Differential effects on nitric oxide-mediated vasodilation in mesenteric and uterine arteries from cytomegalovirus-infected mice

Gombos, Randi; Hemmings, Denise G.

doi:10.1152/ajpheart.01113.2009

Cited by 12 publications

(17 citation statements)

References 57 publications

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“…It is therefore likely to be due to changes in other endothelium-derived hyperpolarizing factors that may contribute to ME-induced vasodilation (4). This is in contrast to our previous study in young active mCMV-infected mice (12).…”

Section: Discussioncontrasting

confidence: 99%

“…The increase in both vasodilation and vasoconstriction may be explained by changes to artery composition and receptor expression. We previously reported changes in distensibility (12), also observed in the current study in arteries from young latently infected mice, which can impact both vasodilation and vasoconstriction. CMV also increases smooth muscle cell proliferation (62), which may contribute to increased vasoconstriction.…”

Section: Discussionsupporting

confidence: 82%

“…The systemic vasculature in aging may compensate for the combined insults of aging and infection with increased endothelium-dependent vasodilation, even in the presence of a latent, not active, mCMV infection (12). Even though there does not appear to be an increased contribution of NO synthase (NOS) activity or increased sensitivity of smooth muscle cells to NO in mesenteric arteries from aged infected mice, it is possible in an in vivo situation that conditions of increased oxidative stress as found in aging could lead to overall reduced NO bioavailability and reduced vasodilation as found using intravital miscroscopy (28).…”

Section: Discussionmentioning

confidence: 99%

“…After incubation in Ca 2ϩ -free EGTA PSS, a distensibility curve was performed on arteries with step increases in pressure from 4 to 170 mmHg. The lumen diameter was unable to be read at 0 mmHg (collapsed vessel), and, therefore, pressure readings began at 4 mmHg as previously described (12). Distensibility was calculated as D2 Ϫ D1/D2 ϫ 100, where D1 is the initial diameter and D2 is the lumen diameter post-pressure change.…”

Section: Rm427mentioning

confidence: 99%

“…Vascular resistance and systemic blood pressure are impacted by the mesenteric vasculature. In our previous studies we showed an overall increase in vasodilation in mesenteric arteries isolated from mice actively infected with mCMV (14), which may be to compensate for increased vasoconstrictory activity (6,12,13). It is unknown whether these effects in mesenteric arteries are maintained during mCMV latency and whether the additional stress of aging would reduce the mCMV-mediated increase in vasodilation allowing vasoconstrictory effects to increase vascular tone.…”

mentioning

confidence: 92%

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Vascular dysfunction in young, mid-aged and aged mice with latent cytomegalovirus infections

Gombos

Brown

Teefy

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Gombos RB, Brown JC, Teefy J, Gibeault RL, Conn KL, Schang LM, Hemmings DG. Vascular dysfunction in young ec50, mid-aged and aged mice with latent cytomegalovirus infections. Am J Physiol Heart Circ Physiol 304: H183-H194, 2013. First published November 2, 2012; doi:10.1152/ajpheart.00461.2012.-Human cytomegalovirus (HCMV) is associated with vascular diseases in both immunosuppressed and immunocompetent individuals. CMV infections cycle between active and latent phases throughout life. We and others have shown vascular dysfunction during active mouse CMV (mCMV) infections. Few studies have examined changes in physiology during latent CMV infections, particularly vascular responses or whether the negative effects of aging on vascular function and fertility will be exacerbated under these conditions. We measured vascular responses in intact mesenteric and uterine arteries dissected from young, mid-aged, and aged latently mCMV-infected (mCMV genomes are present but infectious virus is undetectable) and agematched uninfected mice using a pressure myograph. We tested responses to the ␣ 1-adrenergic agonist phenylephrine, the nitric oxide donor sodium nitroprusside, and the endothelium-dependent vasodilator methacholine. In young latently mCMV-infected mice, vasoconstriction was increased and vasodilation was decreased in mesenteric arteries, whereas both vasoconstriction and vasodilation were increased in uterine arteries compared with those in age-matched uninfected mice. In reproductively active mid-aged latently infected mice, mesenteric arteries showed little change, whereas uterine arteries showed greatly increased vasoconstriction. These vascular effects may have contributed to the decreased reproductive success observed in mid-aged latently mCMV-infected compared with age-matched uninfected mice (16.7 vs. 46.7%, respectively). In aged latently infected mice, vasodilation is increased in mesenteric and uterine arteries likely to compensate for increased vasoconstriction to mediators other than phenylephrine. The novel results of this study show that even when active mCMV infections become undetectable, vascular dysfunction continues and differs with age and artery origin. uterine arteries; mesenteric arteries; infertility; vascular function; pressure myograph HUMAN CYTOMEGALOVIRUS (HCMV) is a member of the ␤-Herpesviridae family (50). In the human population, it infects 40 to 80% of individuals (10). Although in the general population it is thought to be mostly asymptomatic, infection has been associated with tumorigenesis, transplant rejection, vascular diseases such as atherosclerosis and restenosis, and increased mortality and hypertension (9,19,23,26,33,62,64). The mechanisms whereby HCMV infections result in vasculopathy are still unclear.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 82%