Neural Control of Blood Pressure Flashcards

1
Q

SNS & PNS Pharmacology

  • Targets of postganglionic SNS neurons
  • NE & Epi affinities for receptors
  • Effects of Ach release from vagal efferents
  • Effects of binding NE & Epi to beta receptors
A
  • Targets of postganglionic SNS neurons
    • alpha1, alpha2, beta1, & beta2 receptors
  • NE & Epi affinities for receptors
    • alpha1 / alpha2: NE > Epi
    • beta1: NE = Epi
    • beta2: E > NE
  • Effect of Ach release from vagal efferents
    • Ach binds to muscarinic receptors on autorhythmic cells in the SA & AV nodes
    • Increases time required to generate APs –> slows HR
  • Effects of binding NE & Epi to beta receptors
    • NE released from sympathetic nerve terminals
    • Epi released from adrenal medulla
    • NE & Epi bind beta receptors on autorhythmic cells
    • Activate cAMP to phosphorylate channels on autorhythmic cells
    • Increases cation entry
    • Decreases time b/n APs
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2
Q

SNS & PNS influence on myocardial cells

  • Efect of NE/Epi binding to beta receptors on myocardial cells
  • Effect of PNS on myocardial cells
  • Effect of SNS on myocardial cells
A
  • Effect of NE/Epi binding to beta receptors on myocardial cells
    • NE/Epi binding to betaRs –> cAMP production
    • Phosphorylation of voltage-gated Ca2+ channels –> channels open
    • Phospholamban enhances Ca2+ - ATPase activity in the SR so more Ca2+ is sequestered & more Ca2+ can be released next time
    • Increases contraction tension
    • ► SNS increases ventricular contractility
  • Effect of PNS on myocardial cells
    • Decreases HR
    • Slightly/negligibly decreases contractility
    • Negligible effects on ventricles
  • Effect of SNS on myocardial cells
    • Increases contractility & HR
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3
Q

SNS influence on blood flow through arterioles

  • SNS binding in vascular smooth msucle arterioles
  • SNS binding in heart, skeletal muscle, & liver arterioles
  • Effects of large releases / injection of Epi
  • Effects of PNS on blood vessels in genitalia
A
  • SNS binding in vascular smooth muscle arterioles
    • Predominantly alphaRs
    • Binding of NE from sympathetic nerve terminals to alphaRs –> vasoconstriction –> increase TPR –> increase BP
  • SNS binding in heart, skeletal muscle, & liver arterioles
    • Abundance of beta2Rs
    • Binding of Epi from adrenal medula to beta2Rs –> vasodilation
  • Effect of large releases / injection of Epi
    • Acts on both alpha & beta receptors
    • High concentrations of Epi act on alphaRs –> vasoconstriction
  • Effects of PNS on blood vessels in genitalia
    • Release of Ach onto endothelial cells –> NO release
    • –> NO diffusoin into smooth muscle –> activate guanylate cyclase –> increase cGMP
    • –> activate ATPase to pump Ca2+ out of smooth muscle cell –> inhibit actin-myosin interactions
    • –> relaxation –> vasodilation
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4
Q

Baroreceptors & Baroreceptor Reflexes

  • Baroreceptor reflex
  • Afferent limb of the baroreceptor reflex is comprised of receptors associated w/ 2 major arteries
  • Afferents from the aortic arch form…
  • Cell bodies of aortic arch afferents are located in the…
  • Afferents innervating the carotid sinus course in the…
  • Cell bodies of these afferents are located in the…
  • Both artery afferents terminate in the…
A
  • Baroreceptor reflex
    • Monitors BP changes & corrects for them through this negative feedback mechanism to maintain stable BP
  • Afferent limb of the baroreceptor reflex is comprised of receptors associated w/ 2 major arteries
    • Aortic arch & carotid sinus
    • Stretch receptors activated when vessels are distended by blood during increases in BP
  • Afferents from the aortic arch form…
    • Aortic depressor nerve
    • Runs w/ the vagus nerve
  • Cell bodies of aortic arch afferents are located in the…
    • Nodose ganglion in the neck
  • Afferents innervating the carotid sinus course in the…
    • Cranial nerve IX (glossopharyngeal)
  • Cell bodies of these afferents are located in the…
    • Petrosal ganglion
  • Both artery afferents terminate in the…
    • Nucleus of the solitary tract in the medulla
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5
Q

