Influence of raising maternal blood pressure with angiotensin II on utero-placental and feto-placental blood velocity indices in the human

1990 ◽  
Vol 78 (1) ◽  
pp. 95-100 ◽  
Author(s):  
Ph. Loquet ◽  
F. Broughton Pipkin ◽  
E. M. Symonds ◽  
P. C. Rubin

1. The effect of doubling doses of angiotensin II on maternal systemic blood pressure and arcuate and fetal umbilical artery Doppler velocity profiles has been investigated in 10 women in first- and 10 in second-trimester pregnancy. Ten non-pregnant women were also studied. 2. A progressive decrease in the pressor response to angiotensin II in early pregnancy as previously described was confirmed. 3. Angiotensin II induced a significant dose-dependent increase in the pulsatility index (a measure of downstream resistance) in the umbilical artery in both first- and second-trimester patients. There was an apparent increase in the threshold response of the pulsatility index to angiotensin II in the umbilical artery as pregnancy progressed. There was also a significant correlation between changes in maternal systolic or diastolic pressure and change in umbilical artery pulsatility index, but this did not differ between the two trimesters. This suggests that the increase in pulsatility index is related to blood pressure rather than angiotensin II. This is consistent with reports that angiotensin II does not cross the haemo-monochorial placenta. 4. Basal pulsatility index in the arcuate artery fell with increasing gestation. There was a significant inverse association between the evoked change in maternal systemic blood pressure and the change in arcuate artery pulsatility index, suggesting local vasodilatation. 5. We conclude that acutely increasing maternal blood pressure leads to increased vascular resistance on the fetal side of the circulation.

2012 ◽  
Vol 150 (1-3) ◽  
pp. 285-290 ◽  
Author(s):  
Miyoko Kasai ◽  
Takashi Miyazaki ◽  
Tsuneo Takenaka ◽  
Hiroyuki Yanagisawa ◽  
Hiromichi Suzuki

2015 ◽  
Vol 308 (5) ◽  
pp. H376-H385 ◽  
Author(s):  
Istvan Czikora ◽  
Attila Feher ◽  
Rudolf Lucas ◽  
David J. R. Fulton ◽  
Zsolt Bagi

The type 1 angiotensin II (ANG II) receptor (AT1R) undergoes internalization following stimulation by ANG II. Internalization reduces cell surface AT1Rs, and it is required for AT1R resensitization. In this process AT1R may interact with caveolin-1 (Cav1), the main scaffolding protein of caveolae. We hypothesized that the interaction between Cav1 and AT1R delays AT1R resensitization and thereby prevents sustained ANG II-induced resistance artery (RA) constriction under normal conditions and in experimental obesity. In rat and mouse skeletal muscle RA (diameter: ∼90–120 μm) ANG II-induced constrictions were reduced upon repeated (30-min apart) administrations. Upon disruption of caveolae with methyl-β-cyclodextrin or in RA of Cav1 knockout mice, repeated ANG II applications resulted in essentially maintained constrictions. In vascular smooth muscle cells, AT1R interacted with Cav1, and the degree of cell surface interactions was reduced by long-term (15-min), but not short-term (2-min), exposure to ANG II. When Cav1 was silenced, the amount of membrane-associated AT1R was significantly reduced by a short-term ANG II exposure. Moreover, Cav1 knockout mice fed a high-fat diet exhibited augmented and sustained RA constriction to ANG II and had elevated systemic blood pressure, when compared with normal or high-fat fed wild-type mice. Thus, Cav1, through a direct interaction, delays internalization and subsequent resensitization of AT1R. We suggest that this mechanism prevents sustained ANG II-induced RA constriction and elevated systemic blood pressure in diet-induced obesity.


2013 ◽  
Vol 5 (2) ◽  
pp. 60 ◽  
Author(s):  
Mehdi Nematbakhsh ◽  
Fatemeh Eshraghi ◽  
Zahra Pezeshki ◽  
Behzad Zolfaghari ◽  
Tahereh Safari ◽  
...  

2011 ◽  
Vol 5 (1) ◽  
pp. 32-34 ◽  
Author(s):  
Helen L Barrett ◽  
Karin Lust ◽  
Narelle Fagermo ◽  
Leonie K Callaway ◽  
Lee Minuzzo

Moyamoya disease is a rare cerebrovascular occlusive disorder characterized by stenosis in the circle of Willis with the development of a compensatory circulation. It has been associated with significant morbidity in pregnancy including intracranial haemorrhage, ischaemic stroke and epilepsy. We present the case of a 26-year-old woman with a previous diagnosis of moyamoya vasculopathy with bilateral superficial temporal to middle cerebral artery bypass grafting. During the second trimester, she developed significant neurological symptoms related to postural hypotension in the presence of a stenosis of the right-sided graft. The hypotension was treated with fludrocortisone therapy with improvement in blood pressure and symptoms. Moyamoya vasculopathy poses unique challenges to obstetric care. This is the first report of use of fludrocortisone for maintenance of blood pressure during pregnancy in this condition.


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