Terlipressin Versus  Norepinephrine to Correct Refractory Arterial Hypotension after General Anesthesia in Patients Chronically Treated with Renin-Angiotensin System Inhibitors

2003 ◽  
Vol 98 (6) ◽  
pp. 1338-1344 ◽  
Author(s):  
Gilles Boccara ◽  
Alexandre Ouattara ◽  
Gilles Godet ◽  
Eric Dufresne ◽  
Michèle Bertrand ◽  
...  
Keyword(s):  
Blood Pressure ◽  
General Anesthesia ◽  
Arterial Blood Pressure ◽  
Renin Angiotensin System ◽  
Arterial Hypotension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Long Term Treatment ◽  
Systolic Arterial Blood Pressure

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.

scholarly journals Intermittent Hypoxia Increases Arterial Blood Pressure in Humans Through a Renin-Angiotensin System-Dependent Mechanism

Hypertension ◽  
2010 ◽  
Vol 56 (3) ◽  
pp. 369-377 ◽  
Author(s):  
Glen E. Foster ◽  
Patrick J. Hanly ◽  
Sofia B. Ahmed ◽  
Andrew E. Beaudin ◽  
Vincent Pialoux ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Intermittent Hypoxia ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Dependent Mechanism

The Effects of the Antagonists of the Renin—Angiotensin System on Cardiovascular Response to Lower-Body Subatmospheric Pressure in the Anaesthetized Cat

1980 ◽  
Vol 58 (6) ◽  
pp. 549-552 ◽  
Author(s):  
S. A. Adigun ◽  
D. P. Clough ◽  
J. Conway ◽  
R. Hatton
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Negative Pressure ◽  
Cardiovascular Response ◽  
Venous Pressure ◽  
Renin Angiotensin System ◽  
Lower Body ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

1. Lower-body subatmospheric (negative) pressure led to a prompt reduction in central venous pressure and arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. These reflex responses have been used to investigate the role angiotensin plays in blood pressure control. 2. The initial plasma renin activity (2.9 ng of angiotensin I h−1 ml−1) did not change during the brief lowering of pressure. Before pressure was lowered neither the angiotensin-converting enzyme inhibitor nor a competitive antagonist, [Sar1,Ala8]-angiotensin II, lowered arterial pressure. 3. Nevertheless, after inhibition of the renin-angiotensin system by these agents, the reduction in blood pressure induced by lower-body negative pressure became greater and the blood pressure recovery was impaired. 4. The findings suggest that angiotensin, at a blood concentration which has no direct effect on blood pressure, interacts with the sympathetic nervous system to maintain arterial blood pressure.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

Renin-angiotensin system in hypophysectomized rats. I. Control of blood pressure

1984 ◽  
Vol 246 (1) ◽  
pp. E84-E88
Author(s):  
C. D. Simon ◽  
T. W. Honeyman ◽  
J. C. Fray
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Hormone Administration ◽  
Hypophysectomized Rats

The mechanisms whereby the pituitary gland maintains arterial pressure were investigated in rats. The arterial pressure in hypophysectomized rats was 30 mmHg below normal. Saralasin or captopril caused a further fall of 25 and 30 mmHg, respectively, suggesting that the renin-angiotensin system plays a role in blood pressure maintenance in hypophysectomized rats. Growth hormone administration to hypophysectomized rats increased the arterial pressure, but pretreatment with captopril prevented the effect. Plasma renin activity and basal renin secretion (in vitro) was normal in hypophysectomized rats despite a twofold greater renal renin content. Secretory responsiveness to isoproterenol and calcium omission was lower in hypophysectomized rats. It is concluded that the renin-angiotensin system plays a role in maintaining arterial blood pressure in hypophysectomized rats although the responsiveness of the system may be decreased.

