Vascular smooth muscle and prostaglandins

Abstract

Experiments related to mechanisms by which prostaglandin (PG) compounds induce contraction and relaxation of vascular smooth muscles, both arterial and venous, are described. These studies, utilizing isolated rat aortic strips and portal veins, compare the reactivities of these blood vessels to different prostaglandin compounds (i.e., PGE1, F2alpha, B1 and A1) under different environmental conditions (e.g., presence or absence of Ca2+, Mg2+, oxygen, substrate, and PG synthetase inhibitors with and without a variety of smooth muscle agonists) in order to gain some insight into some mechanisms of PG action on blood vessels. PG-induced responses on rat aortic and portal venous smooth muscle appear to be very dependent on [Mg2+]0, oxygen, and availability of glucose. The exact actions (i.e., contraction or relaxation) of different prostaglandin compounds on arterial and venous smooth muscles may be dependent on different [Mg2+]0, oxygen and substrate requirements. Low concentrations of a variety of PG synthetase inhibitors (e.g., aspirin, indomethacin and eicosa-5,8,11,14-tetraynoic acid) potentiate epinephrine, angiotensin, and potassium-induced contractions in aortic muscle but do the reverse to these agonists in portal venous muscle. These PG synthetase inhibitor-induced potentiations and attenuations of agonist-induced responses can be reversed by adding specific PGs in subthreshold contractile doses to the two types of vascular muscles.