Smooth Muscle Histology and Blood Pressure Regulation

Smooth Muscle Histology

• Smooth muscle cells are uni-nucleated, spindle-shaped, and non-striated
• They are autorhythmic, meaning they can contract on their own without external stimulation
• Smooth muscle cells are capable of dividing and regenerating

Regulation of Blood Flow and Pressure

• Blood flow moves from high pressure to low pressure
• The pressure gradient is created through the contraction of the heart muscle
• Contraction of the ventricles generates high blood pressure (BP) in the aorta, which pushes blood through the systemic circulation
• Mean arterial pressure (MAP) is determined by cardiac output (CO) and total peripheral resistance (TPR)
  • MAP = CO x TPR
  • CO = Cardiac output = SV x HR
• Blood pressure varies directly with changes in CO and TPR
• Changes in one variable are quickly compensated for by changes in the other variables

Regulation of Total Peripheral Resistance

• For blood to move through blood vessels (BVs), BP must overcome the opposing pressure in the peripheral circulation (TPR)
• TPR is regulated by the sympathetic nervous system (neural)
  • Vasoconstriction (activation of the sympathetic nervous system) leads to increased resistance (TPR) due to contraction of smooth muscle in blood vessel walls
  • Vasodilation (reduced activation of the sympathetic nervous system) leads to decreased resistance (TPR) due to relaxation of smooth muscle in blood vessel walls
• The parasympathetic system has NO effect on blood vessel diameter regulation

Regulation of Cardiac Output (CO)

• At rest, CO is approximately 5.25 L/min:
  • CO ( mL/min) = HR (75 beats/min) x SV (70 ml/beat)
• Maximal CO is 4-5 times resting CO in non-athletic individuals
• Maximal CO can reach 35 L/min in trained athletes
• Cardiac reserve is the difference between resting and maximal CO
• Resting heart rate (HR) is regulated by the cardioinhibitory center (in the medulla oblongata) via the parasympathetic vagus nerve
• During stress, the cardioacceleratory center increases heart rate and stroke volume via sympathetic stimulation

Regulation of Heart Rate (HR)

• The sinoatrial (SA) node is the heart's rhythm generating center
• The SA node has intrinsic activity of about 100 action potentials/min
• Resting heart rate is considerably lower than the SA node's intrinsic activity
• The SA node is regulated by the autonomic nervous system (ANS)
  • Sympathetic activity:
    • Noradrenaline and adrenaline acting on β1 adrenergic receptors
    • Effect: heart rate increases
  • Parasympathetic activity:
    • Vagus nerve (cranial nerve X) via acetylcholine acting on muscarinic receptors
    • Effect : heart rate decreases
    • Other factors influencing HR
      • Positive chronotropic factors (increase heart rate):
        • Adrenaline, caffeine
      • Negative chronotropic factors (decrease heart rate):
        • Beta-blockers, such as Propranolol
• Tachycardia: abnormally fast heart rate (>100bpm), can lead to fibrillation if persistent
• Bradycardia: heart rate slower than 60 bpm

Regulation of Stroke Volume (SV)

• Intrinsic control:
  • If ventricular wall is stretched before contraction, contractile force increases
  • Increased End Diastolic Volume (EDV) (meaning the ventricle chamber is stretching and putting pressure on the ventricular wall) → SV ↑ → CO ↑
• Extrinsic control:
  • Sympathetic stimulation:
    • Noradrenaline ( & adrenaline injection) acting on β1 adrenergic receptors
    • Effect: increased contractile force

Cardiovascular Changes Associated with Physical Activity

• High intensity interval training (HIIT) has the most significant effects in reducing BP in hypertensive individuals.
• Average blood pressure is 93 mL/g of mercury
• The heart pumps 5L/min → cardiac output
• Blood vessel (BV) branching
  • Coronary vessels → 5%
  • Brain → 15%
  • Gut → 25%
  • Kidneys → 20%
  • Muscles → 20% = 1 L/min is going to the muscles at REST = 3 mL/min/100g of muscle tissue at REST
  • Skin → 5%
• Less resistance = more blood flow = lower BP due to decreased SVR (systemic vascular resistance)
• The sympathetic nervous system (SNS) innervates certain BVs to constrict
  • During exercise:
    • SNS tells coronary arteries to dilate → relaxes the brain and heart
    • SNS constricts the gut → stops 25% of CO to the gut
    • SNS constricts the kidney by a small percent
    • SNS dilates muscles significantly
    • SNS constricts the skin significantly
    • Blood redistribution: 30% of blood is being redirected from the gut to skin, mainly to muscle tissues → increases 1L/min to 20L/min in intense exercise → 200 mL/min/100g of muscle tissues of blood in athletes
• SNS tells those BVs to dilate by increasing:
  • Adrenaline
  • Noradrenaline
  • Nitric-oxide in BVs → tells them to relax
  • Prostaglandins → another chemical that tells BVs to relax
• SNS goes to the heart:
  • Increased contraction
  • Increased HR
• During exercise:
  • Significant increase in BP
  • Increase in CO
  • Increase in HR
  • Increase in contractility → more blood gets pumped out
  • Increase in SVR
  • Increase in mean arterial pressure of mercury (93 mL/g), will continue to increase and can go up to 170 mL/g of mercury
• After exercise, a reflexive drop in SNS
  • Decrease in adrenaline at REST
  • Decrease in noradrenaline at REST
  • Maintained increased nitric-oxide
  • Maintained increased prostaglandins
  • Nitric-oxide and prostaglandins → tells BVs to relax and dilate = drops SVR, heart output back to normal rate, contractility back to normal rate, BV resistance will be reduced (easier for blood to move), BP is lower
• Individuals with hypertension can benefit from increased BP during exercise

This quiz covers key concepts of smooth muscle histology, including the structure and functions of smooth muscle cells. Additionally, it explores the regulation of blood flow and pressure, highlighting the relationship between cardiac output and total peripheral resistance. Test your understanding of these critical physiological mechanisms.