Aminopeptidase A, which generates one of the main effector peptides of the brain renin-angiotensin system, angiotensin III, has a key role in central control of arterial blood pressure

2000 ◽  
Vol 28 (4) ◽  
pp. 435-440 ◽  
Author(s):  
A. Reaux ◽  
X. Iturrioz ◽  
G. Vazeux ◽  
M.-C. Fournie-Zaluski ◽  
C. David ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Renin Angiotensin System ◽  
Central Control ◽  
Angiotensin System ◽  
Arterial Blood ◽  
Angiotensin Iii ◽  
Aminopeptidase A ◽  
The Brain

Overactivity of the brain renin-angiotensin system (RAS) has been implicated in the development and maintenance of hypertension in several experimental animal models. We have recently reported that, in the murine brain RAS, angiotensin II (AngII) is converted by aminopeptidase A (APA) into angiotensin III (AngIII), which is itself degraded by aminopeptidase N (APN), both peptides being equipotent to increase vasopressin release and arterial blood pressure when injected by the intracerebroventricular (i.c.v.) route. Because AngII is converted in vivo into AngIII, the exact nature of the active peptide is not precisely known. To delineate their respective roles in the central control of cardiovascular functions, specific and selective APA and APN inhibitors are needed to block the metabolic pathways of AngII and AngIII respectively. In the absence of such compounds for APA, we first explored the organization of the APA active site by site-directed mutagenesis. This led us to propose a molecular mechanism of action for APA similar to that proposed for the bacterial enzyme thermolysin deduced from X-ray diffraction studies. Secondly, we developed a specific and selective APA inhibitor, compound EC33 [(S)-3-amino-4-mercaptobutylsulphonic acid], as well as a potent and selective APN inhibitor, PC18 (2-amino-4-methylsulphonylbutane thiol). With these new tools we examined the respective roles of AngII and AngIII in the central control of arterial blood pressure. A central blockade of APA with the APA inhibitor EC33 suppressed the pressor effect of exogenous AngII, suggesting that brain AngII must be converted into AngIII to increase arterial blood pressure. Furthermore, EC33, injected alone i.c.v. but not intravenously, caused a dose-dependent decrease in arterial blood pressure by blocking the formation of brain AngIII but not systemic AngIII. This is corroborated by the fact that the selective APN inhibitor PC 18 administered alone via the i.c.v. route increased arterial blood pressure. This pressor response was blocked by prior treatment with the angiotensin type 1 receptor antagonist losartan, showing that blocking the action of APN on AngIII metabolism leads to an increase in endogenous AngIII levels, resulting in arterial blood pressure increase through an interaction with angiotensin type 1 receptors. These results demonstrate that AngIII is a major effector peptide of the brain RAS, exerting a tonic stimulatory control over arterial blood pressure. Thus APA, the enzyme responsible for the formation of brain AngIII, represents a potential central therapeutic target that justifies the development of APA inhibitors, crossing the blood-brain barrier, as central anti-hypertensive agents.

Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system

1995 ◽  
Vol 268 (6) ◽  
pp. H2267-H2273 ◽  
Author(s):  
A. Zanchi ◽  
N. C. Schaad ◽  
M. C. Osterheld ◽  
E. Grouzmann ◽  
J. Nussberger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Sympathetic Nervous

This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS as well as in RS fed rats seems to be sustained by an interaction of several mechanisms, including the activation of the sympathetic nervous system and the renin-angiotensin system.

scholarly journals The Renin-Angiotensin System Modulates Inflammatory Processes in Atherosclerosis: Evidence from Basic Research and Clinical Studies

2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
Fabrizio Montecucco ◽  
Aldo Pende ◽  
François Mach
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Basic Research ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renin Inhibitors ◽  
Arterial Blood ◽  
Inflammatory Processes

Recent evidence shows that the renin-angiotensin system is a crucial player in atherosclerotic processes. The regulation of arterial blood pressure was considered from its first description of the main mechanism involved. Vasoconstriction (mediated by angiotensin II) and salt and water retention (mainly due to aldosterone) were classically considered as pivotal proatherosclerotic activities. However, basic research and animal studies strongly support angiotensin II as a proinflammatory mediator, which directly induces atherosclerotic plaque development and heart remodeling. Furthermore, angiotensin II induces proatherosclerotic cytokine and chemokine secretion and increases endothelial dysfunction. Accordingly, the pharmacological inhibition of the renin-angiotensin system improves prognosis of patients with cardiovascular disease even in settings of normal baseline blood pressure. In the present review, we focused on angiotensin-convertingenzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and renin inhibitors to update the direct activities of the renin-angiotensin system in inflammatory processes governing atherosclerosis.

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