“…ET-1 has been postulated to play a role in the patho physiology of preeclampsia [6] and intrauterine fetal growth retardation [5,11], Because there is systemic hyp oxia in many of these fetuses and because the present study suggests that hypoxia induces an increase in the plasma ET-1 concentration, ET-1 may be directly in volved in the pathogenesis of these disorders. However, there is also the possibility that plasma levels of ET-1 increase secondary to endothelial damage caused by other pathologic factors.…”
Section: Discussionmentioning
confidence: 53%
“…Endothelin-1 (ET-1) is a potent vasoconstrictor and involved in many pathophysiological conditions [1], The production of ET-1 is enhanced in a variety of pathophys iological conditions such as hypoxia [2] and pulmonary hypertension [3], During pregnancy, amniotic fluid levels of ET-1 levels are increased in pregnancies complicated by intra-amniotic infection [4] and fetal growth retardation [5]. Plas ma ET-1 levels in umbilical vessels are also increased in pregnancies complicated by preeclampsia [6], However, the pathophysiological roles and cause-and-effect rela tionships of ET-1 in complicated pregnancies are not well known.…”
The changes in fetal carotid arterial plasma levels of endothelin-1, catecholamines, PO2, PCO2 and pH were measured after intermittent repetitive umbilical cord occlusion in late gestation pregnant goats (n = 9). Endothelin-1 levels increased to 3.58 ± 0.28 pg/ml immediately after the onset of fetal hypoxia, a level significantly higher than the respective values in the control period (p < 0.05). The elevation of fetal plasma endothelin-1 levels correlated inversely with carotid arterial PO2 (r = -0.41, p < a 0.05) and pH (r = -0.43, p < 0.05). The results suggest that increased endothelin-1 levels may contribute to the maintenance of the fetal circulation during fetal asphyxia.
“…ET-1 has been postulated to play a role in the patho physiology of preeclampsia [6] and intrauterine fetal growth retardation [5,11], Because there is systemic hyp oxia in many of these fetuses and because the present study suggests that hypoxia induces an increase in the plasma ET-1 concentration, ET-1 may be directly in volved in the pathogenesis of these disorders. However, there is also the possibility that plasma levels of ET-1 increase secondary to endothelial damage caused by other pathologic factors.…”
Section: Discussionmentioning
confidence: 53%
“…Endothelin-1 (ET-1) is a potent vasoconstrictor and involved in many pathophysiological conditions [1], The production of ET-1 is enhanced in a variety of pathophys iological conditions such as hypoxia [2] and pulmonary hypertension [3], During pregnancy, amniotic fluid levels of ET-1 levels are increased in pregnancies complicated by intra-amniotic infection [4] and fetal growth retardation [5]. Plas ma ET-1 levels in umbilical vessels are also increased in pregnancies complicated by preeclampsia [6], However, the pathophysiological roles and cause-and-effect rela tionships of ET-1 in complicated pregnancies are not well known.…”
The changes in fetal carotid arterial plasma levels of endothelin-1, catecholamines, PO2, PCO2 and pH were measured after intermittent repetitive umbilical cord occlusion in late gestation pregnant goats (n = 9). Endothelin-1 levels increased to 3.58 ± 0.28 pg/ml immediately after the onset of fetal hypoxia, a level significantly higher than the respective values in the control period (p < 0.05). The elevation of fetal plasma endothelin-1 levels correlated inversely with carotid arterial PO2 (r = -0.41, p < a 0.05) and pH (r = -0.43, p < 0.05). The results suggest that increased endothelin-1 levels may contribute to the maintenance of the fetal circulation during fetal asphyxia.
“…8,27 (2) Immunoreactive ET-1 is present in amniotic fluid. [28][29][30][31][32] (3) Prepro-ET-1 mRNA is pre sent in, and immunoreactive ET-1 is produced by, avascular human amnion tissue and amnion epithelial cells maintained in monolayer culture. 33,34 The phys iologic and pathophysiologic role of ET-1 formed in amnion is not known but potentially could evolve about the potency of this peptide in evoking smooth muscle contraction.…”
“…While ET has been identified in the blood [52–54], cerebrospinal fluid [54], urine [55], amniotic fluid [56,57], milk [58], and seminal fluid [59], the concentration of immunoreactive ET in seminal fluid is significantly higher than in any other biological fluid [60]. An immunoreactive form of ET‐1 has been found in large quantities in human seminal fluids from intact and vasectomized men, in whom the testicular contribution to the ejaculate has been eliminated, indicating a prostatic and/or seminal vesicle source [59].…”
OBJECTIVE
To examine the regional differences in the functional (pharmacological) and biochemical properties of endothelin (ET) receptors in the rabbit prostatic urethra.
MATERIALS AND METHODS
The properties of ET receptors in 6‐month‐old male rabbit prostatic urethras were examined using isolated muscle‐bath and radioligand receptor‐binding techniques. Using plasma membrane suspensions, saturation and inhibition experiments with [125I]ET‐1 and unlabelled agonists and antagonists (ETA‐selective antagonist BQ123, and ETB‐selective agonist sarafotoxin 6c, STX6c) were done to determine the ET receptor densities and their subtype specificities in the different regions of the urethra.
RESULTS
The ETs (ET‐1 and ET‐3) produced significant concentration‐dependent contractile responses in the smooth muscle strips from the different regions of the urethra. Although the maximum contractile responses induced by ET‐1 were similar in the different regions, the maximum contractile responses induced by ET‐3 were greater in the distal region than in the proximal or middle regions, suggesting that the contractile response to ET‐1 is more potent than that to ET‐3 in all regions, and that there are region‐specific differences in the responses to ET‐3 but not ET‐1. Moreover, the ET‐3‐induced contractile response was suppressed by BQ788 (a selective antagonist of the ETB receptor) suggesting that the ETB receptor subtype contributes to the contractile responses mediated by ET‐3. The ET receptors were expressed in higher concentrations in the distal than in the proximal or middle regions. BQ123 and STX6c inhibited [125I]ET‐1 binding in all regions with high and low affinity constants, indicating the presence of both ETA and ETB receptor subtypes. The proportions of high‐affinity binding sites for BQ123, representing ETA receptors, were ≈ 68%, 63% and 42% in the proximal, middle and distal regions, respectively. By contrast, the proportions of high‐affinity binding sites for STX6c, representing ETB receptors, were ≈ 27%, 35% and 52% in the proximal, middle, and distal regions, respectively. These data indicate the presence of regional differences in the densities and subtype specificities of ET receptor subtypes, and the existence of regional differences in the rabbit prostatic urethra.
CONCLUSION
The results suggest regional differences in ETB receptor subtypes that mediate contractile responses to ET‐3, reflecting differences in the densities and specificities of the ET receptor subtypes in the rabbit prostatic urethra.
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