Angiotensin II and [Sar1,Ile5,Ala8]Angiotensin II Effect on Contractile Activity and Prostaglandin Production of in Vitro Pregnant Rat Uteri*

Endocrinology ◽  
1980 ◽  
Vol 107 (6) ◽  
pp. 1855-1860 ◽  
Author(s):  
NORMAN H. DUBIN ◽  
RAMESH B. GHODGAONKA
Keyword(s):  
Angiotensin Ii ◽  
Contractile Activity ◽  
Pregnant Rat ◽  
Prostaglandin Production

Uterine prostaglandin production in ovine pregnancy: effects of angiotensin II and indomethacin

1992 ◽  
Vol 263 (1) ◽  
pp. H188-H197 ◽  
Author(s):  
R. R. Magness ◽  
C. R. Rosenfeld ◽  
D. J. Faucher ◽  
M. D. Mitchell
Keyword(s):  
Angiotensin Ii ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Prostaglandin Production ◽  
Eicosanoid Production ◽  
Pregnant Sheep ◽  
Vascular Responsiveness ◽  
Vascular Beds ◽  
Systemic Responses

The ovine and human uteroplacental vascular beds are more refractory to angiotensin II (ANG II)-induced vasoconstriction than the systemic vasculature. ANG II increases in vitro prostacyclin (PGI2) production by uterine but not omental arteries from pregnant sheep. Thus vasodilator prostaglandins may account for this difference in vascular responsiveness. We measured uterine and systemic eicosanoid production and hemodynamic responses in pregnant sheep before and during intravenous ANG II (1.15 and 11.5 micrograms/min). ANG II caused dose-related increases in arterial pressure and systemic and uterine vascular resistance (P less than 0.05). PGI2 metabolite (6-keto-PGF1 alpha) in the uterine vein rose from 166 +/- 70 (SE) to 223 +/- 114 and 631 +/- 323 pg/ml, respectively (P less than 0.05), and arterial levels increased from 67 +/- 24 to 145 +/- 78 and 312 +/- 173 pg/ml, respectively (P less than 0.05). Basal uterine venoarterial differences of 6-keto-PGF1 alpha were 99 +/- 43 pg/ml and increased during 11.5 micrograms ANG II/min to 295 +/- 181 pg/ml (P less than 0.05) but not during 1.15 micrograms/min (64 +/- 30 pg/ml). Responses were similar in gravid and nongravid uterine horns. Unilateral uterine prostaglandin inhibition with indomethacin did not alter basal uterine blood flow or systemic responses to ANG II (0.573-11.5 micrograms/min); however, ipsilateral uterine prostaglandin production fell and uterine vasoconstrictor responses increased (P less than 0.05). During ovine pregnancy ANG II increases uterine PGI2 production. PGI2 appears in part to attenuate ANG II-induced uterine vasoconstriction.

Effects of indomethacin, during pregnancy in the rat, on responses to noradrenaline and angiotensin II in vivo, and responses to phenylephrine in vitro

1990 ◽  
Vol 2 (5) ◽  
pp. 587 ◽  
Author(s):  
C Jansakul ◽  
RG King ◽  
AL Boura
Keyword(s):  
Body Weight ◽  
Angiotensin Ii ◽  
Plasma Volume ◽  
Ang Ii ◽  
Pregnant Rats ◽  
Prostaglandin Production ◽  
Pressor Responses

Pressor responses to both angiotensin II (Ang II) and noradrenaline (NA) were reduced in 20-day-pregnant rats compared with those in non-pregnant animals, regardless of whether the results were expressed in terms of the dose per kilogram of body weight or per millilitre of estimated plasma volume. Inhibition of prostaglandin production with indomethacin (10 mg kg-1, i.v.) was not accompanied by any significant effect on responses to Ang II in either non-pregnant or 20-day-pregnant animals. However, it attenuated the effects of NA in 20-day-pregnant rats. Indomethacin (10(-5) or 3 x 10(-5) M) did not potentiate in vitro vasoconstrictor responses to phenylephrine of endothelium-intact or -denuded thoracic aortic rings from non-pregnant or 20-day-pregnant rats. These results suggest that subsensitivity to Ang II or NA during pregnancy in the rat is not due to dilution of the dose of these autacoids resulting from increased plasma volume, nor to an increased output of vasodilator prostaglandins.

