Neural Control of Blood Pressure Flashcards
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
- 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
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
- 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
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
- 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
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…
- 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
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…
- 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
Neuroanatomical Basis of the Baroreceptor Reflex
- Anatomical substrate of baroreceptor influences on PNS efferents
- Anatomical substrate of baroreceptor influences on SNS efferents
- Net result
- 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
- RVLM relays baroreceptor signals to the spinal cord & controls baseline BP
- –> preganglionic neurons
- Inhibitory interneuron exists
- Net result
- Activate baroreceptor reflex –> decrease contractility, peripheral resistance, & BP
- Inhibit baroreceptor reflex –> increase contractility, peripheral resistance, & BP
Other sensory inputs that influence the activiyt of neurons that mediate the baroreceptor reflex
- Stress / Anxiety
- Exercise
- 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
What happens if the baroreceptor reflex is eliminated
- Normal baroreceptors
- Baroreceptor denervation
- Significance
- 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
Atrial stretch receptors & their role in CV control
- Low-pressure receptors
- Bainbridge reflex
- 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
Atrial stretch receptors & their role in CV control
- Atrial stretch receptors
- Hemorrhage
- Increased osmolarity
- Other inducer of vasopressin release
- 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
3 main triggers for vasopressin release
- 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
Synthesis & secretion of vasopressin from the posterior pituitary
- 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
Atrial Natriuretic Factor
- 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
Longer-term regulation of blood pressure: renin-angiotensin system
- 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
-
Juxtaglomerular (JG) cells detect this condition & release renin
- Decreased BP (by a lot) –> activate baroreceptor reflex –> increased SNS –> largest augmentation in renin release
Angiotensin II
- 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