Angiotensin II, vasopressin, and sympathetic activity in conscious rats with endotoxemia

Schaller, M. D.; Waeber, Bernard; Nussberger, Jürg; Brunner, Heinrich

doi:10.1152/ajpheart.1985.249.6.h1086

Cited by 72 publications

(86 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Two hours after the beginning of LPS infusion, the diminished pressor and carotid, mesenteric and hindquarters vasoconstrictor effects of methoxamine are consistent with reports of vascular hyporeactivity to a variety of vasoconstrictor agents in other rat models (Fink et al, 1985;Schaller et al, 1985;Guc et al, 1990;Hollenberg et al, 1993) and in man (Chernow et al, 1982). It is generally agreed that NOmediated mechanisms are involved (see Moncada et al, 1991) and, if so, it is interesting that not all vascular beds responded uniformly and that the pattern of hyporesponsiveness changed with time during LPS infusion (see below).…”

Section: Discussionsupporting

confidence: 87%

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Waller

Gardiner

Bennett

1994

British J Pharmacology

View full text Add to dashboard Cite

1 The aim of the study was to assess the regional haemodynamic responsiveness to vasoconstrictor and vasodilator challenges during continuous 24 h infusion of lipopolysaccharide (LPS) in conscious Long Evans rats.2 Rats were chronically instrumented for the measurement of regional haemodynamics (either internal and common carotid or renal, superior mesenteric and hindquarters) and received 3 min of infusions of acetylcholine (22 nmol min-'), methoxamine (120 nmol min-'), salbutamol (0.83 nmol min-') and bradykinin (14.4 nmol min-') at 2, 6 and 24 h after the start of saline or LPS (150 ;g kg-' h-') infusion (rats with carotid probes received only acetylcholine and methoxamine). 3 During infusion of LPS there was a changing haemodynamic profile. After 2 h, there was a modest hypotension and vasodilatation in the internal carotid, renal and hindquarters vascular beds. After 6 h, arterial blood pressure had returned to baseline, there was still vasodilatation in the renal vascular bed but vasoconstriction in the internal and common carotids and the hindquarters. After 24 h, there was hypotension, tachycardia and generalized vasodilatation. 4 Acetylcholine caused a fall in blood pressure, tachycardia and hyperaemic vasodilatation in the carotid and renal vascular beds. Throughout the infusion of LPS, the carotid vasodilator response was enhanced after 2 h, reduced after 6 h and enhanced again after 24 h, whereas the renal vasodilator response to acetylcholine was either reduced (6 h) or absent (2 and 24 h); at this juncture the hypotensive response to acetylcholine was also enhanced and the tachycardia was reduced. 5 Methoxamine caused a rise in blood pressure, a fall in heart rate, and vasoconstriction in all the vascular beds monitored. During infusion of LPS, the pressor response to methoxamine was consistently reduced as were the vasoconstrictor responses in the carotid and mesenteric vascular beds, whereas the renal and hindquarters vasoconstrictor responses to methoxamine were only significantly reduced at some time points (renal 6 h, hindquarters 2 and 6 h).6 Salbutamol caused hypotension, tachycardia and hyperaemic vasodilatation, particularly in the hindquarters vascular bed. Throughout the infusion of LPS, the cardiovascular responses to salbutamol were substantially attenuated.7 Bradykinin caused hypotension, tachycardia and hyperaemic vasodilatation in the renal, mesenteric and hindquarters vascular beds. During the infusion of LPS, the hypotensive response to bradykinin was consistently augmented, and the tachycardia was consistently reduced, but the regional haemodynamic profile changed with time. Thus, after 2 h, the mesenteric vasodilator response was augmented and the hindquarters vasodilator response was reduced; after 6 h, the mesenteric vasodilator response appeared normal, but the renal and hindquarters vasodilator responses were reduced; after 24 h, the hindquarters vasodilator response was markedly augmented and the renal response had changed to a vasoconstriction.8 The present findings indica...

show abstract

Section: Discussionsupporting

confidence: 87%

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Waller

Gardiner

Bennett

1994

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…The renin-angiotensin system in sepsis Activation of the RAS during sepsis is a well know phenomenon, observed in experimental [17] and clinical studies [18][19][20]. However, so far, most of our knowledge about the RAS system during septic shock has come from a few experimental studies performed with healthy rodents [17,[21][22][23][24][25][26], sheep [27,28] or pigs [7].…”

Section: Angiotensin II Receptorsmentioning

confidence: 99%

“…However, so far, most of our knowledge about the RAS system during septic shock has come from a few experimental studies performed with healthy rodents [17,[21][22][23][24][25][26], sheep [27,28] or pigs [7]. The role of exogenous angiotensin II administration or its inhibition in sepsis is poorly understood [29].…”