Baroreceptors & Baroreceptor Reflexes

  • When BP increases…
  • Activation of the baroreceptor reflex (increased firing of baroreceptor afferents) leads to…
  • Decreased firing of baroreceptor afferents leads to…
A
  • When BP increases…
    • Baroreceptor terminals stretch –> afferents fire more
    • Adaptation (resetting): afferents begin to adapt to prolonged stretch within a few minutes of a sustained change in BP
    • Afferents signal acute changes in pressure, not a specific pressure
  • Activation of the baroreceptor reflex (increased firing of baroreceptor afferents) leads to…
    • Increased PNS outflow to heart
    • Decreased SNS outflow to heart & blood vessels
    • –> decreased CO & TPR –> decreased BP
  • Decreased firing of baroreceptor afferents leads to…
    • Increased SNS outflow to heart & blood vessels
    • Decreased PNS outflow to heart
    • –> increased CO & TPR –> increased BP
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6
Q

Neuroanatomical Basis of the Baroreceptor Reflex

  • Anatomical substrate of baroreceptor influences on PNS efferents
  • Anatomical substrate of baroreceptor influences on SNS efferents
  • Net result
A
  • Anatomical substrate of baroreceptor influences on PNS efferents
    • Baroreceptor inputs
    • –> PNS preganglionic neurons in the dorsal motor nucleus of the vagus near the nucleus ambiguus
    • –> nucleus of the solitary tract
  • Anatomical substrate of baroreceptor influences on SNS efferents
    • Inhibitory interneuron exists
      • Increase baroreceptor activity –> decrease SNS efferent firing
      • SNS preganglionic neurons are located in the spinal cord
    • Baroreceptor inputs
    • –> brainstem
    • –> caudal ventrolateral medulla (CVLM)
      • Site of inhibitory interneurons
      • Activate CVLM –> decrease BP
      • Inhibit CVLM –> increase BP
    • –> rostral ventrolateral medulla (RVLM)
      • RVLM relays baroreceptor signals to the spinal cord & controls baseline BP
        • Activate RVLM –> increase BP
        • Inhibit RVLM –> decrease BP
      • Baroreceptor stimulation inhibits firing of neurons in the RVLM whose axons terminate in the sympathetic intermediolateral cell column
      • Locaiton: in the brainstem, dorsolateral to the inferior olivary nucleus in the rostral medulla w/ Epi-utilizing cells
    • –> preganglionic neurons
  • Net result
    • Activate baroreceptor reflex –> decrease contractility, peripheral resistance, & BP
    • Inhibit baroreceptor reflex –> increase contractility, peripheral resistance, & BP
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7
Q

Other sensory inputs that influence the activiyt of neurons that mediate the baroreceptor reflex

  • Stress / Anxiety
  • Exercise
A
  • Stress / Anxiety
    • Alteratoins in firing rate of RVLM cells
    • –> make connections w/ sympathetic preganglionic neurons in the spinal cord
    • –> change BP
  • Exercise
    • Decreased excitability of neurons in the nucleus tractus solitarius
    • Decreased “gain” of the baroreceptor reflex
    • Permits increases in BP during exercise that would otherwise be corrected by the baroreceptor reflex
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8
Q

What happens if the baroreceptor reflex is eliminated

  • Normal baroreceptors
  • Baroreceptor denervation
  • Significance
A
  • Normal baroreceptors
    • BP remains stable over an extended period
  • Baroreceptor denervation
    • BP is more labile
    • Mean BP remains near 100 mmHG
    • BP would initially increase b/c the system would think that BP = 0
    • Over time, the system adapts, & BP won’t be as high
  • Significance
    • Baroreceptor inputs don’t establish the set point in BP
    • Baroreceptor inputs are essential in maintaining BP within a narrow range
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9
Q

