Aging Reduces Venous Distensibility and the Venodilatory Response to Nitroglycerin in Normal Subjects

Gascho, Joseph; Fanelli, Claude; Zelis, Robert

doi:10.1097/00132586-199006000-00034

Cited by 10 publications

(11 citation statements)

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“…Defective endothelium-dependent relaxation characterizes many pathophysiological states, including diabetes (14-16), aging (17,18), atherosclerosis (31,32), and some forms of hypertension (33,34). This study demonstrates that nitric oxide activity is modulated in part by acquired protein modifications that occur within the vascular wall.…”

Section: Discussionmentioning

confidence: 75%

“…Such an interaction would prevent endothelial cell-derived nitric oxide from activating smooth muscle relaxation. Interest in this possibility was motivated by observations that defective endothelium-dependent relaxation is a prominent feature in situations where high levels of advanced glycosylation end products occur, such as in diabetes (14)(15)(16) and in aging (17,18).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes.

Bucala

Tracey²,

Cerami³

1991

J. Clin. Invest.

1,109

619

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Nitric oxide (an endothelium-derived relaxing factor) induces smooth muscle relaxation and is an important mediator in the regulation of vascular tone. Advanced glycosylation end products, the glucose-derived moieties that form noncnzymatically and accumulate on long-lived tissue proteins, have been implicated in many of the complications of diabetes and normal aging. We demonstrate that advanced glycosylation products quench nitric oxide activity in vitro and in vivo. Acceleration of the advanced glycosylation process in vivo results in a time-dependent impairment in endothelium-dependent relaxation. Inhibition of advanced glycosylation with aminoguanidine prevents nitric oxide quenching, and ameliorates the vasodilatory impairment. These results implicate advanced glycosylation products as important modulators of nitric oxide activity and endothelium-dependent relaxation. (J. Clin. Invest. 1991. 87:432-438.)

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Section: Discussionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes.

Bucala

Tracey²,

Cerami³

1991

J. Clin. Invest.

1,109

619

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“…Inactivation of nitric oxide by vascular wall AGEs may very well explain the progressive impairment in endo thelium-dependent (i.e. nitric oxide-me diated) responses that occurs in the coronary and systemic circulation of diabetic or aged patients [24][25][26],…”

Section: Advanced Glycosylation and Vascular Reactivitymentioning

confidence: 99%

Advanced Glycosylation Endproducts in Diabetic Renal Disease: Clinical Measurement, Pathophysiological Significance, and Prospects for Pharmacological Inhibition

Bucala¹,

Vlassara²

1995

Blood Purif

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Glucose reacts nonenzymatically with amino groups to produce a class of stable, crosslinking moieties termed advanced glycosylation endproducts (AGEs). These products act to increase vascular permeability, enhance subintimal protein and lipoprotein deposition, inactivate nitric oxide, and exert a number of toxic effects on endothelial cells. Loss of normal renal function has been found recently to cause a marked increase in the circulating levels of plasma AGEs, suggesting that these moieties may comprise one component of the so-called uremic ‘middle molecules’. AGEs also form on the lipid and the protein components of LDL, forming a modified form of LDL (AGE-LDL) which is not taken up by tissue LDL receptors. Aminoguanidine offers a specific therapeutic modality for inhibiting advanced glycosylation in vivo and has been observed recently to reduce both hemoglobin-AGE and circulating LDL levels.

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“…Advancing age produces several changes in cardiovascular structure and function in humans [4,5], among which an impairment in cardiopulmonary, integrative baroreflex sympatho-circulatory control [6,7], and a stiffness of the peripheral venous wall [8,9] have mainly been proposed to have influences on cardiovascular stability in the elderly. Japanese Journal of Physiology, 52, 69-76, 2002 Key words: muscle sympathetic nerve activity, cardiopulmonary baroreflex, arterial baroreflex, calf blood flow, gravitational stress.…”

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confidence: 99%

Age-Related Changes in Vasomotor Reflex Control of Calf Venous Capacitance Response to Lower Body Negative Pressure in Humans.

Iwase

Niimi

et al. 2002

JJP

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The venous system plays an important role in fluid shifts and blood pressure regulation. In humans, it has been supposed that the capacity of the leg veins may be reduced by a vasomotor reflex when standing [1]. If this is so, this is a portion of the compensatory response to gravitational stress. However, how the vasomotor reflex controls calf venous capacitance is unclear.Currently, little information in available concerning a relationship between vasomotor sympathetic activity, which can be recorded as muscle sympathetic nerve activity (MSNA) [2,3], and calf venous capacitance, especially under the effect of aging. Advancing age produces several changes in cardiovascular structure and function in humans [4,5], among which an impairment in cardiopulmonary, integrative baroreflex sympatho-circulatory control [6,7], and a stiffness of the peripheral venous wall [8,9] have mainly been proposed to have influences on cardiovascular stability in the elderly. Japanese Journal of Physiology, 52, 69-76, 2002 Key words: muscle sympathetic nerve activity, cardiopulmonary baroreflex, arterial baroreflex, calf blood flow, gravitational stress.Abstract: The present study was performed to test the hypothesis that calf venous capacitance would be reduced by mild gravitational stress through a vasomotor reflex in humans, and this response could be diminished with advancing age. Nine young (31Ϯ1 years, meanϮSE) and 9 elderly (69Ϯ1 years) healthy males were exposed to a lower body negative pressure (LBNP) of 15 mmHg. Venous occlusion plethysmography was used to measure calf venous capacitance and calf blood flow. Muscle sympathetic nerve activity (MSNA) was recorded microneurographically from the tibial nerve along with cardiovascular variables. It was found that baseline MSNA was higher [21Ϯ4 (meanϮSE) vs. 37Ϯ5 bursts · min Ϫ1, young vs. elderly; pϽ0.05] and calf venous capacitance was lower (1.71Ϯ0.12 vs. 1.44Ϯ0.10, ml · 100 ml Ϫ1 , young vs. elderly; pϽ 0.05) in the elderly group. At 15 mmHg-LBNP, heart rate and mean arterial pressure both remained unchanged, MSNA was enhanced, and calf blood flow was reduced in all subjects. Calf venous capacitance during LBNP decreased in the young, but did not change in the elderly. A significant negative correlation between percent changes in MSNA and percent changes in calf venous capacitance existed in the young group (yϭϪ0.171xϪ11.863, rϭϪ0.682; pϭ0.0432), but disappeared in the elderly group. The ratio of percent changes in calf venous capacitance to percent changes in MSNA was markedly lower in the elderly (pϽ0.01). In conclusion, these results substantiate our hypothesis that calf venous capacitance is reduced by mild LBNP through the vasomotor reflex, and this response is diminished in the elderly.

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Aging Reduces Venous Distensibility and the Venodilatory Response to Nitroglycerin in Normal Subjects

Cited by 10 publications

References 0 publications

Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes.

Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes.

Advanced Glycosylation Endproducts in Diabetic Renal Disease: Clinical Measurement, Pathophysiological Significance, and Prospects for Pharmacological Inhibition

Age-Related Changes in Vasomotor Reflex Control of Calf Venous Capacitance Response to Lower Body Negative Pressure in Humans.

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