PHY3171 Lecture Notes - Lecture 13: Smooth Muscle Tissue, Gap Junction, Calcitonin Gene-Related Peptide
10 Feb 2019
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Document Summary
Endothelial cell lining in all blood vessels stops clotting. In some arteries: the endothelium projects through the lamina to the underlying smooth muscle these are gap junctions: cytoplasmic continuity between endothelial and smooth muscle cells. Allows for ions to go through these gap junction. What causes constriction: nerves na, circulating ang ii, bradykinin, local tissue factors, mechanical pressure stretch of blood vessel causes contraction, endothelium endothelin, prostaglandins - thromboxane. What causes relaxation: endothelium no, most important, circulating anp, nerves cgrp, local tissue factors, mechanical stress. 3 things: no, blocking no increased map and decrease blood flow. In bigger arteries: prostacyclin (pgi2, extremely potent in blood clotting - anticoagulant, not as strong as relaxing smooth muscle as no, less important in smaller arteries, edhf. Every hole in the iel, is where you can see potassium channels source of delivering hyperpolarisation. Ion channels are on the tip of endothelial cell. Gap junction between endothelial cells and smooth muscle cell.
