Renal vascular responses to CORM-A1 in the mouse

Ryan, Michael J.; Jernigan, Nikki L.; Drummond, Heather A.; McLemore, Gerald R.; Rimoldi, John M.; Poreddy, Sambasiva R.; Gadepalli, Rama S; Stec, David E.

doi:10.1016/j.phrs.2006.01.012

Cited by 64 publications

(47 citation statements)

References 30 publications

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“…Although determining the cellular mechanism for the attenuated CO response is beyond the scope of this study, we hypothesize based on our previous study that cyclic guanosine monophosphate (cGMP)signaling may be impaired in Ang II-infused mice. 25 Similar to nitric oxide, CO has been shown to act through a cyclic guanosine monophosphate-mediated mechanism to cause vessel relaxation. 26 While acutely, CoPP can inhibit HO-1, 27 it has been shown by several investigators to significantly induce HO-1 in vivo such that total HO activity is increased chronically.…”

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Induction Does Not Improve Vascular Relaxation in Angiotensin II Hypertensive Mice

Stec

Vera

McLemore

et al. 2008

American Journal of Hypertension

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Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Induction Does Not Improve Vascular Relaxation in Angiotensin II Hypertensive Mice

Stec

Vera

McLemore

et al. 2008

American Journal of Hypertension

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“…In other in vitro and in vivo investigations involving either mice or rats [24][25][26][27], COHb concentrations varied following CORM exposure, with little increase seen with CORMs that release CO quickly (e.g., CORM-3, tricarbonyldichloro(glycinato)ruthenium (II)), contrasted with COHb values between 8% to 17% after exposure to slow releasing CORMs (e.g., CORM-A1, sodium boranocarbonate, Na 2 [H 3 BCO 2 ]). In sum, when exposed to CO at low or high concentrations (based on COHb), platelet function and measures of intravascular thrombus formation were decreased in mice and rats [18][19][20][21][22][23].…”

Section: Clinical Preclinical and In Vitro Evidence That Co Is An Anmentioning

confidence: 99%

Carbon monoxide: Anticoagulant or procoagulant?

Nielsen

Pretorius

2014

Thrombosis Research

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Within the past decade there have been several investigations attempting to define the impact of exogenous and endogenous carbon monoxide exposure on hemostasis.Critically, two bodies of literature have emerged, with carbon monoxide mediated platelet inhibition cited as a cause of in vitro human and in vitro/in vivo rodent anticoagulation. In contrast, interaction with heme groups associated with fibrinogen, α 2 -antiplasmin and plasmin by carbon monoxide has resulted in enhanced coagulation and decreased fibrinolysis in vitro in human and other species, and in vivo in rabbits. Of interest, the ultrastructure of platelet rich plasma thrombi demonstrates an abnormal increase in fine fiber formation and matting that are obtained from humans exposed to carbon monoxide.Further, thrombi obtained from humans and rabbits have very similar ultrastructures, whereas mice and rats have more fine fibers and matting present. In sum, there may be

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“…The mean location of the catheter tip was 0.9 Ϯ 0.6 mm below the right renal artery. With the animal on its ventral side, the right kidney was approached retroperitoneally and a perivascular flow probe (0.5 PSB; Transonic Systems, Ithaca, NY) was positioned around the right renal artery and held in place using a micromanipulator, as previously described (39,46).…”

Section: Animalsmentioning

confidence: 99%

Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus

Venegas-Pont

Mathis

Iliescu

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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-Inflammation and immune system dysfunction contributes to the development of cardiovascular and renal disease. Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that carries a high risk for both renal and cardiovascular disease. While hemodynamic changes that may contribute to increased cardiovascular risk have been reported in humans and animal models of SLE, renal hemodynamics have not been widely studied. The renin-angiotensin system (RAS) plays a central role in renal hemodynamic control, and although RAS blockade is a common therapeutic strategy, the role of RAS in hemodynamic function during SLE is not clear. This study tested whether mean arterial pressure (MAP) and renal hemodynamic responses to acute infusions of ANG II in anesthetized animals were enhanced in an established female mouse model of SLE (NZBWF1). Baseline MAP was not different between anesthetized SLE and control (NZWLacJ) mice, while renal blood flow (RBF) was significantly lower in mice with SLE. SLE mice exhibited an enhanced pressor response and greater reduction in RBF after ANG II infusion. An acute infusion of the ANG II receptor blocker losartan increased RBF in control mice but not in mice with SLE. Renin and ANG II type 1 receptor expression was significantly lower, and ANG II type 2 receptor expression was increased in the renal cortex from SLE mice compared with controls. These data suggest that there are fewer ANG II receptors in the kidneys from mice with SLE but that the existing receptors exhibit an enhanced sensitivity to ANG II. inflammation; angiotensin receptor; autoimmune INFLAMMATION AND IMMUNE SYSTEM dysregulation are recognized as prominent contributors to the development and progression of cardiovascular and renal disease. Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder associated with a high risk for the development of renal and cardiovascular disease, which are major causes of mortality in these patients (43). Almost all patients with SLE have at least some evidence of renal damage on biopsy (4, 11), and measures of declining renal function, including elevated serum creatinine and blood urea nitrogen or reduced filtration fraction, are commonly reported (11,20,28).The renin-angiotensin system (RAS) is well known for its critical role in renal hemodynamic control and blood pressure regulation and is a common therapeutic target in patients with SLE. Although renal dysfunction and blockade of the RAS system are common to patients with SLE, renal hemodynamic responses to ANG II have not been previously investigated. In the present study, we tested the hypothesis that during SLE, there is an enhanced renal hemodynamic response to acute infusion of ANG II. This hypothesis was tested using an experimental mouse model of SLE.The New Zealand Black/White F1 hybrid (NZBWF1) is an established and widely used model of lupus nephritis (8). Like humans with SLE, female NZBWF1 mice exhibit declining renal function with age (5, 23, 29, 42), and we previously reporte...

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Renal vascular responses to CORM-A1 in the mouse

Cited by 64 publications

References 30 publications

Heme Oxygenase-1 Induction Does Not Improve Vascular Relaxation in Angiotensin II Hypertensive Mice

Heme Oxygenase-1 Induction Does Not Improve Vascular Relaxation in Angiotensin II Hypertensive Mice

Carbon monoxide: Anticoagulant or procoagulant?

Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus

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