Atrial stretch receptors & their role in CV control

  • Low-pressure receptors
  • Bainbridge reflex
A
  • Low-pressure receptors
    • Located in atria & pulmonary arteries
    • Detect increaess in pressure in low-pressure partsof the circulation from increased blood volume
    • Work with baroreceptors to make BP regultaion more precise
      • Ex. decreased atrial & arterial baroreceptor activity means BP has dropped b/c of decreased blood volume (ex. hemorrhage)
  • Bainbridge reflex
    • Activates SNS & PNS to prevent accumulation of blood in CV system
    • Activate stretch receptors –> brainstem-mediated reflex –> increase HR & contractility
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10
Q

Atrial stretch receptors & their role in CV control

  • Atrial stretch receptors
  • Hemorrhage
  • Increased osmolarity
  • Other inducer of vasopressin release
A
  • Atrial stretch receptor signals –> hypothalamus –> release vasopressin
    • AKA antidiuretic hormone, arginine vasopressin (AVP)
    • Controls water reabsorption in the kidney
    • Activate stretch receptors –> decrease vasopressin –> decrease blood volume
  • Hemorrhage –> severely decreased blood volume –> very high vasopressin release –> activate baroreceptor reflex + vasoconstriction
  • Decreased blood volume or increased solute concentration –> increased blood osmolarity –> activated hypothalamus –> increased vasopressin
  • Renin release from kidney –> increased angiotensin II –> vasopressin release
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11
Q

3 main triggers for vasopressin release

A
  • Increased osmolarity
    • Hypothalamus –> vasopressin release
  • Decreased atrial stretch
    • Low blood volume –> decreased atrial stretch receptor –> hypothalamus –> vasopressin release
  • Decreased BP
    • Decreased carotid & aortic baroreceptors –> hypothalamus –> vasopressin release
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12
Q

Synthesis & secretion of vasopressin from the posterior pituitary

A
  • Posterior pituitary gland secretes oxytocin & vasopressin
  • Peptides are…
    • Synthesized in separate neurons in the hypothalamus
    • Packaged into secretory vesicles
    • Transported to the nerve terminals int eh posterior pituitary to await release
  • Secretion
    • Neurons integrate neural inputs
    • Sufficient excitation generates an AP
    • AP propagates to the nerve terminal to cause hormone release
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13
Q

Atrial Natriuretic Factor

A
  • Released from the atria when venous pressure (atrial stretch) is high
    • –> vasodilation
    • –> decreases cardiac return
    • –> decreases workload of heart that’s overloaded w/ blood
  • Promotes secretion of water & salt by the kidney
    • –> decrease blood volume
  • Inhibits release of aldosterone from the adrenal cortex
    • Aldosterone promotes the reabsorption of salt & water
    • Inhibiting aldosterone causes salt & water to be lost
  • Acts in the brain to potentiate the baroreceptor reflex
    • –> decreases BP
    • –> inhibits vasopressin release
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14
Q

Longer-term regulation of blood pressure: renin-angiotensin system

A
  • BP remiand low for several minutes
    • Juxtaglomerular (JG) cells detect this condition & release renin
      • SNS can also release renin when NE binds to betaRs
    • Renin converts angiotensinogen into angiotensin I
    • Angiotensin cnverting enzyme (ACE) converts angiotensin I into angiotensin II
    • Angiotensin II is concentrated in blood vessels of the lung
  • Decreased BP (by a lot) –> activate baroreceptor reflex –> increased SNS –> largest augmentation in renin release
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15
Q

Angiotensin II

A
  • Vasoconstrictor
    • Increases TPR & BP
  • Stimulates release of vasopressin (ADH) from pituitary
    • Causes water retention & increased blood volume
  • Stimulates thirst via the brain
  • Affects parts of the medulla that control SNS outflow
    • Increases HR & vasoconstriction
  • Causes adrenal cortex to release aldosterone
    • Causes kidney to reabsorb salt & water into the blood
    • Increases blood volume
  • Potentiates the release of NE from SNS terminals
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16
Q

Inhibiting angiotensin II

A
  • Treats hypertension
  • Selective Angiotensin-2 Type 1 antagonists
    • Block receptor subtype in blood vessels
    • Blcok adrenal cortex production of aldosterone
    • Fewer side effects than ACE inhibitors
  • ACE inhibitors & angiotensin receptor blockers
    • Side effect: hyperkalemia (elevated blood K+)
    • Aldosterone reabsorbs Na+ & water but eliminates K+
    • Blocking aldosterone secretion increases plasma K+