scholarly journals Role of interventions for atherosclerotic renal artery stenoses

2011 ◽  
Vol 54 (2) ◽  
pp. 563-570 ◽  
Author(s):  
Vikram S. Kashyap ◽  
Fabrice Schneider ◽  
Jean-Baptiste Ricco
2001 ◽  
Vol 280 (1) ◽  
pp. H327-H333 ◽  
Author(s):  
Laurent P. Audoly ◽  
Xiaoping Ruan ◽  
Victoria A. Wagner ◽  
Jennifer L. Goulet ◽  
Stephen L. Tilley ◽  
...  

The kidney plays a central role in long-term regulation of arterial blood pressure and salt and water homeostasis. This is achieved in part by the local actions of paracrine and autacoid mediators such as the arachidonic acid-prostanoid system. The present study tested the role of specific PGE2 E-prostanoid (EP) receptors in the regulation of renal hemodynamics and vascular reactivity to PGE2. Specifically, we determined the extent to which the EP2 and EP3 receptor subtypes mediate the actions of PGE2 on renal vascular tone. Renal blood flow (RBF) was measured by ultrasonic flowmetry, whereas vasoactive agents were injected directly into the renal artery of male mice. Studies were performed on two independent mouse lines lacking either EP2or EP3 (−/−) receptors and the results were compared with wild-type controls (+/+). Our results do not support a unique role of the EP2 receptor in regulating overall renal hemodynamics. Baseline renal hemodynamics in EP2−/− mice [RBF EP2−/−: 5.3 ± 0.8 ml · min−1 · 100 g kidney wt−1; renal vascular resistance (RVR) 19.7 ± 3.6 mmHg · ml−1 · min · g kidney wt] did not differ statistically from control mice (RBF +/+: 4.0 ± 0.5 ml · min−1 · 100 g kidney wt−1; RVR +/+: 25.4 ± 4.9 mmHg · ml−1 · min · 100 g kidney wt−1). This was also the case for the peak RBF increase after local PGE2 (500 ng) injection into the renal artery (EP2−/−: 116 ± 4 vs. +/+: 112 ± 2% baseline RBF). In contrast, we found that the absence of EP3receptors in EP3−/− mice caused a significant increase (43%) in basal RBF (7.9 ± 0.8 ml · min−1 · g kidney wt−1, P < 0.05 vs. +/+) and a significant decrease (41%) in resting RVR (11.6 ± 1.4 mmHg · ml−1 · min · g kidney wt−1, P < 0.05 vs. +/+). Local administration of 500 ng of PGE2 into the renal artery caused more pronounced renal vasodilation in EP3−/− mice (128 ± 2% of basal RBF, P < 0.05 vs. +/+). We conclude that EP3 receptors mediate vasoconstriction in the kidney of male mice and its actions are tonically active in the basal state. Furthermore, EP3receptors are capable of buffering PGE2-mediated renal vasodilation.


Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Karina M Mata ◽  
Wei Li ◽  
Ossama M Reslan ◽  
Waleed T Siddiqui ◽  
Lauren A Opsasnick ◽  
...  

Pregnancy (Preg) is associated with hormonal and vascular changes, and estrogen (E2) may promote systemic vasodilation during Preg; however, the specific E2 receptor (ER), post-ER signaling mechanisms and vascular bed involved are unclear. To test if Preg is associated with distinct expression/activity of ERs in different blood vessels, BP and plasma E2 were measured in virgin and day-19 Preg rats, and the aorta, carotid, mesenteric and renal artery were isolated for measurement of ERα, ERβ and GPR30 expression, and the responses to E2 and specific ER agonists PPT (ERα), DPN (ERβ) and G1 (GPR30). BP was in Preg (89±6) < virgin (98±4mmHg), and plasma E2 was in Preg (120.5±5.8) > virgin (94.3±7.5pg/ml). Western blots revealed increased ERα and ERβ in aorta and mesenteric artery and GPR30 in aorta of Preg vs virgin. Immunohistochemistry revealed that the increases in ERs were mainly in intima and media. E2 and PPT caused greater relaxation of aorta of Preg (52.8±5.5, 49.3±11.4) than virgin (30.0±3.9, 19.3±3.8%) and of mesenteric artery of Preg (77.9±4.7, 75.4±4.5) than virgin (57.4±5.9, 46.5±9.5%), but similar relaxation in carotid and renal artery of Preg vs virgin. DPN and G1 caused greater relaxation in mesenteric and renal artery (15 to 30%) than aorta and carotid artery (<10%), but only aortic relaxation to G1 was in Preg (26.2±4.4) > virgin (5.3±6.7%). The NOS inhibitor L-NAME ± EDHF blocker tetraethylammonium or endothelium removal reduced PPT relaxation in aorta, suggesting an endothelium-dependent mechanism, but did not affect E2, PPT, DPN or G1-induced relaxation in other vessels, suggesting endothelium-independent mechanisms. PPT caused relaxation of Ca 2+ entry-dependent KCl contraction of mesenteric artery that was in Preg (69.7±5.5) > virgin rats (52.9±8.11%). Thus, during pregnancy, an increased ERα expression in endothelial and smooth muscle layers of aorta and mesenteric artery is associated with increased ERα-mediated relaxation via endothelium-derived vasodilators and direct inhibition of Ca 2+ entry pathways, supporting a role of aortic and mesenteric arterial ERα in pregnancy-associated systemic vasodilation. GPR30 may contribute to aortic dilation while the enhanced ERβ may mediate other genomic vascular effects during pregnancy.


1978 ◽  
Vol 43 (3) ◽  
pp. 437-446 ◽  
Author(s):  
S Ichikawa ◽  
J A Johnson ◽  
W L Fowler ◽  
C G Payne ◽  
K Kurz ◽  
...  

1983 ◽  
Vol 245 (4) ◽  
pp. H683-H689 ◽  
Author(s):  
J. R. Haywood ◽  
G. D. Fink ◽  
J. Buggy ◽  
S. Boutelle ◽  
A. K. Johnson ◽  
...  

This study examined the role of the anteroventral third ventricle (AV3V) in the renin-dependent two-kidney, one-clip model of renal hypertension. AV3V lesion and sham lesion rats were subjected to the placement of a clip on one renal artery or a sham operation. The sham lesion-renal artery clip rats experienced an increase in systolic blood pressure; however, AV3V lesioned animals experienced only a transient rise in arterial pressure during the 1st wk after clip. Body fluid regulation studies during the course of the hypertension revealed that there were no differences in water intake and urine volume between the lesion- and sham lesion-renal artery clip animals. Although significantly greater plasma and blood volumes were demonstrated in the AV3V lesion-sham clip rats compared with sham lesion animals, no differences in vascular volumes were detected in the renal artery clip rats. Finally, the rats were water deprived for 3 days to maximally stimulate vasopressin release. Urine osmolality increased significantly in all groups of rats except the AV3V lesion-renal artery clip animals protected against the hypertension.


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