Control of arterioles in animals

Control of arterioles in animals

Control of arterioles in animals involves Neural regulation and Hormonal regulation

Neural regulation by vasomotor centers

It is located bilaterally in the medullary reticular formation and lower pons and includes the Vasoconstrictor and Vasodilator centers.

This centre receives sensory signals through vagus and glossopharyngeal nerves. The output signals from these centers regulate their vasoconstrictor or vasodilator activities on blood vessels through sympathetic and parasympathetic divisions of ANS.

Vasoconstrictor centre is a bilaterally located centre, extends from the middle pons to upper spinal cord. It projects its vasoconstrictor fibers through sympathetic system. Under normal conditions, the vasoconstrictor area transmits continuous signals through the sympathetic vasoconstrictor nerve fibers which maintain a partial state of contraction of the blood vessels called as sympathetic vasoconstrictor tone.

Vasodilator centre is located close to the vasoconstrictor area medially in the  floor of the ventricles of the medulla oblongata that inhibits the vasoconstrictor area producing vasodilatation.

Vasoconstrictor and vasodilator centers show reciprocal inhibition. These centers are controlled by higher neurons from hypothalamus and cerebral cortex and also from sensory impulses from the peripheral organs and chemical composition of blood.

Vasoconstrictor nerves

The sympathetic nerves (thoraco-lumber outflow) innervate the small arteries, large arterioles and veins. They provide peripheral resistance and function to maintain the tonus of the arterioles, thus regulate BP. On the other hand, the capillaries and precapillary sphincters are free from sympathetic innervations.

The venules have fewer adrenergic fibres than large veins which themselves are less richly innervated than the arterioles.

Sympathetic innervation to veins causes either constriction or dilatation of the veins and regulates BP by altering the blood volume of the circulatory system. Nor-epinephrineis the sympathetic neurotransmitter. Sympathetic stimulation also causes the release of epinephrinefrom adrenal medulla.

Both epinephrine and norepinephrine acts through α  and β receptors on the blood vessels. NEP excites mainly α  receptors and causes vasoconstriction.

By its action on α1-adrenergic receptors, causes vasoconstriction in arterioles of all organs of the body. Epinephrine acts both on α  and β adrenergic receptors. Its action on α  adrenergic receptors in cutaneous and renal arterioles causes vasoconstriction.

Epinephrine causes vasodilatation in the cardiac and skeletal muscles via its effect on β receptors. Neuropeptide-Y potentiates the vasoconstrictor effect of adrenergic receptors in primates. All vasoconstrictor fibers are sympathetic fibers and these fibers are in tone.

Vasoconstrictor or vasodilator effect can be produced by altering vasoconstrictor tone without involving vasodilator fibers. Stimulation of sympathetic fibers to veins causes vasoconstriction.

Vasodilator fibers

Vasodilator fibers are of three types, parasympathetic, sympathetic cholinergic and antidromic fibers. These fibers do not exert tonic activity on blood vessels.

