Nervous and Hormonal Control of Vascular Tone

Cards (43)

  • What is intrinsic control of circulation?
    • Intrinsic control of circulation refers to the local regulation of blood flow within tissues and organs independent of external neural or hormonal influences.
    • It ensures that tissues receive adequate perfusion based on their metabolic needs.
  • What are the main mechanisms of intrinsic control of vascular tone? #
    The four main mechanisms of intrinsic vascular control are:
    • Myogenic mechanism
    • Metabolic control
    • Endothelial-derived factors
    • Autoregulation
  • What is the myogenic mechanism in intrinsic vascular control?
    • Myogenic mechanism: Vascular smooth muscle responds to changes in pressure.
    • Increased arterial pressure → Smooth muscle contracts (vasoconstriction) → Prevents excessive blood flow.
    • Decreased arterial pressure → Smooth muscle relaxes (vasodilation) → Maintains adequate perfusion.
  • How does metabolic control regulate vascular tone?
    • Metabolic control regulates blood flow by responding to local metabolic demands.
    • An increase in tissue metabolism leads to:↓O₂ ↑CO₂ ↑H⁺ (decreased pH)↑ Adenosine.
    • These factors cause vasodilation increasing blood flow to meet metabolic demand.
  • What are the endothelial-derived factors that regulate vascular tone?
    • Nitric oxide (NO): Potent vasodilator
    • Prostacyclin (PGI₂): Vasodilator
    • Endothelin-1 (ET-1): Potent vasoconstrictor
    • These factors help modulate vascular resistance and blood flow.
  • What is autoregulation in vascular control?
    Autoregulation is the ability of an organ to maintain constant blood flow despite changes in arterial pressure.
    • It involves:
    1. Myogenic response (vascular smooth muscle contraction or relaxation)
    2. Metabolic response (vasodilator metabolites adjusting flow)
    3. Common in the brain heart and kidneys.
  • What is extrinsic control of circulation?
    Extrinsic control involves regulation of vascular tone by external factors such as the autonomic nervous system (ANS) and hormones to maintain overall blood pressure and distribution of blood flow.
  • How does the sympathetic nervous system (SNS) control vascular tone? The SNS controls vascular tone primarily via α-adrenergic and β-adrenergic receptors:
    • α₁ receptors → Vasoconstriction (most arteries and veins)
    • β₂ receptors → Vasodilation (skeletal muscle coronary arteries liver)
    • The SNS maintains systemic vascular resistance (SVR) and adjusts blood flow distribution.
  • What is the role of the parasympathetic nervous system (PNS) in vascular control?
    • The PNS has minimal direct control over vascular tone.
    • However it influences heart rate and can cause vasodilation in specific regions (e.g. via acetylcholine-induced NO release in erectile tissue and salivary glands).
  • What are the key hormones involved in extrinsic vascular control?
    • Epinephrine (adrenal medulla) → β₂-mediated vasodilation (skeletal muscle liver) and α₁-mediated vasoconstriction (gut skin).
    • Norepinephrine (SNS) → α₁-mediated vasoconstriction (increased blood pressure).
    • Angiotensin II (RAAS) → Potent vasoconstrictor (maintains blood pressure).
    • Vasopressin (ADH) → Vasoconstriction and water retention to increase BP.
    • Atrial Natriuretic Peptide (ANP) → Vasodilation and natriuresis reducing BP.
  • How does the Renin-Angiotensin-Aldosterone System (RAAS) regulate circulation?
    • Renin (kidney) converts angiotensinogenangiotensin I.
    • ACE (lungs) converts angiotensin Iangiotensin II.
    • Angiotensin II:Vasoconstriction (↑ BP)
    • Aldosterone release (↑ Na⁺ & H₂O retention → ↑ blood volume)
  • What is the effect of baroreceptors on vascular tone?
    • Located in the carotid sinus and aortic arch baroreceptors detect BP changes.
    • High BP → Increased baroreceptor firing → SNS inhibitionVasodilation HR BP.
    • Low BP → Decreased baroreceptor firing → SNS activationVasoconstriction HR BP.
  • How do intrinsic and extrinsic mechanisms work together to regulate circulation?
    • Intrinsic control ensures local tissue perfusion based on metabolic needs.
    • Extrinsic control (SNS hormones) regulates systemic BP and redistributes blood flow as needed.
    • Example: During exercise:
    1. Intrinsic: Skeletal muscles vasodilate due to increased metabolism.
    2. Extrinsic: SNS causes vasoconstriction in non-essential areas (gut skin) to redirect blood to muscles.
  • Which neurotransmitter is primarily responsible for sympathetic vasoconstriction?
    Noradrenaline (norepinephrine) which binds to α1-adrenergic receptors on vascular smooth muscle cells.
  • What is the effect of α1-adrenergic receptor activation on blood vessels? Activation of α1-adrenergic receptors causes vasoconstriction by increasing intracellular calcium in smooth muscle cells leading to contraction.
  • Which blood vessels are mainly controlled by sympathetic vasoconstrictor nerves?
    Arterioles and small arteries which regulate total peripheral resistance (TPR) and blood pressure.
  • How does sympathetic vasoconstriction help maintain blood pressure?
    By increasing vascular resistance it maintains blood pressure especially during conditions like hemorrhage or standing up (orthostatic response).
  • What is basal sympathetic tone and why is it important?
    Basal sympathetic tone is the continuous low-level activity of sympathetic nerves ensuring resting vascular tone and preventing excessive vasodilation.
  • Which areas of the brain regulate sympathetic vasoconstrictor activity?
    The medulla oblongata (particularly the rostral ventrolateral medulla RVLM) controls sympathetic outflow.
  • How does the baroreceptor reflex influence sympathetic vasoconstriction?

