Nervous and hormonal control of vascular tone Flashcards
Sympathetic vasoconstrictor system
Sympathetic vasoconstrictor nerves
- Action potential moves down axon and arrives at variscosity.
- Depolarisation at variscosity activates Ca2+ channels.
- Ingress of Ca2+ causes release of neurotransmitters (mainly noradrenaline.)
- NA diffeses to the vascular smooth muscle cells where it binds mainly α1- contraction, Some α2 - contraction, and β2 - relaxation. Modulation of responses in both constriction and dilation.
- Noradrenaline is taken up again and recycled/broken down.
Varicosity
- Relase of NA is modulated by angiotensin II actinf on AT1 receptor increasing NA release.
- Metabolites prevent vasoconstriction to maintain blood flow: K+, adenosine, histamine and seretonin etc. feedback and inhibit NA release.
- NA can negatively feedback itself via α2 receptors to limit its own release.
Sympathetic vasoconstrictor nerves
- Controlled by brainstem
* 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. - Innervate most arterioles and veins
* NA activates α1-adrenoreceptors on vascular smooth muscle cells causing vasoconstriction.
* Sympathetic nerve activity is tonic - 1 action potential per second.
* Decrease in parasympathetic activity producing vasodilation is important for treatment of cardiovascular disease.
Main roles of sympathetic vasoconstrictor nerves
- Distinct sympathetic pathways innervate different tissues - Switching on vasoconstriction in some vessels and off in other vessels.
- Control resistance arterioles - produces vascular toe allows vasodilatation/vasoconstriction controlling TPR. Maintains arterial blood pressure and blood flow to brain myocardium and kidney etc.
- Pre-capillary vasoconstriction - leads to downstream capillary pressure drop so increased absorption of interstitial fluid into plasma to maintain blood volume (important in hypovolemia)
- Control venous blood volume - Venoconstriction leads to decreased venous blood volume increasing venous return. This increases stroke volume via Starling’s law and so increases cardiac output.
Vasodilator nerves
- Vasodilatation occurs when vascular tone produced by sympathetic vasoconstrictor nerves is inhibited.
- Specific vasodilator nerve s are parasympathetic.
Examples of Parasympathetic and Sympathetic vasodilators
- Parasympathetic:
* Salivary glands - release Ach and vasoactive intestinal peptide (VIP).
* Pancreas and intestinal mucosa - Release VIP, both need high blood flow to maintain fluid secretion. Ach and VIp tact on endothelium cause release of Nitric Oxide –> vasodilatation.
* Male genitalia/erectile tissue - Release NO by parasympathetic nerves produces cGMP –>vasodilation. Sildenafil/viagra enhances affect of NO by inhibiting breakdown of cGMP by phosphodiesterase-5. - Sympathetic:
* Skin/sudomotor fibres - release Ach/VIP causing vasodilatation via NO, increased blood flow increases sweat and allows heat to exit via exit. Sympathetic activity vasoconstriction only reduces blood flow, limits sweat and limits cooling.
Sensory (nociceptive C fibres) Vasodilator fibres
Stimulatiom of C-fibres by trauma and infection release substance P or CPRP.
Inflammation is part of Lewis triple triple response:
1. Redness caused by capillary vasodilation.
2. Flare, redness in surrounding area due to arteriolar dilation mediated by axon reflex.
3. Wheal, exudation of fluid from capillaries and venules.
Hormonal control of circulation
- Vasoconstrictors : Adrenaline, Angiotensin II, Vasopressin.
- Vasodilators : Atrial natriuretic peptide.
- Others : Insulin, Oestrogen, Relaxin.
Adrenaline / epinephrine
Adrenaline released from adrenal medulla via Ach on nicotinic receptors in these cases:
* Excercise
* Fight or flight
* Hypotension
* Hypoglycaemia
Main roles - Metabolic and CVS effects:
* Glucose mobilisation- Skeletal muscle glycogenolysis, fat lipolysis - β3.
* Stimulation of heart rate and contractility during normal exercise - β1.
* Vasodilatation of coronary and skeletal muscle artetries - β2.
Adrenaline vs Noradrenaline on resistance vessels
Effect of iv adrenaline versus iv noradrenaline on circulation
Renin-angiotensin-aldosterone system (RAAS)
Vasopressin (antidiuretic hormone - ADH)
Stretch receptors in the left atrium send continuous signals causes to NTS —>The NTS sends out inhibitory nerves to the CVLM —> CVLM signals stimulate pituitary to relase vasopressin so stretching of the heart inhibits this.
