Prostanoid receptors: ontogeny and implications in vascular physiology

Abstract

Prostanoids exert significant effects on circulatory beds. They play a role in the response of the vasculature to adjustments in perfusion pressure and oxygen and carbon dioxide tension, and they mediate the actions of numerous factors. The role of prostanoids in governing circulation of the perinate is suggested to surpass that in the adult. Prostanoids are abundantly generated in the perinate. They have been implicated in autoregulation of blood flow as studied in brain and eyes. Prostaglandins are also dominant regulators of ductus arteriosus tone. The effects of these autacoids are mediated through specific G protein-coupled receptors. In addition to the pharmacological characterization of the prostanoid receptors, important advances in understanding the biology of these receptors have been made in the last decade. Their cloning and the development of animals with disrupted genes of these receptors have been very informative. The involvement of prostanoid receptors in the developing subject, especially on brain and ocular vasculature and on ductus arteriosus, has also begun to be investigated; the expression of these receptors changes with development. Some but not all of the ontogenic changes in these receptors are attributed to homologous regulation. Interestingly, in the process of elucidating their effects, functional perinuclear prostaglandin E2 receptors have been uncovered. This article reviews prostanoid receptors and addresses implications on the developing subject with attention to vascular physiology.

Vaginal Misoprostol vs Vaginal Misoprostol With Estradiol for Labor Induction: A Prospective Double Blind Study

“…PGE 2 exerts its effects on blood vessels through actions on multiple counterbalanced signaling pathways in vascular smooth muscle cells. EP 1 and EP 3 receptors induce vasoconstriction whereas EP 2 and EP 4 receptors provoke vasodilatation [5]. PGE 2 can act as an important modulator of cervical vascular tone.…”

Prostacyclin release and receptor activation: differential control of human pulmonary venous and arterial tone

“…These subtypes include the DP, EP, FP, IP and TP receptors that preferentially respond to PGD 2 , PGE 2 , PGF 2a , PGI 2 and TxA 2 , respectively. This classification does not exclude the effect, for example, of PGI 2 and TxA 2 on EP receptors (Coleman et al, 1994;Wright et al, 2001). An activation of some subtypes (TP, EP 1 , EP 3 , FP) induces vasoconstriction whereas the other receptor subtypes (IP, EP 2 , EP 4 , DP) are responsible for vasodilation.…”

Evidence for the involvement of the cyclooxygenase-metabolic pathway in diclofenac-induced inhibition of spontaneous contraction of rat portal vein smooth muscle cells

“…It has also been indicated that products of the COX pathway are important in the regulation of vascular smooth muscle contraction (Wright et al, 2001). While meclofenamate, a COX inhibitor, has been reported to inhibit spontaneous contractions of the rat portal vein (Enero, 1979), the detailed mechanism of action is not clear.…”

“…Because such contractions are very sensitive to extracellular calcium, the rat portal vein has been used to examine the effects of drugs on vascular contraction (Sutter, 1990). Products of the cyclooxygenase (COX) pathway have been shown to be involved in the regulation of physiological activities (Wright et al, 2001). Spontaneous contractions of the rat portal vein have been shown to be potentiated by prostaglandin E1 (PGE1) (Miwa et al, 1997) and arachidonic acid (Vidulescu et al, 2000).…”

“…In this study, we have examined the effect of diclofenac, another COX inhibitor (Mitchell et al, 1994), on spontaneous contractions of smooth muscle cells of the rat portal vein, as well as on their membrane potential and intracellular Ca 2+ concentration. Products of the COX pathway act on prostanoid receptors, which use different intracellular mediators (Wright et al, 2001). To identify the product involved in this spontaneous contraction, we examined the effects of prostanoid receptor…”