Section: Angiotensin II Receptorsmentioning

confidence: 99%

“…Despite the high angiotensin II plasma levels, pronounced hypotension, associated with a reduced vasopressor effect of angiotensin II, has been reported [17]. Moreover, RAS activation contributes to oxidative stress and endothelial dysfunction [24], which has been associated with development of kidney [33] and pulmonary [25,26] injury and with the severity of organ dysfunction [19].…”

Section: Angiotensin II Receptorsmentioning

confidence: 99%

See 1 more Smart Citation

Angiotensin II in Septic Shock

Corrêa

Jeger

Pereira

et al. 2014

Critical Care Medicine

View full text Add to dashboard Cite

show abstract

“…Inappropriate low plasma vasopressin levels have been suggested to contribute to the hypotension in advanced vasodilatory septic shock (14). In models of acute sepsis, vasopressin is markedly increased (26,32,33); in addition, a reduced pressor response to the exogenous hormone has been shown (8,26,30). The pathogenetic mechanisms of this phenomenon, called vasoplegia, are not clearly understood.…”

mentioning

confidence: 99%

Cytokine-mediated downregulation of vasopressin V_1Areceptors during acute endotoxemia in rats

Bucher¹,

Hobbhahn²,

Taeger³

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

The reduced pressure response to vasopressin during acute sepsis has directed our interest to the regulation of vasopressin V1A receptors. Rats were injected with lipopolysaccharide for induction of experimental gram-negative sepsis. V1A receptor gene expression was downregulated in the liver, lung, kidney, and heart during endotoxemia. Inasmuch as the concentrations of proinflammatory cytokines such as interleukin-1␤, tumor necrosis factor-␣, and interferon-␥ were highly increased during sepsis, the influence of these cytokines on V1A receptor expression was investigated in primary cultures of hepatocytes and in the aortic vascular smooth muscle cell line A7r5. V1A receptor expression was downregulated by the cytokines in a nitric oxide-independent manner. Blood pressure dose-response studies after injection of endotoxin showed a diminished responsiveness to the selective V1 receptor agonist Phe 2 ,Ile 3 ,Orn 8 -vasopressin. Our data show that sepsis causes a downregulation of V1A receptors and suggest that this effect is likely mediated by proinflammatory cytokines. We propose that this downregulation of V1A receptors contributes to the attenuated responsiveness of blood pressure in response to vasopressin and, therefore, contributes to the circulatory failure in septic shock. blood pressure; hepatocytes; vascular smooth muscle; A7r5 cell line; nitric oxide SHOCK DUE TO SEPSIS HAS INCREASED in incidence during the past 50 years and is now one of the most common causes of death in intensive care units. Despite considerable therapeutic advances, mortality from septic shock remains high. Pathogenetically, sepsis and septic shock are characterized by systemic vasodilation, leading to arterial hypotension, multiple organ dysfunction, and death (21). The pathogenetic mechanism of this vasodilation is multifactorial and not clearly understood. Nitric oxide (NO) production due to induction of NO synthase isoform II (NOS II) has been assumed to mediate sepsis-induced vasodilation (16,21). However, findings that arterial hypotension, as well as vascular hyporeactivity, is only slightly alleviated by NOS II inhibition suggest that other or additional pathways may be involved in septic circulatory failure (5,22,27,31). Alterations in vasoconstrictor mechanisms have been reported. Inappropriate low plasma vasopressin levels have been suggested to contribute to the hypotension in advanced vasodilatory septic shock (14). In models of acute sepsis, vasopressin is markedly increased (26,32,33); in addition, a reduced pressor response to the exogenous hormone has been shown (8,26,30). The pathogenetic mechanisms of this phenomenon, called vasoplegia, are not clearly understood. One could imagine that the receptors for vasoconstrictors could be altered during sepsis, leading to diminished pressor effects in response to the respective agonist. We previously demonstrated that sepsis leads to a systemic downregulation of ANG II type 1 receptors (4). Therefore, we were interested also in the regulation of the receptor mediating the ...

show abstract

Angiotensin II, vasopressin, and sympathetic activity in conscious rats with endotoxemia

Cited by 72 publications

References 0 publications

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Angiotensin II in Septic Shock

Cytokine-mediated downregulation of vasopressin V_1Areceptors during acute endotoxemia in rats

Contact Info

Product

Resources

About

Angiotensin II, vasopressin, and sympathetic activity in conscious rats with endotoxemia

Cited by 72 publications

References 0 publications

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Angiotensin II in Septic Shock

Cytokine-mediated downregulation of vasopressin V1Areceptors during acute endotoxemia in rats

Contact Info

Product

Resources

About

Cytokine-mediated downregulation of vasopressin V_1Areceptors during acute endotoxemia in rats