scholarly journals Pressor and renal regional hemodynamic effects of urotensin II in neonatal pigs

2013 ◽  
Vol 217 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Hitesh Soni ◽  
Adebowale Adebiyi
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Peptide Hormone ◽  
Urotensin Ii ◽  
Hemodynamic Effects ◽  
Angiotensin Ii Receptor ◽  
Hemodynamic Changes ◽  
Newborn Pigs ◽  
Dose Dependent Decrease ◽  
Kidney Maturation

Renal expression of the peptide hormone urotensin II (UII) and its receptor (UTR) are dependent on kidney maturation and anatomical regions. However, renal regional hemodynamic effects of UII in neonates are unclear. Here, we investigated regional hemodynamic responses to acute intrarenal arterial administration of UII in newborn pigs. Western immunoblotting and immunofluorescence confirmed UTR expression and membrane localization in newborn pig renal afferent arterioles and afferent arteriolar smooth muscle cells respectively. Intrarenal arterial bolus injections of human UII (hUII; 1–100 ng/kg) resulted in a dose-dependent decrease in total renal blood flow (RBF) and an increase in mean arterial pressure (MAP) and renal vascular resistance (RVR) in newborn pigs. Moreover, hUII dose dependently reduced cortical blood flow (CBF) but increased medullary blood flow (MBF) in the piglets. hUII-induced MAP elevation and hemodynamic changes were inhibited by urantide, a UTR antagonist, but not losartan, a type 1 angiotensin II receptor antagonist. U-73122, a phospholipase C (PLC) inhibitor, and 2-aminoethoxydiphenyl borate, an inositol 1,4,5 trisphosphate (IP3) receptor antagonist, attenuated hUII-induced MAP and RVR elevations, RBF and CBF reductions, but not MBF increase. These findings indicate that intrarenal arterial administration of hUII elevates blood pressure and induces region-selective renal hemodynamic changes in newborn pigs. Our data also suggest that the PLC/IP3signaling pathway contributes to hUII-induced alterations in MAP, RBF, RVR, and CBF but not MBF in newborn pigs.

Hemodynamic effects of the angiotensin II receptor antagonist irbesartan in patients with cirrhosis and portal hypertension

2001 ◽  
Vol 121 (2) ◽  
pp. 389-395 ◽  
Author(s):  
Michael Schepke ◽  
Eva Werner ◽  
Erwin Biecker ◽  
Peter Schiedermaier ◽  
Jörg Heller ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Hemodynamic Effects ◽  
Angiotensin Ii Receptor ◽  
Angiotensin Ii Receptor Antagonist

scholarly journals Hemodynamic effects of urotensin II and its specific receptor antagonist palosuran in cirrhotic rats

Hepatology ◽  
2007 ◽  
Vol 47 (4) ◽  
pp. 1264-1276 ◽  
Author(s):  
Jonel Trebicka ◽  
Ludger Leifeld ◽  
Martin Hennenberg ◽  
Erwin Biecker ◽  
Andreas Eckhardt ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Urotensin Ii ◽  
Hemodynamic Effects ◽  
Specific Receptor

Hemodynamic effects of a combination of clonidine and propranolol in conscious cirrhotic rats

1989 ◽  
Vol 67 (10) ◽  
pp. 1369-1372 ◽  
Author(s):  
Dominique Roulot ◽  
Christophe Gaudin ◽  
Alain Braillon ◽  
Tatsuya Sekiyama ◽  
Yannick Bacq ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Pressure ◽  
Biliary Cirrhosis ◽  
Hemodynamic Effects ◽  
Hemodynamic Changes ◽  
Flow Measurements ◽  
Before And After ◽  
Radioactive Microsphere Method ◽  
Blood Flow Measurements

The hemodynamic effects of the combination of clonidine and propranolol were studied in conscious rats with portal hypertension owing to secondary biliary cirrhosis. Pressure and blood flow measurements (radioactive microsphere method) were performed in three groups of eight rats before and after drug administration. The combined effects of clonidine (2 μg/100 g body wt., i.v.) and propranolol (0.2 mg/min for 10 min) were compared with those observed after administration of either clonidine alone or propranolol alone. The association of clonidine and propranolol induced significant decreases in portal pressure (30%) and portal tributary blood flow (43%), the magnitude of these changes being significantly more marked than that after administration of either clonidine alone (12 and 20%, respectively) or propranolol alone (16 and 17%, respectively). After the combination, no significant change in arterial pressure was observed, but cardiac output significantly decreased and systemic vascular resistance significantly increased. Renal blood flow decreased to a similar extent (40%) in the three groups. These findings indicate that the combination of clonidine and propranolol is more effective for reversing splanchnic hemodynamic changes than clonidine alone or propranolol alone. The additive effects of this association are in agreement with the action of clonidine and propranolol at different levels (central and peripheral) and on different receptors (α and β). It suggests that an increase in sympathetic activity may play a major role in hemodynamic changes observed in experimental cirrhosis.Key words: portal hypertension, cirrhosis, splanchnic blood flow, α2-adrenergic agonist, β-blocker.

Angiotensin II receptor antagonist CV-11974 and cerebral blood flow autoregulation

1995 ◽  
Vol 13 (7) ◽  
pp. 755???762 ◽  
Author(s):  
Tina Vraamark ◽  
Gunhild Waldemar ◽  
Svend Strandgaard ◽  
Olaf B. Paulson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Angiotensin Ii Receptor ◽  
Angiotensin Ii Receptor Antagonist ◽  
Cerebral Blood Flow Autoregulation

Telmisartan prevents high-fat diet-induced neurovascular impairments and reduces anxiety-like behavior

2021 ◽  
pp. 0271678X2110034
Author(s):  
Gianna Huber ◽  
Mikolaj Ogrodnik ◽  
Jan Wenzel ◽  
Ines Stölting ◽  
Lukas Huber ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Fat Diet ◽  
Neurovascular Unit ◽  
Laser Speckle ◽  
Angiotensin Ii Receptor ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Whisker Pad ◽  
Receptor Blockers

Angiotensin II receptor blockers (telmisartan) prevent rodents from diet-induced obesity and improve their metabolic status. Hyperglycemia and obesity are associated with reduced cerebral blood flow and neurovascular uncoupling which may lead to behavioral deficits. We wanted to know whether a treatment with telmisartan prevents these changes in obesity. We put young mice on high-fat diet and simultaneously treated them with telmisartan. At the end of treatment, we performed laser speckle imaging and magnetic resonance imaging to assess the effect on neurovascular coupling and cerebral blood flow. Different behavioral tests were used to investigate cognitive function. Mice developed diet-induced obesity and after 16, not 8 weeks of high-fat diet, however, the response to whisker pad stimulation was about 30% lower in obese compared to lean mice. Simultaneous telmisartan treatment increased the response again by 10% compared to obese mice. Moreover, telmisartan treatment normalized high-fat diet-induced reduction of cerebral blood flow and prevented a diet-induced anxiety-like behavior. In addition to that, telmisartan affects cellular senescence and string vessel formation in obesity. We conclude, that telmisartan protects against neurovascular unit impairments in a diet-induced obesity setting and may play a role in preventing obesity related cognitive deficits in Alzheimer’s disease.

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