    Increased blood pressure activates baroreceptors which inhibit sympathetic outflow leading to vasodilation. Conversely low BP increases sympathetic activity causing vasoconstriction.
  • How do hormones interact with sympathetic vasoconstriction? Adrenaline (from the adrenal medulla) can reinforce vasoconstriction via α1 receptors while angiotensin II enhances sympathetic activity.
  • What are sensory vasodilator nerves and how do they differ from sympathetic vasoconstrictor nerves?
    Sensory vasodilator nerves belong to the afferent (sensory) nervous system and cause vasodilation via neurotransmitter release unlike the efferent sympathetic vasoconstrictor nerves.
  • What neurotransmitters are released by sensory vasodilator nerves?
    • Substance P calcitonin gene-related peptide (CGRP)
    • Vasoactive intestinal peptide (VIP) contribute to vasodilation.
  • What is the function of substance P in sensory vasodilation? Substance P binds to neurokinin-1 (NK1) receptors leading to endothelial nitric oxide (NO) release and vasodilation.
  • How does CGRP contribute to vasodilation?
    CGRP directly acts on vascular smooth muscle causing relaxation and dilation.
  • Where are sensory vasodilator nerves most prominent?
    They are particularly important in the skin (for thermoregulation) mucosal tissues and coronary circulation.
  • How do sensory vasodilator nerves contribute to neurogenic inflammation? They release vasoactive substances like substance P leading to increased blood flow plasma leakage and local immune responses.
  • What triggers the activation of sensory vasodilator nerves?
    • Tissue
    • Injury
    • Heat inflammation
    • Pain stimuli activate these nerves leading to reflexive vasodilation.
  • How do sensory vasodilator nerves contribute to the axon reflex?
    The axon reflex occurs when sensory nerves release vasodilators upon stimulation (e.g. skin injury) leading to local vasodilation without central nervous system involvement.
  • What is vascular tone? Vascular tone refers to the degree of contraction of blood vessels particularly in the smooth muscle of arterioles which regulates blood pressure and blood flow distribution.
  • How do hormones regulate vascular tone? Hormones regulate vascular tone by acting on blood vessel receptors to cause vasoconstriction (increasing blood pressure) or vasodilation (decreasing blood pressure) depending on physiological needs.
  • What is the effect of adrenaline on different vascular beds?
    • Skeletal muscle & coronary arteries: Vasodilation via β2 receptors to increase blood flow during exercise.
    • Skin gastrointestinal tract and kidneys: Vasoconstriction via α1 receptors to redistribute blood flow.
  • How does adrenaline affect blood pressure? Adrenaline increases systolic blood pressure by increasing cardiac output but may decrease diastolic pressure due to β2-mediated vasodilation.
  • What receptors does angiotensin II act on? Angiotensin II binds to AT₁ receptors on vascular smooth muscle causing vasoconstriction and increased blood pressure.
  • What is angiotensin II and how does it regulate vascular tone? Angiotensin II is a potent vasoconstrictor formed from angiotensin I by angiotensin-converting enzyme (ACE). It plays a critical role in blood pressure regulation and fluid balance.
  • How does angiotensin II contribute to long-term blood pressure regulation?
    • Stimulates aldosterone release from the adrenal cortexsodium and water retention.
    • Increases sympathetic nervous system activity.
    • Promotes vasoconstriction increasing systemic vascular resistance (SVR).
  • What is vasopressin (ADH) and how does it regulate vascular tone? Vasopressin (antidiuretic hormone ADH) is released from the posterior pituitary and primarily regulates water balance but also contributes to vasoconstriction.
  • What receptors does vasopressin (ADH) act on for vascular tone regulation?
    • V1 receptors on vascular smooth musclevasoconstriction
    • V2 receptors in the kidneys → increased water reabsorption
  • When is vasopressin (ADH) released?
    • Low blood pressure
    • Dehydration
    • High plasma osmolality to conserve water and increase blood pressure.
  • What is atrial natriuretic peptide (ANP) and how does it affect vascular tone? ANP is a hormone secreted by the atria of the heart in response to high blood volume and acts as a vasodilator.