limbs. This decreases central venous pressure and stoke volume. The fall in blood pressure is too small to be seen as the heart detects it and corrects the shortfall by increasing sympathetic drive by increasing heart rate and total peripheral resistance.

If there is a decrease in plasma osmolarity, receptors detect this and insert aquaporins in the loop of Henle. This increases water reabsorption.

Stretch receptors do this. Blood volume affects central venous pressure. The increase in blood volume promotes ANP release from atrial myocytes. Decrease in sympathetic activity.

Atria stretches, stimulating the brain stem to decrease ADH release. this decreases sodium and water reabsorption in the kidneys

Increases in parasympathetic and decrease in sympathetic drive. Decrease in heart rate, vasodilation. Decrease in cardiac output and total peripheral resistance. Decrease in blood flow to the brain which causes fainting.