Cardiovascular regulatory mechanisms
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Transcript of Cardiovascular regulatory mechanisms
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By Ronald Ombaka Esq.
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Why regulate?
Agents of regulation
Crucial centers for regulation
Intergration of regulation with practice
Objectives
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Why do we need a CVS……….
To deliver and remove metabolic substrates and wastes from; points of entry; to points of use; to points of excretion/elimination, respectively.
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Why regulate?
For homeostasis (sustain metabolic tissue requirements-oxygen and nutrients- as per demand and waste elimination-CO2 & other products of metabolism-)
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Neural
Humoral
On integration Neuro-humoral
Agents of regulation:
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Purely Autonomic
-Sympathetic
-Parasympathetic
Key terms: RVLM; DVN; NTS; Carotid and Aortic sinuses
Neural
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The medulla oblongata located within the brainstem, the
hypothalamus, and the cortical regions work together to regulate autonomic function.
The medulla contains the ANS centers, the hypothalamus modulates medullary activity in relation to requirements, higher cortical centers alter CVS func in relation to stress, anxiety, exercise etc
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Afferent fibers from peripheral baroreceptors and
chemoreceptors, as well as respiratory stretch receptors, enter the medulla at the nucleus tractussolitarius (NTS).
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The NTS relays inhibitory nerves to the
RVLM(sympathetic nervous system cell nuclei); and excitatory signals to the DVN (parasympathetic nervous system nuclei)
Therefore NTS activity = sympathetic activity and parasympathetic activity.
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Cell bodies are found in collections of neurons called the
dorsal vagal nucleus (DVN) and nucleus ambiguus (NA).
activity here is associated with
reduces sinoatrial (SA) nodal firing (negative chronotropy)
slows AV nodal conduction (negative dromotropy)
NB: Increased baroreceptor firing causes excitation of these centers.
Parasympathetic innervation;
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Existing parasympathetic nerves do not play a
significant role in the regulation of systemic vascular resistance and arterial blood pressure.
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The sympathetic adrenergic neuron cell bodies lie
within the Rostral ventral lateral medulla (RVLM).
Increased activity of these neurons produces cardiac stimulation and systemic vasoconstriction.
Sympathetic activation increases chronotropy, dromotropy, and inotropy.
Sympathetic innervation;
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Activation of one arm of the ANS is assoc with
reciprical inhibition of the other arm.
Example; Standing up causes baroreceptor reflex to reduce parasympathetic outflow and concurrent increase in sympathetic outflow. Thus sustaining normal BP despite reduced venous return.
RECIPROCAL SYMPATHETIC AND VAGAL ACTIVITY:
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Input from higher centers eg sudden fear or emotion can
cause vagal stimulation and withdrawal of sympathetic tone = bradycardia and vasodilation = hypotension. Hence a vasovagal syncope.
Fear and anxiety can lead to sympathetic activation.
Chronic sympathetic activation induced by long-term emotional stress can result in sustained hypertension, cardiac hypertrophy, and arrhythmias.
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Check effector receptor location & function;
Alpha and Beta receptors
Muscarine and nicotinic receptors
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Arterial blood pressure is regulated through
negative feedback systems.
Arterial baroreceptors are found in the carotid sinus (at the bifurcation of external and internal carotids) and in the aortic arch.
Baroreceptor Feedback Regulation of Arterial Pressure:
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The sinus nerve, a branch of the glossopharyngeal nerve
(cranial nerve IX), innervates the carotid sinus.
Afferent fibers from the carotid sinus synapse at the NTS. (Recall, NTS modulates the activity of sympathetic neurons within
the RVLM and medullary vagal nuclei.)
The aortic arch baroreceptors are innervated by the aortic nerve, which then combines with the vagus nerve prior to synapsing at NTS.
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The arterial baroreceptors respond to the stretching
of the vessel walls produced by increases in arterial blood pressure which subsequently causes increeased firing.
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Overall, the receptors of the carotid sinus respond to
pressures ranging from about 60 to 180 mm Hg.
If arterial blood pressure decreases from normal, it lowers the firing rate of the carotid sinus baroreceptors and vice versa.
Carotid sinus is more sensitive than aortic sinus
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Scenario examples; Standing up, Carotid massage, Valsalva manouvre
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The primary role of these receptors is to regulate pCO2;
pO2; pH within normal limits.
Also interact with medullary cardiovascular centers directly -hypoxic environs, poor gaseous exchange, hypotension increase
firing of nerves in RVLM- and indirectly via pulmonary stretch receptors - causes inhibition of vagal discharge from DVN-.
Central receptors also respond similarly.
Chemoreceptor Feedback Regulation of Arterial Pressure:
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Pediatric bradycardia with hypoxia-
Normal response to hypoxia-
Analogy:
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Some affect blood vessels and the heart directly
Others affect blood volume
Examples
circulating catecholamines
the renin-angiotensin- aldosterone system
atrial natriuretic peptide
antidiuretic hormone (vasopressin)
HUMORAL CONTROL
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Circulating catecholamines originate from two
sources :
The adrenal medulla -catecholamines(80% epinephrine, 20% norepinephrine)
Sympathetic nerves innervating blood vessels (principally norepinephrine)
Circulating Catecholamines
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Catecholamine activity is governed by receptor
distribution (e.g. the affinity of epinephrine for β-adrenoceptors is much greater than for α-adrenoceptors.)
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Therefore, at low to moderate circulating levels of
epinephrine, heart rate, inotropy, and dromotropy are stimulated (primarily β1-adrenoceptor mediated).
At high plasma concentrations, the cardiovascular actions of epinephrine are different because epineph-rine binds to α-adrenoceptors as well as to β-adrenoceptors.
NB- Check Nor-epi receptor affinities??
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Renin is primarily produced in the kidney
(Juxtaglomerular cells)
Production is dictated by;
B1 stimulation in the kidney
Renal artery hypotension
Reduced Na delivery to distal tubules
The Renin-Angiotensin-Aldosterone system
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Angiotensinogen
Renin
Angiotensin I
ACE (In lung endothelium)
Angiotensin II
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Constricts resistance vessels( Increasing SVR)
Enhances sympathetic adrenergic activity (Locally and centrally)
Acts upon the adrenal cortex to release aldosterone(Thus increase in blood volume)
Stimulates the release of vasopressin from the posterior pituitary
Stimulates thirst centers within the brain
Stimulates cardiac and vascular hypertrophy.
Angiotensin II actions
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It is synthesized stored and released by atrial myocytes in
response to Atrial distension (think heart failure, vol, overload)
Angiotensin II
Sympathetic stimulation.
Function- Longterm regulation of Na, water ,blood vol. homeostasis.
Actions tend to be the opposite of angiotensin II action.
Atrial Natriuretic Peptide
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Vassopressin(ADH)
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It is released from the posterior pituitary
Action sites at kidneys and blood vessels
The most important physiologic action of AVP is that it increases water reabsorption by the kidneys.(via V2 receptors)
This hormone also constricts arterial blood vessels through V1 vascular receptors
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NB: Consider all the afore mentioned as a finely tuned intergrated system working in sync not as compartments.
THE END
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