• BIO 461 Principles of Physiology
  • Module 1.0. Homeostasis, Membranes, Electrophysiology and ANS
  • Module 2.0. Skeletal Muscle and Special Senses
  • Module 3.0. Cardiovascular System
  • Module 4.0. Urinary and Respiratory Systems
  • Module 5.0. Digestive, Endocrine and Reproductive Systems
  • Appendix A. Gender
  • Appendix B. The Placebo Effect
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  • 3.5.5

    Myogenic and Paracrine Regulation of Vasoconstriction and Vasodilation

    An important characteristic of all tissues is the ability to “locally” control blood flow by regulating arteriolar resistance. Tissues utilize two methods of local control, myogenic and paracrine regulation. Myogenic regulation occurs because of the intrinsic property of smooth muscle cells to contract in response to stretch. This reflexive contraction to stretch occurs because of the presence of mechanically gated Ca2+ channels. Once Ca2+  enters the cell it induces the contraction cascade. This intrinsic property is effective at reducing blood flow via vasoconstriction in response to systemic increases in blood pressure. Although effective, the myogenic regulation is limited to specific circumstances and can only increase resistance. When the tissues require more precise regulation of blood flow they turn to local chemical regulation called paracrine signaling.

    Metabolically active endothelial cells can release paracrines in response to metabolic activity. For example, an increase in metabolic activity would decrease local O2 levels while simultaneously increasing local CO2 levels. Both of these conditions would result in vasodilation of associated arterioles, resulting in more blood flow which helps to eliminate CO2 and replenish O2. This process of increasing local blood flow in response to increased metabolic activity is called active hyperemia.

    Sometimes O2 levels decrease and CO2 levels increase without a change in metabolic activity. This can happen when blood flow to a given tissue becomes occluded via a clot or injury. In addition to experiencing decreases in O2 and increases in CO2, the endothelial cells will also begin producing nitric oxide (NO) and adenosine, both potent vasodilators.  If blood flow is suddenly restored to the occluded area, the tissue will have maximally dilated arterioles as the blood re-enters. This response is called reactive hyperemia.

    Depending on the length of occlusion, paracrine metabolites can accumulate at higher than normal levels, resulting in a significant trigger of vasodilation when blood flow resumes. This rapid increase can cause an inflammatory response that results in more cellular damage. This is called a reperfusion injury. If the occlusion occurs in vessels supplying the brain, a reperfusion injury can worsen the initial effects of a stroke. It the occlusion occurs in vessels supplying the heart, a reperfusion injury can worsen the effects of a myocardial infarction.   

    Not all paracrine signals are associated with changes in local metabolism, instead some are associate with inflammation (bradykinin and histamine; vasodilators) and some with clotting cascades (serotonin and ADP; vasoconstrictors).

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