scholarly journals Activation of renin-angiotensin system in maintenance of high blood pressure in uncomplicated pheochromocytoma A case report.

1983 ◽  
Vol 22 (3) ◽  
pp. 227-230
Author(s):  
Hiromi MURATANI ◽  
Terukazu KAWASAKI ◽  
Yuhei KAWANO ◽  
Isao ABE ◽  
Kenshi KUMAMOTO ◽  
...  
2004 ◽  
Vol 22 (7) ◽  
pp. 1323-1332 ◽  
Author(s):  
Huan Wang ◽  
Jun Nawata ◽  
Noriko Kakudo ◽  
Koichiro Sugimura ◽  
Jun Suzuki ◽  
...  

2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Sandrita Simonyte ◽  
Renata Kuciene ◽  
Jurate Medzioniene ◽  
Virginija Dulskiene ◽  
Vaiva Lesauskaite

1976 ◽  
Vol 51 (s3) ◽  
pp. 19s-21s ◽  
Author(s):  
J. Giese

1. The syndrome of malignant hypertension in man and animals has three fundamental components: high blood pressure, activation of the renin—angiotensin system and the rapid development of necrotizing arteriolar disease. 2. The high blood pressure can be associated with different conformations of the arteriolar microcirculation. The emergence of an arteriolar reaction pattern characterized by the formation of focal dilatations, with intervening constricted segments, is of fundamental pathophysiological importance. 3. Activation of the renin system is reflected in an increased renin secretion rate from the kidneys and an increased rate of angiotensin II generation in the pulmonary vascular bed. 4. The crucial pathogenetic process, leading eventually to severe arteriolar wall damage, is a penetration of plasmatic macromolecules into the wall of distended arteriolar segments, as observed in states of severe experimental hypertension. 5. Renin can induce vascular disease, but hypersecretion of renin is not a necessary condition for the development of hypertensive arteriolar necrosis.


2003 ◽  
Vol 98 (6) ◽  
pp. 1338-1344 ◽  
Author(s):  
Gilles Boccara ◽  
Alexandre Ouattara ◽  
Gilles Godet ◽  
Eric Dufresne ◽  
Michèle Bertrand ◽  
...  

Background Terlipressin, a precursor that is metabolized to lysine-vasopressin, has been proposed as a drug for treatment of intraoperative arterial hypotension refractory to ephedrine in patients who have received long-term treatment with renin-angiotensin system inhibitors. The authors compared the effectiveness of terlipressin and norepinephrine to correct hypotension in these patients. Methods Among 42 patients scheduled for elective carotid endarterectomy, 20 had arterial hypotension following general anesthesia that was refractory to ephedrine. These patients were the basis of the study. After randomization, they received either 1 mg intravenous terlipressin (n = 10) or norepinephrine infusion (n = 10). Beat-by-beat recordings of systolic arterial blood pressure and heart rate were stored on a computer. The intraoperative maximum and minimum values of blood pressure and heart rate, and the time spent with systolic arterial blood pressure below 90 mmHg and above 160 mmHg, were used as indices of hemodynamic stability. Data are expressed as median (95% confidence interval). Results Terlipressin and norepinephrine corrected arterial hypotension in all cases. However, time spent with systolic arterial blood pressure below 90 mmHg was less in the terlipressin group (0 s [0-120 s] vs. 510 s [120-1011 s]; P < 0.001). Nonresponse to treatment (defined as three boluses of terlipressin or three changes in norepinephrine infusion) occurred in zero and eight cases (P < 0.05), respectively. Conclusions In patients who received long-term treatment with renin-angiotensin system inhibitors, intraoperative refractory arterial hypotension was corrected with both terlipressin and norepinephrine. However, terlipressin was more rapidly effective for maintaining normal systolic arterial blood pressure during general anesthesia.


2012 ◽  
Vol 302 (3) ◽  
pp. R313-R320 ◽  
Author(s):  
Curt D. Sigmund

The purpose of this review is two-fold. First, I will highlight recent advances in our understanding of the mechanisms regulating angiotensin II (ANG II) synthesis in the brain, focusing on evidence that renin is expressed in the brain and is expressed in two forms: a secreted form, which may catalyze extracellular ANG I generation from glial or neuronal angiotensinogen (AGT), and an intracellular form, which may generate intracellular ANG in neurons that may act as a neurotransmitter. Second, I will discuss recent studies that advance the concept that the renin-angiotensin system (RAS) in the brain not only is a potent regulator of blood pressure and fluid intake but may also regulate metabolism. The efferent pathways regulating the blood pressure/dipsogenic effects and the metabolic effects of elevated central RAS activity appear different, with the former being dependent upon the hypothalamic-pituitary-adrenal axis, and the latter being dependent upon an interaction between the brain and the systemic (or adipose) RAS.


Sign in / Sign up

Export Citation Format

Share Document