Your body's vascular system is like a complex highway network, constantly adjusting to keep traffic flowing smoothly. Neural signals and hormones act as traffic controllers, fine-tuning blood flow and pressure to meet your body's changing needs.

Exercise and health issues can shake up this delicate balance. Regular workouts improve your vascular system's efficiency, while conditions like high blood pressure or blood loss force your body to adapt, sometimes with long-term consequences.

Neural and Hormonal Regulation of Vascular Homeostasis

Neural mechanisms of vascular homeostasis

• Autonomic nervous system controls vascular tone and blood pressure
  • Sympathetic nervous system (SNS) increases vascular tone and blood pressure
    • Releases norepinephrine binds to α1-adrenergic receptors on vascular smooth muscle cells
    • Causes vasoconstriction increasing peripheral resistance and blood pressure (fight-or-flight response)
  • Parasympathetic nervous system (PNS) decreases heart rate and contractility
    • Releases acetylcholine binds to muscarinic receptors on the heart (sinoatrial node)
    • Reduces cardiac output and blood pressure (rest and digest state)
• Baroreceptors detect changes in blood pressure send signals to the brainstem
  • Located in the carotid sinus (carotid arteries) and aortic arch
  • Increased blood pressure stimulates baroreceptors triggering a reflex decrease in SNS activity increase in PNS activity (negative feedback loop)
  • Decreased blood pressure has the opposite effect increasing SNS activity decreasing PNS activity (maintains homeostasis)

Hormonal control of blood pressure

• Renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and fluid balance
  • Juxtaglomerular cells in the kidneys release renin in response to decreased renal perfusion pressure or sympathetic stimulation
    1. Renin converts angiotensinogen to angiotensin I
    2. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II
  • Angiotensin II effects:
    • Vasoconstriction increasing peripheral resistance and blood pressure (potent vasoconstrictor)
    • Stimulates aldosterone release from the adrenal cortex (zona glomerulosa)
    • Increases thirst (hypothalamus) and antidiuretic hormone (ADH) release (posterior pituitary)
  • Aldosterone promotes sodium and water retention in the kidneys increasing blood volume and pressure (distal tubules and collecting ducts)
• Atrial natriuretic peptide (ANP) counteracts RAAS
  • Released by atrial myocytes in response to increased atrial stretch (volume overload)
  • Promotes natriuresis (sodium excretion) and diuresis (water excretion) (acts on kidneys)
  • Reduces blood volume and pressure (opposes actions of angiotensin II and aldosterone)

Local regulation of vascular tone

• Vasomotor tone is the degree of constriction in blood vessels, influenced by various factors
• Autoregulation maintains constant blood flow despite changes in perfusion pressure
• Endothelium-derived factors play a crucial role in regulating vascular tone:
  • Nitric oxide (NO) causes vasodilation
  • Endothelin is a potent vasoconstrictor produced by endothelial cells
  • Prostaglandins can cause either vasodilation or vasoconstriction depending on the specific type

Effects of Exercise and Pathological Conditions on Vascular Homeostasis

Exercise effects on vascular function

• Acute effects of exercise:
  • Increased cardiac output and blood flow to active muscles (up to 20-fold)
  • Vasodilation in active muscles due to local metabolic factors ($\uparrow$CO2, $\downarrow$pH, $\uparrow$temperature)
  • Vasoconstriction in inactive tissues (gastrointestinal tract, kidneys) to redistribute blood flow (shunting)
• Chronic adaptations to regular exercise:
  • Improved endothelial function increased nitric oxide production (vasodilator)
  • Increased capillary density in skeletal muscle (angiogenesis)
  • Enhanced vasodilation in response to exercise (functional hyperemia)
  • Reduced resting blood pressure improved blood pressure regulation (lowers risk of hypertension)

Vascular system in pathological conditions

• Hypertension:
  • Chronically elevated blood pressure (systolic $\geq$ 140 mmHg or diastolic $\geq$ 90 mmHg)
  • Increased peripheral resistance due to vasoconstriction structural changes in blood vessels (hypertrophy)
  • Can lead to endothelial dysfunction, atherosclerosis (plaque formation), organ damage (heart, brain, kidneys)
• Hemorrhage:
  • Significant blood loss leading to reduced blood volume and pressure (hypovolemia)
  • Compensatory mechanisms:
    • Baroreceptor reflex increases SNS activity triggers vasoconstriction (maintains perfusion to vital organs)
    • RAAS activation promotes sodium and water retention (restores blood volume)
    • ADH release promotes water retention (concentrates urine)
  • Severe hemorrhage can lead to hypovolemic shock (inadequate tissue perfusion)
• Circulatory shock:
  • Inadequate tissue perfusion and oxygen delivery (hypoperfusion)
  • Types include hypovolemic (hemorrhage), cardiogenic (heart failure), distributive (sepsis)
  • Compensatory mechanisms similar to hemorrhage but may be insufficient to maintain adequate perfusion
  • Can lead to organ dysfunction and failure if untreated (multiple organ dysfunction syndrome)