The Dossier

Local, Humoral, and Neural control of resistance.

Changes in resistance control filtration, flow, diffusion.

Bleeding causes neurally mediated constriction of blood vessels.

Blood-Brain barrier protects it from vasoconstrictor stimuli.

VSM capable of graded contraction.

Spontaneous tone due to high leak of Ca

Agonist tone via neural (NE) or humoral (Epi)

Stretch induced – myogenic response

Endothelial cell cooperation: Mechanical, Electrical, Chemical (paracrine factors)

No is produced from arginine, activates GC to produce cGMP which reduces intra Ca and desensitizes myosin to Ca. Phosphodiesterase 5 removes the cGMP (Viagra inhibitsP5)

Endothelium derived hyperpolarizing factor (EDHF) – dilates, with secondary reduction in Ca

Arachidonic Acid metabolites

Endothelin – constriction peptide, potent, hypertension.

Intrinsic control at precapillary vasculature. Pre dilation accompanied by post dilation.

Reactive hyperemia – excess flow that follows reduced flow. Recovery depends on contration of VSM.

Autoregulation stabilizes blood flow and capillary pressure in the face of changing arterial blood pressure.

Functional hyperemia – increased flow with increased metabolic activity.

Myogenic mechanism very important in autoregulation and reactive hyperemia.

Look at flow to metabolic rate ratio to determine myogenic vs. metabolic component.

Vasomotor Center – CNS control from dorsal medulla

• Regulates cardiac function with SNS and PNS
• Vascular regulation only by SNS
• Sympathetic tone
• Traube Herring Waves – cyclical pressure changes associated with respiration

Depressor Area – Ventromedial and caudal medulla

• Dilation through vasomotor and spinal pathways

Hypothalamus

• stimulation of anterior causes decreased blood pressure, vasodilation, and bradycardia
• stimulation of posterolateral causes tachycardia and vasoconstriction
• cutaneous thermal receptors induce vasodilation or vasoconstriction in response to temperature.

Cerebral Cortex

• blushing and fainting
• connections to vasculature via hypothalamus

Cardiovascular sensors

• Peripheral Blood Gas – carotid and aortic, glossopharangeal and vagus nerves
  • Control respiration
  • cardiac acceleration and vasoconstriction
• Central Blood Gas – vasomotor
• Blood Pressure Sensors – carotid and aorta
  • work through vasomotor via intermediate inhibitory nucleus
  • sensitive to both mean and pulse pressure
  • increased sympathetic activation of VSM in artery increases sensitivity of sinus
  • rapidly adapting
  • stretch receptors work through glosspharangeal and vagus nerves to inhibit vassomotor center
    • inhibits sympathetics
    • increased parasympathetic flow – HR
• Blood Pressure Sensors – low pressure side – atria, ventricles, pulmonary artery
  • Atrial A receptors are stimulated by contraction, B stimulated by distension
  • Important in blood volume control
  • Stimulation inhibits release of angiotensin, aldosterone, vasopressin
• Enteric Sensors
• Cutaneus Receptors – Superficial produce constriction, deep produce vasodilation

• Sympathetic Adrenergic Fibers – NE, ATP , NPY

• receptors in blood vessels
  • alpha – contraction of smooth muscle (DOMINANT with NE)
  • beta – relaxation of smooth muscle
• Epi is a more potent beta stimulator at low doses, at high doses alpha are stimulated
• Arterioles and venules are both innervated but NOT capillaries

Extracellular fluid compartment is divided between interstitial fluid and plasma.

If venous pressure rises, more fluid is filtered from capillaries. The initial change in tissue weight is due to the expansion of the vessels.

Driving pressure is Arterial pressure – Venous pressure. This affects flow.

Sympathetic stimulation constricts arterioles more than venules, so the capillary pressure falls.

Contraction of veins shifts blood from the periphery to the central circulation, called venous volume mobilization. Happens during hemorrhage.

Skin is the most sensitive to sympathetic stimulation, brain is the least.

Sympathetic cholinergic fibers use ACh to induce active vasodilation. Not major. These fibers are not tonically active and do not innervate capacitance vessels. They are activated by emotion and anticipation of exercise.

Parasympathetic Dilator Fibers use ACh. Fibers of cranial origin supply the head and viscera. Sacral origin serve pelvis.

Salivary glands: parasympathetic discharge > dilation of glands > formation of kallikrein > formation of bradykinin from plasma proteins > vasodilation

Bradykinin also formed in sweat glands and is involved in cutaneous vasodilation.

NO at work in penis for vasodilation.

Cutaneous sensory neurons release substance P which degranulates mast cells and increases capillary permeability.

Adrenal Medullary Hormone – Epi – Release is stimulated by lots of things including baraoreceptor, works on muscle and skin.

Adrenal cortical hormones

• Corticosterone – permissive role
• Aldosterone – Major action in the kidney, increases salt and water retention, elevates BP.

Angiotensin II – formation initiated by low NaCl and low BP in kidney. Vasoconstrictor. ACE inhibitors

Antidiuretic Hormone – ADH – Vasopressin – released by posterior pituitary – vasoconstrictor – hemorrhage.

Histamine – released by mast cells – dilates arterioles, constricts venules, increases capillary permeability.

Prostas from AA – synthesized on demand, release associated with injury.