scholarly journals Effects of epidermal growth factor, interleukin 1 and nitric oxide on prostaglandin production by guinea-pig uterus

Reproduction ◽  
2002 ◽  
pp. 317-322 ◽  
Author(s):  
JE Keeble ◽  
NL Poyser
Keyword(s):  
Nitric Oxide ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Guinea Pig ◽  
Sodium Nitroprusside ◽  
Spontaneous Activity ◽  
Contractile Activity ◽  
Prostaglandin Production ◽  
Epidermal Growth

Initial experiments in the present study investigated the effects of epidermal growth factor (EGF), interleukin 1beta (IL-1beta) and sodium nitroprusside (a nitric oxide donor) on the output of prostaglandins from guinea-pig uterus on day 7 of the oestrous cycle. Superfusion of day 7 guinea-pig uterus in vitro with either EGF or sodium nitroprusside increased the output of PGF(2alpha) and 6-keto-PGF(1alpha), but not of PGE(2). IL-1beta had no effect on the output of these three prostaglandins. EGF still increased the output of PGF(2alpha), but did not increase the output of 6-keto-PGF(1alpha) in a calcium-depleted superfusate. Subsequent experiments investigated the effect of sodium nitroprusside on contractile activity of day 7 guinea-pig uterus. Basal spontaneous activity of both the intact uterus and isolated myometrium superfused in vitro was low. Sodium nitroprusside increased the contractile activity of these tissues two- to fourfold. EGF did not affect the contractile activity of the uterus, indicating that sodium nitroprusside-induced contractions are not due to increased prostaglandin production. Overall, the findings indicate that EGF and nitric oxide may act as mediators in the mechanism by which oestradiol acting on a progesterone-primed uterus stimulates the increase in PGF(2alpha) production by the guinea-pig uterus necessary for luteolysis. Nitric oxide may increase the spontaneous activity of the uterus when this activity is low.

Locally produced angiotensin II induces ovulation by stimulating prostaglandin production in in vitro perfused rabbit ovaries.

Endocrinology ◽  
1993 ◽  
Vol 133 (4) ◽  
pp. 1609-1616 ◽  
Author(s):  
Y Yoshimura ◽  
M Karube ◽  
T Oda ◽  
N Koyama ◽  
S Shiokawa ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin Production

scholarly journals (Pro)renin receptor: another member of the system controlled by angiotensin II?

2011 ◽  
Vol 13 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Luciana G Pereira ◽  
Carine P Arnoni ◽  
Edgar Maquigussa ◽  
Priscila C Cristovam ◽  
Juliana Dreyfuss ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Mesangial Cells ◽  
At1 Receptor ◽  
Receptor Internalization ◽  
Prorenin Receptor ◽  
Receptor Blockers ◽  
And Function ◽  
At1 Receptor Blockers

The prorenin receptor [(P)RR] is upregulated in the diabetic kidney and has been implicated in the high glucose (HG)-induced overproduction of profibrotic molecules by mesangial cells (MCs), which is mediated by ERK1/2 phosphorylation. The regulation of (P)RR gene transcription and the mechanisms by which HG increases (P)RR gene expression are not fully understood. Because intracellular levels of angiotensin II (AngII) are increased in MCs stimulated with HG, we used this in vitro system to evaluate the possible role of AngII in (P)RR gene expression and function by comparing the effects of AT1 receptor blockers (losartan or candesartan) and (P)RR mRNA silencing (siRNA) in human MCs (HMCs) stimulated with HG. HG induced an increase in (P)RR and fibronectin expression and in ERK1/2 phosphorylation. These effects were completely reversed by (P)RR siRNA and losartan but not by candesartan (an angiotensin receptor blocker that, in contrast to losartan, blocks AT1 receptor internalization). These results suggest that (P)RR gene activity may be controlled by intracellular AngII and that HG-induced ERK1/2 phosphorylation and fibronectin overproduction are primarily induced by (P)RR activation. This relationship between AngII and (P)RR may constitute an additional pathway of MC dysfunction in response to HG stimulation.

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