Pituitary site of action of endothelin: Selective inhibition of prolactin release in vitro

Samson, Willis K.; Skala, Karl D.; Alexander, B. D.; Huang, Fang

doi:10.1016/0006-291x(90)90393-2

Cited by 122 publications

(47 citation statements)

References 18 publications

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“…The ETA receptor has a higher affinity for ET-1 or ET-2 compared with ET-3, whereas the ETB receptor has equal affinity for the three members of the ET family. In rat cultured anterior pituitary cells and rat PC12 pheochromocytoma cells, evidence was provided for an ET receptor subtype which was selective for ET-3 (Martin et al, 1990; Samson et al, 1990), designated ETc ; the cDNA clone for this receptor has not yet been isolated. The solubilization of ETA and ETB receptors from rat lung (Kondoh et al, 1991) and the purification of the ETB receptor (52 kD) from bovine lung (Kozuka et al, 1991;Hagiwara et al, 1992) have been described.…”

Section: Introductionmentioning

confidence: 99%

Endothelin receptor subtypes in human and guinea‐pig pulmonary tissues

Hay

Luttmann

Hubbard

et al. 1993

British J Pharmacology

109

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1 In this study the endothelin (ET) receptor subtypes mediating contractions produced by ET-1 in human and guinea-pig pulmonary tissues were investigated. In addition the receptor responsible for ET-1-induced prostanoid release in human bronchus was determined.2 In human bronchus and human pulmonary artery ET-l (0.1 nM-0.3 JIM) was a potent and effective contractile agent (pD2 = 7.58 + 0.15, n = 6, and 8.48 + 0.11, n = 7, respectively). BQ-123 (1-10 JiM), a potent and selective ETA receptor antagonist, potently antagonized ET-1-induced contraction in human pulmonary artery (pKB = 6.8 with 1 JIM BQ-123, n = 7) but had no effect in human bronchus (n = 6). 3 Sarafotoxin S6c (0.1 nM-0. IliM), the ETB-selective agonist, did not contract human pulmonary artery (n = 5), but potently and effectively contracted human bronchus: pD2 = 8.41 ± 0.17, maximum response =74.4 ± 3.1% of 1O JM carbachol; n = 5. BQ-123 (1-1 I1M) did not antagonize sarafotoxin S6c-induced contraction in human bronchus (n = 5). 4 ET-1 potently contracted guinea-pig trachea, bronchus, pulmonary artery and aorta (pD2 = 8.15 + 0.14, 7.72 + 0.12, 8.52 + 0.12, and 8.18 ± 0.12, respectively, n = 6-14). BQ-123 (0.1-101M) antagonized ET-1-induced contractions in guinea-pig pulmonary artery (pKB = 6.7 with 1 JIM BQ-123, n = 6), aorta (pKB = 7.1 with 1 JIM BQ-123, n = 6) and trachea (pKB = 6.2 with 1 AIM BQ-123, n = 6) but was without marked effect in bronchus (n = 4). In contrast, sarafotoxin S6c (0.1 nM-0.l JIM) did not contract guinea-pig aorta (n = 4) or guinea-pig pulmonary artery (n = 6) but potently and effectively contracted guinea-pig bronchus: pD2= 8.55 + 0. 1; maximum contraction = 63.6 ± 3.1% of 1O JIM carbachol, n = 4. Sarafotoxin S6c (0.1 nM-0. 1 JIM) was a much less effective agonist in guinea-pig trachea: maximum contraction = 13.9 ± 2.5% of 10 JM carbachol, n = 4; P < 0.0001, compared to bronchus. Contractions produced by sarafotoxin S6c in guinea-pig bronchus or trachea were unaffected by (IO IM, n=4). 5 Significant differences were observed in the efficacy, relative to carbachol, but not the potency of sarafotoxin S6c in guinea-pig airways, with a much greater maximum contractile response in bronchus (69.6 ± 2.4% of 1O JM carbachol, n = 6) or lower region of the trachea (48.5 ± 5.9% of 1OJIM carbachol, n = 6) than in the middle region of the trachea (14.4 ± 4.0% of 10 JiM carbachol, n = 6) or the upper region of the trachea (19.3 ± 2.7% of 1O JM carbachol, n = 6). There were minimal regional differences in either ET-1-induced contraction or the potency of BQ-123 (3 JIM) for inhibition of responses to ET-1 in guinea-pig airways. 6 Release of various prostanoids in human bronchus induced by ET-1 (0.3 JiM) was essentially abolished with 10 IM These data provide evidence that distinct ET receptors mediate ET-1-induced contraction in human pulmonary artery, guinea-pig pulmonary artery and guinea-pig aorta (ETA subtype) compared with human bronchus and guinea-pig bronchus (non-ETA, perhaps ETB subtype). Contractions to ET-1 in guinea-pig trache...

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Section: Introductionmentioning

confidence: 99%

Endothelin receptor subtypes in human and guinea‐pig pulmonary tissues

Hay

Luttmann

Hubbard

et al. 1993

British J Pharmacology

109

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“…Studies by MacCumber et al (1 990) have suggested that ET in brain is produced largely by the glial cells, but it can act on both glia and neurons in a paracrine fashion. There is increasing evidence that ET exerts a modulatory role in neurosecretory events (Shichiri et al, 1989;Lin et al, 1990b;Samson et al, 1990;Warner et al, 1990;Kanyicska et al, 1991). However, its ability to "cross talk" with other agonists that transmit signals through hydrolysis of poly-PI and increase in [Ca2+], has not been examined in detail.…”

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confidence: 99%

Endothelin‐Mediated Calcium Response and Inositol 1,4,5‐Trisphosphate Release in Neuroblastoma‐Glioma Hybrid Cells (NG108‐15): Cross Talk with ATP and Bradykinin

Chau

Lin

Chang

et al. 1993

Journal of Neurochemistry

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“…Endothelin peptides, which are differentially expressed in tissues of the peripheral and central nervous system, have profound effects on prolactin secretion (Samson et al, 1990;Kanyicska et al, 1991;Samson and Skala, 1992;Kanyicska et al, 1995;Stojilkovic et al, 2010). The endothelin receptors ETa are located on the lactotrophs (Stojilkovic et al, 2010).…”

Section: Factors Inhibiting Prolactin Secretionmentioning

confidence: 99%