Nervous and Hormonal Control of Vascular Tone Flashcards
What is the difference between local and extrinsic control? (Give examples)
Local control:
Regulate local blood flow to organs/tissues
Important- regional hyperaemia (increase in blood flow)
Vasodilators e.g. inflammation, local metabolites such as Nitric oxide, prostaglandins, endothelin, K+, H+
Extrinsic control:
Regulate TPR to control blood pressure
Brain function selectivity alters blood flow to organs according to need e.g. during exercise, temperature regulation etc.
Nerves:
Vasoconstrictors e.g. noradrenaline
Vasodilators e.g. acetylcholine, nitric oxide
Hormones:
Vasoconstrictor e.g. adrenaline, angiotensin II
Vasodilators e.g. anti-natriuretic peptide (ANP)
How do sympathetic vasoconstrictor nerves work?
- An action potential moves down the axon and arrive at a varicosity
- Depolarisation at the varicosity activating voltage gated Ca2+ channels
- Ingress of calcium causes release of neurotransmitters- mainly noradrenaline
- NA diffuses to the vascular smooth muscle cells where it binds mainly a1- contraction, some a2- contraction and b2- relaxation.
Modulation of responses in both constriction and dilatation - The noradrenaline is then taken up again and recycled or broken down
Adrenaline from the adrenals and released into the circulation can also act at a1 or b2 Receptors.
What parts of the brainstem control the sympathetic vasoconstrictor nerves?
Rostral ventrolateral medulla (RVLM)- this is controlled by other areas such as…
Caudal ventrolateral medulla (CVLM) and hypothalamus
Provides central control of blood flow and blood pressure
What do sympathetic vasoconstrictor nerves innervate, and how?
Innervate most arterioles and veins:
NA activates a1- adrenoceptors on vascular smooth muscle cells causing vasoconstriction
Sympathetic nerve activity is tonic (1 action potential per second)
Tonic sympathetic activity sets vascular tone
Decrease in sympathetic activity producing vasodilation is an important principle in pharmacological treatment of cardiovascular disease e.g. hypertension
What are the main roles of sympathetic vasoconstrictor nerves?
Distinct sympathetic pathways innervate different tissues:
Switching on vasoconstriction in some vessels and off in other vessels (producing vasodilation)
E.g. exercise, increased sympathetic nerve stimulation to GI (less blood flow), reduce sympathetic nerve stimulation to skin (more blood flow, cool down)
Precapillary vasoconstriction:
Leads to downstream capillary pressure drop so increased absorption of interstitial fluid into blood plasma to maintain blood volume (important in hypovolemia)
Control resistance arterioles:
Produces vascular tone allows vasodilation/increased blood flow to occur, control TPR
Maintain arterial blood pressure and blood flow to brain myocardium and kidney etc.
Control venous blood volume:
Venoconstriction leads to decreased venous blood volume increasing venous return, this increases stroke volume via Starling’s law
What are vasodilator nerves?
Vasodilation usually occurs as vascular tone produced by sympathetic vasoconstrictor nerves is inhibited
A few specialised tissues contain vasodilator nerves, as well as vasoconstrictor nerves
Normally these have a specific function controlling a specific vascular bed rather than global functions
A few sympathetic vasodilator nerves exist e.g. sensory (nociceptive C fibres) vasodilator fibres
Specific vasodilator nerves are mainly parasympathetic
Some blood vessels are innervated by parasympathetic cholinergic fibres (e.g. coronary vessels)
These release acetylcholine (Ach) which binds to muscarinic receptor on the smooth muscle and/or endothelium
M3 receptors located on the vascular endothelium can coupled to the formation of nitric oxide (NO) causing vasodilation
However, Ach can also cause contraction through smooth muscle M2 and M3 receptors
Cerebral arteries appear to have M3 muscarinic receptors that vasodilate in response to Ach
How and where do the sympathetic vasodilator nerves work?
Skin (sudomotor fibres)- release acetylcholine (Ach) and vasoactive intestinal peptide (VI) causing vasodilatation via NO associated routes
Increased blood flow causes more sweat and also allows heat loss via skin
Sympathetic activity vasoconstriction would reduce blood flow, limit sweat production and limit cooling
Emotional centres in the brain have some control over these fibres, head, face, upper chest, involved in blushing
How and where do parasympathetic vasodilator nerves work?
Salivary glands- release acetylcholine (Ach) and vasoactive intestinal peptide (VIP) Pancreas and intestinal mucosa- release VIP Both these tissues need high blood flow to maintain fluid secretion Ach/VIP act on endothelium to cause release of nitric oxide (NO)- vasodilation Male genitalia (erectile tissue)- release NO Release of NO by parasympathetic nerves causes production of cGMP which leads to vasodilation Sildenafil (Viagra) enhances this effect of NO by inhibiting the breakdown of cGMP by phosphodiesterase-5
What happens when you stimulate the sensory (nociceptive C fibres) vasodilator fibres?
Stimulation of sensory axon reflex (C-fibres) by trauma, infection etc.
Release substance P or calcitonin gene-related peptide (CGRP)
Act on:
Mast cells to release histamine
Endothelium and vascular smooth muscle
Both produce vasodilatation called flare in skin
Inflammation is part of the Lewis triple response:
1. Local redness
2. Wheal
3. Flare
What are the different hormones that affect vascular tone?
Vasoconstrictors: Adrenaline Angiotensin II (ang II) Vasopressin (anti-diuretic hormone, ADH) Vasodilators: Atrial natriuretic peptide (ANP) Others e.g. Insulin, oestrogen, relaxin Also effects on vasculature
How does adrenaline affect vascular tone?
Adrenaline is released from adrenal medulla- via action of acetylcholine on nicotinic receptors during:
Exercise
Fight-flight-fear response (increase sympathetic drive)
Hypotension (baroreceptor reflex)
Hypoglycaemia
Main roles- metabolic and CVS effects:
Glucose mobilisation (skeletal muscle glycogenolysis, fat lipolysis)
Stimulation of heart rate and contractility during normal exercise
Vasodilation of coronary and skeletal muscle arteries
How do adrenaline and noradrenaline compare in terms of resistance vessels?
In most tissue vasoconstriction due to a1 adrenoceptors
Skeletal muscle and coronary arteries have more b2 and a1 adrenoceptors
Adrenaline higher affinity for beta over alpha, mainly acts at b2 to dilate vessels
Noradrenaline higher affinity for alpha, mainly acts at a1 receptors to constrict vessels
How does vasopressin (ADH) affect vascular tone?
Stretch receptors in the left atrium send continuous signals causes to Nucleus Tractus Solitarius (NTS).
The NTS sends out inhibitory nerves to the Caudal Ventrolateral Medulla (CVLM)
CVLM signals stimulate pituitary to release vasopressin so stretching of the heart inhibits this
Dehydration of haemorrhage NTS inhibition is switched off and CVLM stimulates vasopressin
NTS is the thermostat that sets the level at which the CVLM is inhibited
Hypothalamus response stimulated by an increase in osmolarity i.e. dehydration or low blood volume
Vasopressin (ADH) released from the posterior of pituitary gland causes increased reabsorption of fluid by kidney and also causes vasoconstriction- both effects maintain blood pressure
How does atrial natriuretic peptide (ANP) work?
ANP released by specialised atrial myocytes
Secreted by increased filling pressures which stimulate stretch receptors
Act at ANP receptors on vascular smooth muscle cells increasing cGMP pathways (like nitric oxide)
Systemic vasodilatation- opposes action of noradrenaline, RAAS, ADH
How does RAAS work?
Yes… pls edit
