TI: Angiotensinogen: a candidate gene involved in preeclampsia? [letter]
TI: angiotensinogen: кандидат ген, вовлеченный в преэклампсию? [Письмо]
AU: Arngrimsson-R; Purandare-S; Connor-M; Walker-JJ; Bjornsson-S; Soubrier-F; Kotelevtsev-YV; Geirsson-RT; Bjornsson-H
SO: Nat-Genet. 1993 Jun; 4(2): 114-5
MESH: Alleles-; Base-Sequence; Disease-Susceptibility-genetics; Iceland-; Molecular-Sequence-Data; Polymorphism-Genetics; Pre-Eclampsia-classification; Pre-Eclampsia-ethnology; Pre-Eclampsia-urine; Pregnancy-; Prospective-Studies; Proteinuria-etiology; Repetitive-Sequences,-Nucleic-Acid; ScotlandMESH: *Angiotensinogen-genetics; *Pre-Eclampsia-genetics
TI: Decreased levels of amniotic fluid oxytocinase activity in preeclampsia.
TI: Сниженные уровни амниотической жидкости oxytocinase активность в преэклампсии.
AU: Roy-AC; Viegas-OA; Sen-DK; Ratnam-SS
AD: Department of Obstetrics and Gynaecology, National University of Singapore, Republic of Singapore.
SO: Gynecol-Obstet-Invest. 1993; 35(3): 166-8
AB: Oxytocinase (EC 3.4.11.3) activity was determined in 80 amniotic fluid samples obtained from 40 normotensive primigravidas (median age 27 years) and 40 primigravidas (median age 29 years) with pregnancies complicated by preeclampsia between 32 and 39 weeks of gestation. The enzyme activity was significantly lower in preeclampsia than in normal pregnancy with matched gestations (p < 0.01). Considering the possible involvement of vasopressin and angiotensin II in preeclampsia, it is suggested that the enzyme which degrades these pressor hormones may play a role in the pathogenesis of hypertensive pregnancy.
: oxytocinase (ЕВРОПЕЙСКОЕ ЭКОНОМИЧЕСКОЕ СООБЩЕСТВО 3.4.11.3) активность была определена в 80 амниотических жидких образцах, полученных от 40 normotensive primigravidas (срединный возраст 27 лет) и 40 primigravidas (срединный возраст 29 лет) с беременностями, осложненными преэклампсией между 32 и 39 неделями беременности. Активность фермента была значительно ниже в преэклампсии чем в нормальной беременности согласованными беременностями (p < 0.01). Рассматривая возможную причастность(вовлечение) вазопрессина и angiotensin II в преэклампсии, это предложено, что фермент, который деградирует эти вазопрессорные гормоны, может играть роль в патогенезе гипертензивной беременности.
TI: [Hemoconcentration via ANP in pre-eclampsia. A recently discovered peptide antagonist to the RAA system]
TI: [hemoconcentration через ANP в преэклампсии. Недавно обнаруженный антагонист пептида к RAA системе]
TO: Hemokoncentration via ANP vid preeklampsi. Nyupptackt peptid antagonist till RAA-systemet.
AU: Poulsen-H; Stjernquist-M; Sjoberg-NO
AD: Samtliga vid kvinnokliniken, Malmo allmanna sjukhus.
SO: Lakartidningen. 1993 May 26; 90(21): 2033-8
MESH: Atrial-Natriuretic-Factor-blood; Blood-Volume; Models,-Cardiovascular; Pre-Eclampsia-blood; Pre-Eclampsia-etiology; PregnancyMESH: *Atrial-Natriuretic-Factor-physiology; *Pre-Eclampsia-physiopathology; *Renin-Angiotensin-System-physiology
TI: Is endothelin involved in the pathogenesis of hypertension?
TI: эндотелин вовлечен в патогенез артериальной гипертензии?
AU: Vanhoutte-PM
AD: Baylor College of Medicine, Center for Experimental Therapeutics, Houston, TX 77030.
SO: Hypertension. 1993 Jun; 21(6 Pt 1): 747-51
AB: Endothelins are a family of potent vasoconstrictor peptides released by endothelial cells. The production of endothelin-1 (ET-1) can be stimulated by aggregating platelets and angiotensin II. It is inhibited by increases in intracellular concentration of cyclic GMP. ET-1 causes biphasic changes in arterial blood pressure and of peripheral resistance in several vascular beds: an initial transient decrease (due to release of nitric oxide, prostacyclin, or both from the endothelium) followed by a sustained increase (mainly due to direct activation of vascular smooth muscle). The vasoconstriction induced by the peptide is inhibited by increases in cyclic GMP. Few studies, except in pregnant women with preeclampsia or eclampsia, indicate that the circulating levels of the peptide are augmented in hypertension. Likewise, the information available on changes in responsiveness to endothelins in blood vessels from hypertensive animals is controversial. Until the effect of selective antagonists on the production or action of the peptide can be determined in hypertensive patients, caution must be exerted when implying a role for endothelin in the pathophysiology of hypertension.
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