1. Parasympathetic vasodilator fibers
   • These are the cranio-sacral outflow as chorda tympani (branch of facial nerve), glossopharyngeal, vagus and pelvic nerves.
   • The neurotransmitter of these fibers is acetyl choline, which act through the cholinergic muscarinic M₃ type receptors, located on the endothelial cells and the smooth muscle cells of most arterioles.
   • M₃ receptors are innervated by parasympathetic fibers in the coronary circulation and in the external genitalia and by sympathetic cholinergic fibers in skeletal muscles.
   • Activation of M₃ receptors on the endothelial cells causes vasodilatation and it also releases nitrous oxide from endothelial cells.
   • This nitrous oxide also produces vasodilatation by acting through smooth muscle cells of arterioles.
   • Stimulation of these fibers results in vasodilatation in coronary vessels, tongue, salivary gland, external genitalia, bladder and rectum. 
2. Sympathetic vasodilators
   • Two types of fibers are adrenergic and cholinergic vasodilator fibers.
     • Sympathetic adrenergic fibers
       • Stimulation of   β₁ receptor causes relaxation of renal arterioles.
       • Sympathetic stimulation of  β₂ adrenergic receptors causes vasodilatation.
       • Epinephrine acts on  β₂ adrenergic receptors to effect vasodilatation of coronary vessels, skeletal muscle, pulmonary and splanchnic arterioles and systemic veins.
       • β₂ receptors are found on the coronary and skeletal muscle arterioles. These receptors are not innervated by sympathetic nerves but they respond to circulating epinephrine released from the adrenal medulla in response to sympathetic stimulation.
       • It causes anticipatory increase in blood flow to heart and skeletal muscles during fight or flight reaction.
     • Cholinergic sympathetic vasodilator fibers
       • They are limited to the arterioles of active skeletal muscles, causes an anticipatory increase in blood flow even before exercise to overcome fatigue (in dog and cat).
       • Sympathetic cholinergic fibers to cholinergic muscarinic M₃ receptors cause cutaneous vasodilatation.
3. Antidromic fibers
   • These fibers originate from dorsal roots of spinal cord and show bidirectional conduction of impulses.
   • The antidromic fibers divide at their peripheral end, one branch supplying the receptors of the skin or muscle and the other to the nearby arterioles.
   • The receptor are sensitive to trauma, heat, cold and frostbite.
   • When the receptor are stimulated, the impulses reache the blood vessel concerned by travelling in opposite direction (antidromic) and result in vasodilatation. Since the reflex operates on the sensory nerve and its branch to the blood vessel without involving CNS, it is referred as the axon reflex.

Humoral regulation of arterioles

• Effect of epinephrine, norepinephrine and renin – angiotensin on arterioles has already been dealt.
• ADH, angiotensin II, dopamine, prostaglandins and high cAMP act on epsilon receptors will result in vasoconstrictions.
• Atrial natriuretic factor (ANF)release is stimulated by stretching of atria due to increased blood volume. In the kidney tubules it causes increased GFR, decreased Na⁺ reabsorption (natriuresis), diuresis by inhibition of renin, aldosterone and ADH activities. It also exhibits vasodilator effect through cGMP mechanism.
• Neuropeptide Y has direct vasoconstrictor properties, regulates the release of atrial natriuretic factor and angiotensin-II.
• The vasoconstrictor actions of serotonin and K⁺ and norepinephrine are potentiated by neuropeptide Y, whereas it inhibits renin release. It is involved in moment by moment regulation of blood pressure and blood flow.
• Vasoactive inhibitory polypeptide (VIP) causes vasodilatation and renin release.
• Serotonin by its effect on S₁ and S₂ receptors causes vasodilatation and vasoconstriction, respectively. Serotonin and K⁺ ions stimulate the release of atrial natriuretic factor; tend to reduce BP by vasodilatation.
• Prostaglandins are local hormones, synthesized by vascular endothelium. PGE₂ and prostacyclin (PGI₂) are vasodilators, whereas thromboxane A₂ and PGF_2α are vasoconstrictors.
• Acetylcholine, insulin, glucagon and prostaglandins are coronary vasodilators, whereas vasopressin (ADH) and oxytocin are coronary vasoconstrictors.
• Thyroxine causes increased blood flow through coronary vessels.
• Bradykinin and histamine cause very powerful vasodilatation and play a key role in the regulation of blood flow in the skin and gastrointestinal glands.
• Histamine acts on H₁ and H₂ histamine receptors cause the release of endothelium derived relaxing factor (EDRF) and low cAMP, results in vasodilatation.
• High CO₂, H⁺ and lactic acid, the metabolic products cause local vasodilatation.
• Adenosine, ATP, K⁺ ions are the vasodilator substances.
• An increase in Ca⁺⁺ ions causes vasoconstriction, whereas increased concentrations of Na⁺,K⁺ and Mg⁺ result in vasodilatation.
• GABA and glycine are the neurotransmitters of δ receptors cause vasodilatation.
• Adenosine released during tissue anoxia stimulates adenosine A₂ receptors activates cAMP mechanism results in profound vasodilatation. ADP and ATP causes release of nitrous oxide from endothelial cells, act on P₂ receptors cause vasodilatation .