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Drugs in pregnancy and lactation
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Numerous prostaglandin receptors have been identified and their role in renal development becomes increasingly clear [43]. Four prostaglandin E2 receptor subtypes have been identified in the kidney as well: EP1, EP2, EP3, and EP4. They are localised both on glomerular vessels (EP1, EP2, and EP4) and on different parts of the tubule (EP1, EP3, and EP4). Overexpression of some prostaglandin receptors (EP2 and EP4) has been demonstrated in the glomerular afferent vessels of the developmental kidney, allowing for increased activity of vasodilator prostanoids. The vasodilation of the afferent arteriole via these receptors is the way by which prostaglandins counter-act the high vascular resistance generated by the ANG II mediated vasoconstriction of efferent arterioles. It is the main mechanism for maintaining glomerular filtration in fetal and early postnatal life. Overexpression of the tubular EP3 receptor (located in the distal tubule and collecting duct) is needed for amniotic fluid formation and to excrete water during the first days of life [44–46]. In addition, it has been postulated that the down-regulation of the apical collecting duct water channel AQP2 also results in the excretion of hypotonic urine in utero and during the first days of life [47,48]. Embryonic calcium-sensing receptor expression is another mechanism involved in the blockade of arginine vasopressin action, resulting in hypotonic urine, during antenatal life [49].
Diverse Receptors and G Proteins Control the Generation of cAMP, Inositol Phosphates, and Tension in the Myometrium
Published in Robert E. Garfield, Thomas N. Tabb, Control of Uterine Contractility, 2019
Simone Harbon, Lien Do Khac, Zahra Tanfin, Olivier Goureau, Denis Leiber
A classification of different subtypes of prostaglandin receptors has been proposed by Coleman39 and Coleman et al.,40 based on functional criteria using the rank order of potencies of natural PGs and a few relatively selective agonists and antagonists. The five main types of receptors are TP, DP, IP, FP, and EP for thromboxane A2, PGD2, PGI2, PGF2a, and PGE2, respectively. The EP receptors may further be subdivided into EP1, EP2, and EP3 subtypes.40 Using such a pharmacological approach, we have attempted to characterize in rat myometrium, the specificity of PG receptor interaction with different second messenger generating systems and to associate these interactions with PG functional activity.38
Migraine: diagnosis and treatment
Published in Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby, Headache in Clinical Practice, 2018
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby
Prostaglandin production may be enhanced in menstrual migraine. The effectiveness of the NSAIDs129 may be a result of blocking prostaglandin synthesis by inhibiting the enzyme COX. The meclofenamates, in addition, are prostaglandin receptor antagonists. One NSAID, ketoprofen, inhibits the formation of leukotnenes by inhibiting 5-lipooxygenase. NSAIDs in adequate doses can be used abortively or prophytactically 1–2 days before the expected onset of headache and continued for the duration of vulnerability. If the first NSAID is ineffective, other classes of NSAIDs should be tried (Figure 6.24).129
Headaches related to latanoprost in open-angle glaucoma
Published in Clinical and Experimental Optometry, 2021
Henrietta Wang, Katherine Masselos, Michael Kalloniatis, Jack Phu
The side effects of PGAs are typically localised to the eye: conjunctival hyperaemia, eyelash changes (such as hypertrichosis), iris colour changes, periorbital skin darkening, periorbital fat atrophy, and potentially induction of inflammatory events such as herpetic eye disease, uveitis and cystoid macular oedema.7,10–12 However, pharmacological evidence suggests that headaches may be a potential side-effect with prostaglandin therapy.13,14 Although focused primarily on prostaglandin receptors other than the F2α receptor targeted by ophthalmic PGAs, there is evidence to suggest that the prostaglandin family of drugs may induce headaches or activate migraines in some individuals.13,14 One case series has suggested that topical PGAs may be associated with ‘migraine headaches’ in certain patients, concluding that this phenomenon could be explained pharmacologically by latanoprost activation of the trigeminovascular pathway underlying migraine headache pathogenesis.15 The present case series challenges this hypothesis by presenting three cases of patients with primary open-angle glaucoma who were prescribed latanoprost, and subsequently developed symptoms of headaches which subsided without drug cessation.
Relations between second-trimester aneuploidy screening results and prediction of labour induction success in term pregnancies
Published in Journal of Obstetrics and Gynaecology, 2021
Gokhan Karakoc, Mert Turgal, Hasan Eroglu, Caner Cakir, And Yavuz, Aykan Yucel
In the vaginal prostaglandin group, we found lower MoM values of the oestriol level in the caesarean section group than the vaginal delivery group (p < .001). Such a relation was not evident in the balloon dilatation group (p = .064). The former occurrence may be related to an increasing number of prostaglandin receptors due to lower oestriol levels may be representable for this relation. In a prospective clinical study including 24 patients who had underwent labour induction, maternal serum oestriol levels prior to labour were possibly indicators of a favourable labour outcome (Goharkhay et al. 2001). Our results are consistent with these findings. On the contrary, in a recent study were found that oestriol levels did not differ between vaginal and caesarean delivery groups after dinoprostone administration (Konopka et al. 2013).
Selexipag for the treatment of pulmonary arterial hypertension
Published in Expert Review of Respiratory Medicine, 2021
Léon Genecand, Julie Wacker, Maurice Beghetti, Frédéric Lador
Cyclooxygenase metabolizes arachidonic acid (AA) into PGI2,Prostaglandin D2, prostaglandin E2, prostaglandin G2a, and thromboxane, regrouped under the term ‘prostanoids’ [7]. Prostanoids act via their receptors including prostaglandin D receptor, prostaglandin E receptor (1–4), prostaglandin F receptor, and PGI2 receptor (IP receptor). Vascular endothelial cells are the main producers of PGI2, which act mainly via the IP receptor leading to vasodilatation, antiplatelet and antiproliferative actions [7]. Reductions of PGI2 urinary metabolites and of PGI2 synthase expression in the pulmonary arteries have been shown in PAH patients [8]. Nonspecific binding of PGI2 to prostaglandin receptors in the gastric mucosa has been described and could explain some side effects [9].