Role of Nitric Oxide in the Progression of Cardiovascular Remodeling Induced by Carotid Arterio-Venous Shunt in Rabbits.

Miyamoto, Takuya; Takeishi, Yasuchika; Shishido, Tetsurou; Takahashi, Hitomi; Itoh, Makoto; Tomoike, Hitonobu

doi:10.1536/jhj.44.127

Cited by 8 publications

(13 citation statements)

References 29 publications

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Section: Cardiac Outputmentioning

confidence: 99%

“…[13][14][15] Arterial enlargement in response to a chronic increase in arterial flow also appears to involve NO because NOS inhibition blunts arterial enlargement caused by an arteriovenous shunt in vivo. [13][14][15] In the heart, a chronic increase in cardiac output can be experimentally induced by creating an arteriovenous anatomosis. Cardiac output progressively increases over several weeks and is associated with structural enlargement of the LV chamber 14,31 and activation of the Akt pathway, 31 a pathway known to be important in regulating myocardial growth.…”

Section: Cardiac Outputmentioning

confidence: 99%

“…[13][14][15] In the heart, a chronic increase in cardiac output can be experimentally induced by creating an arteriovenous anatomosis. Cardiac output progressively increases over several weeks and is associated with structural enlargement of the LV chamber 14,31 and activation of the Akt pathway, 31 a pathway known to be important in regulating myocardial growth. 32 NOS activation appears to be important in this response because NOS inhibition blunts the increase in cardiac output and the ventricular enlargement induced by arteriovenous anastomosis.…”

Section: Cardiac Outputmentioning

confidence: 99%

mentioning

confidence: 99%

“…For example, activation of eNOS in endothelial cells exposed to high shear stress promotes arterial vasodilation and eventual structural enlargement. [13][14][15] In the current study, we hypothesized that eNOS plays a central role in mediating cardiovascular adaptations to preg-nancy. Therefore, we determined the effect of pregnancy on cardiac structure and function using ultrasound in lightly anesthetized mice, and on arterial blood pressure, heart rate, and plasma volume in awake mice in both the eNOS knockout and in the background strain for the knockout mice C57Bl/6J (B6).…”

mentioning

confidence: 99%

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Cardiovascular Function in Mice During Normal Pregnancy and in the Absence of Endothelial NO Synthase

Kulandavelu

Adamson

2006

Hypertension

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Abstract-In humans, the increased cardiovascular demands of pregnancy are met by increases in cardiac output (CO), stroke volume (SV), plasma volume (PV), and cardiac and aortic inner dimensions and a concurrent decrease in arterial pressure that indicates a fall in total peripheral vascular resistance. The mechanisms responsible for these changes are incompletely understood, but NO synthase (NOS) is believed to play a central role. We assessed whether C57Bl/6J (B6) mice show similar changes and whether these changes are altered in mice lacking the gene for endothelial NOS (eNOS). The CO of B6 mice increased 28% by day 9.5 of gestation because of a 25% increase in SV, and increased 48% by day 17.5 because of a 41% increase in SV. The increase in SV at day 17.5 was associated with a 27% increase in PV, a 15% decrease in arterial pressure, and 10% to 15% increases in aortic and left-ventricular inner dimensions. In the absence of eNOS, CO increased 22% by day 9.5 because of increases in SV (14%) and heart rate (9%), but increased no further by day 17.5. SV near term was lower than B6 mice despite similar 26% increases in PV and 14% decreases in arterial pressure in association with blunted left-ventricular chamber enlargement. Key Words: nitric oxide synthase Ⅲ pregnancy Ⅲ cardiac output Ⅲ arterial pressure Ⅲ blood flow velocity Ⅲ echocardiography Ⅲ remodeling I n the first half of pregnancy, the maternal cardiovascular system preadapts in anticipation of the physiological demands of pregnancy and the growing perfusion and exchange requirements of the conceptus and changes further in the last half of gestation when the most rapid growth of the conceptus occurs. Failure to make or to sustain these changes may result in impaired fetal growth and/or preeclampsia, the 2 most common and serious complications of human pregnancy. 1,2 Although the mechanisms are not fully understood, there is considerable evidence that NO plays an important role in mediating maternal cardiovascular changes during pregnancy in humans, rats, and other species. [3][4][5][6] During pregnancy in humans, there is a 30% decrease in the circulating levels of asymmetrical dimethylarginine, 7 an endogenous inhibitor of NO synthase (NOS) activity. Furthermore, a nonselective NOS inhibitor caused a greater decrease in blood flow in the forearm circulation of pregnant versus nonpregnant women, 3 which suggests that an increase in bioactive NO contributes to the decrease in peripheral vascular resistance during pregnancy in humans. NO also appears to be important in rats during pregnancy because plasma and urinary levels of nitrites and nitrates (metabolites of NO) and cGMP (second messenger of NO) are increased in pregnant rats, 5,8 although whether similar changes occur in human pregnancy is less certain. 5,9 Furthermore, treatment of rats in late pregnancy with nonselective NOS inhibitors blunts or indeed reverses the normal decrease in arterial blood pressure, 4,6 abolishes the normal increase in plasma volume, 6 and causes fetal intrauterine growt...

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