0704 - Neural Regulation of BP - RM Flashcards
What are the sensors, integrators and effectors of the arterial baroreflex?
Pressoreceptors in the aortic arch and carotid sinus measure wall tension in the vessels (fire more with higher pressure), provide a system of negative feedback. They respond better to pulsatile than steady, set-point pressure.
Travels via CN IX (carotid sinus) and CN X (aortic arch) to several nuclei (tractus solitarius (initial), ambiguus (effector), and rostral vasopressor/caudal vasodepressor areas) in the brainstem, which coordinates with other areas of the brain (particularly hypothalamus). There is a set point (maximal slope in HR vs BP plot), that can be reset by exercise. Where the set-point is not achieved, effectors set in.
Effect is vasodilation or constriction throughout the vasculature (sympathetic) or all VA-innervated areas (and lumbosacral cord) (VA). SY activity occurs through the SY chain (T1-L3), whereas VA activity is through VA and lumbosacral cord (S2-S4). Both systems act together, but in opposite directions (i.e. max SY is min VA and vice versa).
What are the sensors, integrators and effectors of the cardiopulmonary reflexes?
Affector fibres arise in the heart - 80% small, unmyelinated from cardiac mechanoreceptors (wall tension in ventricle), ventricular chemosensors (mediate pain via SY fibres - lead to increase SY activity), and coronary artery baroreceptors (perfusion pressure). Remaining 20% are myelinate veno-atrial mechanoreceptors. SY fiibres send pain through spinal cord to brain, remainder send afferents to nucleus tractus solitarius.
Veno-atrial stretch receptors most important for us. Measure atrial blood volume in low-pressure part of circulation and control VR. Do this by activating on high venous pressure (Bainbridge Effect), which increases SY activity to SA node without dropping VA activity - provides tachycardia only. Stretching of the receptors also increases naturesis by renal vasodilation and ANP release, and decreases ADH release (via hypothalamus) - lowering blood volume.
Outline the anatomy of the AB reflex pathway
Vagal - Afferent fibres through nucleus tractus solitarius, relayed to nucleus ambiguus for direct efferents via VA, while also inhibiting rostral vasopressor area, which acts with raphe nucleus (serotonin) to inhibit outputs to SY preganglionic neurons.
Symp - Afferent fibres through NTS, to other areas including hypothalamus and cerebellum. Integration in peri-aqueductal grey, with stimulation from rostral vasopressor area then to SY preganglionic neurons in spinal cord, and SY ganglion, providing SY efferents cardiac and vasomotor fibres.
How are HR, SV, and TPR regulated?
All of these parameters are regulated by AB reflex.
HR - VA innervation directly on SA and AV node, changes pacemaker activity. SY innervation across whole heart, which also changes pacemaker activity.
SV - SY innervation of myocardium increases strength of contraction, increasing SV.
TPR - SY innervation contracts whole vasculature, increasing TPR via vasomotor fibres.
Outline the nature and effect of the AB reflex.
AB reflex provides short-term, beat by beat stabilisation of blood pressure around a set point that can be altered by exercise. It does this via VA innervation of the heart when BP high (decrease HR, SV, and TPR), and SY innervation of heart and vasculature when BP low (increase HR, SV, and TPR). The two systems (VA and SY) work together but in opposite directions, and the reflex can be altered by inputs from respiratory and other centres. Activated in times of orthostasis, blood loss, dehydration, shock etc.
Outline the nature and effect of the cardiopulmonary reflex
A reflex to control venous return. Low pressure receptors (particularly atrial and venous stretch receptors), when activated, give tachycardia (move shift the pressure). Activate SY without changing VA to increase venous return over longer-term. Allows for this by renal vasodilation (increasing Na+ filtration), producing ANP and decreasing ADH, lowering volume.
Which reflex controls HR, SV, TPR, and VR?
AB controls HR, SV, and TPR, and CP mainly VR
How does the AB reflex establish beat to beat control?
Fast acting and more responsive to pulsatile than steady-state pressure - quick response via sensors in aortic arch or carotid sinus to increase either VA or SY innervation and decrease the other, leading to a very rapid systemic (via TPR as well as HR, SV) response.
How are the BP reflexes modulated by respiration?
During inspiration, HR increases because the inspiratory centre reduces vagal output (makes Nucleus Ambiguus briefly unresponsive to AB receptor input) - this disinhibits the SA node, resulting in increased HR. The converse is true during expiration.
How are the BP reflexes modulated by shock?
During asphyxia/shock, carotid and aortic chemoreceptors sense P(O2) and P(CO2). If change in arterial pressure is more than 80 torr (asphyxia, shock etc):
TPR increases as renal, splanchnic and muscle vascular beds are constricted.
Splanchnic veins constrict, decreasing pooling, increasing MSF pressure, increasing SV and therefore CO.
BP increases due to TPR and CO increasing.
Tachycardia comes on due to increased respiratory rate (inspiration).
