Intrauterine infusion of BQ-610, an endothelin type A receptor antagonist, delays luteolysis in dairy heifers

Keator, Christopher S.; Schreiber, David; Hoagland, T.A.; McCracken, J. David; Milvae, R. A.

doi:10.1016/j.domaniend.2007.11.002

Cited by 10 publications

(18 citation statements)

References 40 publications

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“…Infusion of the EDNRA-specific antagonist BQ610 maintained serum concentrations of progesterone, suggesting a luteotropic role of the antagonist and hence, luteolytic role of the endogenous peptide. Consistent with this, intrauterine infusion of BQ610 on Days 16 to19 of the estrous cycle appeared luteotropic in a study from Connecticut, delaying luteal regression in cattle for ~24 h (67). Unfortunately, a compilation of all the literature describing the pharmacological manipulation of luteal function in vivo will not answer the most pertinent question of whether EDN1 is luteolytic or luteotropic.…”

Section: Corpus Luteummentioning

confidence: 58%

Endothelins in regulating ovarian and oviductal function

Bridges

Cho

2011

Front Biosci

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In the last 30 years, remarkable progress has been made in our understanding of the biological role of endothelins in the regulation of reproductive function and fertility. A peptide hormone identified for its ability to regulate blood pressure has now been shown as a potent mediator of several reproductive pathways. Ligand-and receptor-specific roles have been identified and/or postulated during follicular development and ovulation as well as in the function and regression of the corpus luteum. In this review we have attempted to organize endothelin-mediated ovarian processes in a process-specific manner, rather than compile a review of ligand-or isoform-specific actions. Further, we have included a discussion on "post-ovarian" or oviductal function, as well as the future directions that we believe will increase our understanding of endothelin biology as a whole. KeywordsEndothelin; ovary; oviduct; ovulation; follicle; corpus luteum INTRODUCTION ENDOTHELINSEndothelins were first identified in a hallmark paper by Yanigasawa et al. (1) as potent vasoactive peptides, regulating vascular tone and blood pressure. However, diversity in biological function became readily apparent with many other roles for these peptides now described. Three isoforms of endothelins (EDN1, 2 and 3) coded by three different genes (2) have been identified to date (3). These 21 amino acid peptides are derived by cleavage of the biologically inactive "big-endothelin" by the action of at least 2 endothelin converting enzymes (ECE1 and ECE2). The biological effects of endothelin production are then determined via activation of one of two G-protein coupled receptors, endothelin receptors A and B (EDNRA and EDNRB). EDNRA has a high affinity for both EDN1 and EDN2 (and a low affinity for EDN3) whereas EDNRB has a similar affinity for all the isoforms (4).Genetic deletion of components of the endothelin system has highlighted the importance of these peptides rather than defining tissue specific effects. Endothelin-1 knockout mice die of respiratory failure at birth (5), EDN2 knockout mice exhibit growth retardation and juvenile NIH Public Access Author ManuscriptFront Biosci (Schol Ed). Author manuscript; available in PMC 2011 January 28. Published in final edited form as:Front Biosci (Schol Ed). ; 3: 145-155. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript lethality (6), EDN3 knockout mice exhibit aganglionic megacolon and die young (7), EDNRA knockout mice are embryonic lethal (8) and EDNRB knockout mice die close to the age of puberty (9). Researchers have therefore relied heavily on the use of agonists and antagonists to study the function of these peptides, however conditional transgenic models are now becoming more readily available. As expected from their structure, the three purified peptide ligands are available for commercial purchase, albeit not always in a species-specific state. Similarly, a plethora of antagonists can be purchased, selective (or not) in their antagonism to either EDNRA or EDNRB. W...

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Section: Corpus Luteummentioning

confidence: 58%

Endothelins in regulating ovarian and oviductal function

Bridges

Cho

2011

Front Biosci

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“…While the endothelin receptor type that is responsible for this CL regression pathway is not known, it would be worth to see whether EDNRB is the EDN1 receptor for an initiating the luteolytic pathway; loss of EDNRB may deter the luteolytic pathway, leaving the CL live longer and keep it larger. Interestingly, it was shown that luteolysis was inhibited by EDNRA antagonism but not by EDNRB antagonist (Doerr et al, 2008; Keator et al, 2008; Watanabe et al, 2006), indicating EDNRA plays as an initiator of luteolysis. Therefore, further study is warranted to determine specific endothelin-driven physiological events that are mediated by EDNRA and EDNRB in regulating the luteolytic pathway.…”

Section: Discussionmentioning

confidence: 99%

Endothelin B receptor is not required but necessary for finite regulation of ovulation

et al. 2012

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Aims In the ovary, endothelins regulate a variety of ovarian functions that include but not limited to folliculogenesis, steroidogenesis, oocyte maturation, ovulation and corpus luteum (CL) function. Two cognate receptors, EDNRA and EDNRB are constitutively expressed in the ovary, and mediate the regulatory endothelin actions. However, the physiological significance of the presence of the two receptors that often elicit opposite responses upon activation by an endothelin is yet to be determined. This study was proposed to test the hypothesis that both receptors are present in the ovary to lend an endothelin a finite regulation of ovulation. Main methods A rescued EDNRB knockout (rEDNRB-KO) mouse that is deficient of EDNRB expression in all cells but adrenergic cell lineage was used to test the impact of the loss of function of EDNRB on ovulation. The EDNRB gene deletion and its confirmation at mRNA level were assessed by molecular biology techniques, and the number and size of corpus lutea was determined by ovary histology. Key findings Female rEDNRB-KO mice had larger litter sizes (numbers of pups per birth) and their ovaries contained more corpus lutea than wild type littermates. Significance This result shows that without EDNRB excessive ovulation occurs, suggesting a role of EDNRB in having the extent of ovulation confined.

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“…This led investigators to consider whether other types of cells were missing from the steroidogenic cell cultures (i.e., endothelial cells [18][19][20] and immune cells [21], and the results of many in vitro experiments suggested that the luteolytic effect of PGF 2a likely involved communication among these heterogeneous cells. Support for a critical role of the endothelial cell-derived protein, endothelin 1, in luteal regression was also obtained from in vivo experiments [22][23][24][25].…”

Section: What Is the Mechanism Of Action Of Pgf 2a In The Cl?mentioning

confidence: 96%

It Takes Two to Tango but Four for the Finale

Pate

2012

Biology of Reproduction

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Intrauterine infusion of BQ-610, an endothelin type A receptor antagonist, delays luteolysis in dairy heifers

Cited by 10 publications

References 40 publications

Endothelins in regulating ovarian and oviductal function

Endothelins in regulating ovarian and oviductal function

Endothelin B receptor is not required but necessary for finite regulation of ovulation

It Takes Two to Tango but Four for the Finale

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