The prolactin family hormones regulate vascular tone through NO and prostacyclin production in isolated rat aortic rings

Abstract

Aim: Prolactin family hormones include growth hormone, placental lactogen and prolactin, which are able to regulate angiogenesis via NO and prostaglandins. However, their effects on vascular tone are not fully understood. The aim of this study was to evaluate the effects of prolactin family hormones on rat vascular tone in vitro. Methods: Aortic rings were prepared from adult male rats and precontracted with phenylephrine, then treated with the hormones and drugs. The tension was measured with isometric force displacement transducer connected to a polygraph. NO production and prostacyclin release in physiological solution was determined. Cultured rat aortic endothelial cells (RAECs) were treated with the hormones and drugs, and the phosphorylation of eNOS at serine 1177 was assessed using Western bolt analysis. Results: Administration of growth hormone or placental lactogen (0.01-100 nmol/L) induced endothelium-dependent vasodilation. Both the hormones significantly increased the phosphorylation of eNOS in RAECs and NO level in physiological solution. Preincubation with L-NAME blocked growth hormone-or placental lactogen-induced vasodilation and NO production. Preincubation with an antibody against growth hormone receptors blocked growth hormone-and placental lactogen-induced vasodilation. Addition of a single dose of prolactin (0.01 nmol/L) induced sustained vessel relaxation, whereas multiple doses of prolactin induced a biphasic contractionrelaxation effect. The vascular effects of prolactin depended on endothelium. Prolactin significantly increased the level of prostacyclin I 2 in physiological solution. Preincubation with indomethacin or an antibody against prolactin receptors blocked prolactin-induced vasodilation. Conclusion: The prolactin family hormones regulate rat vascular tone, selectively promoting either relaxation or contraction of vascular smooth muscle via activation of either growth hormone receptors or prolactin receptors within the endothelium.

Trophoblastic debris modifies endothelial cell transcriptome in vitro: a mechanism by which fetal cells might control maternal responses to pregnancy

“…In combination these results suggest that regulatory factors, either RNAs or proteins, were transferred to the endothelial cells from the trophoblastic debris and induced the transcription of placental genes in the endothelial cells. Of biologic relevance to our study, it has been shown that CSH1 can induce endothelium dependent vasodilation through nitric oxide production 25 which, since nitric oxide is key physiologic vasodilator, may be important in the normal physiologic adaptation of the maternal cardiovascular system to pregnancy.…”

Vasodilator Activity of Compounds Isolated from Plants Used in Mexican Traditional Medicine

“…Involvement of the NO/cGMP and the H 2 S/K ATP channel pathways in the vasodilator effect of compounds 3 , 15 , and 18 was evaluated by incubating intact endothelium aortic rings for 20 min in the presence of inhibitors of specific enzymes of each of these pathways: (1) NO/cGMP pathway: 100 μM N G -nitro-l-arginine methyl ester (L-NAME, inhibitor of eNOS); and (2) H 2 S/K ATP channel pathway: 10 mM dl-propargylglycine (PAG, inhibitor of CSE) [ 34 , 78 , 79 ].…”

Affinin (Spilanthol), Isolated from Heliopsis longipes, Induces Vasodilation via Activation of Gasotransmitters and Prostacyclin Signaling Pathways

“…To determine the involvement of the prostacyclin pathway in the vasodilator effect of affinin, aortic segments were pre-incubated for 20 min in the presence of 1 µM indomethacin (INDO, inhibitor of COX) [ 78 , 79 ]. In addition, to assess whether activation of K + channels was involved in the vasodilation produced by affinin, the effect of pretreatment with the non-selective potassium channel blocker, 1 mM tetraethyl ammonium (TEA) and 10 µM glibenclamide (a specific blocker of the K ATP channels) was evaluated [ 80 , 81 ].…”