Venous Tone in the Developmental Stages of Spontaneous Hypertension

Martin, Douglas; Rodrigo, Manoj C.; Appelt, Christopher W.

doi:10.1161/01.hyp.31.1.139

Cited by 46 publications

(47 citation statements)

References 32 publications

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“…These findings are in agreement with published data that ET-1 produces O 2 Ϫ via its ET A receptors in rebound pulmonary hypertension 23 and that the O 2 Ϫ scavenger tempol reduces blood pressure in Ang II-induced hypertensive rats. 2,4 More important, those studies also concur with our recent investigations demonstrating the presence of an intact and sustained ET-1-induced venoconstriction mediated by ET A (but not ET B ) receptors in DOCA-salt hypertension. 19 The latter findings argue for a shift in the balance of ET-1-induced contractions that predominate in veins versus arteries in this model, which might contribute to a rise in blood pressure by increasing cardiac output and shifting blood to the arteries.…”

Section: Discussionsupporting

confidence: 89%

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NADPH Oxidase–Derived Superoxide Augments Endothelin-1–Induced Venoconstriction in Mineralocorticoid Hypertension

Watts

Banes

et al. 2003

Hypertension

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Abstract-Deoxycorticosterone acetate (DOCA)-salt hypertension is characterized by low renin/angiotensin but increased arterial superoxide levels. We have recently reported that the arterial endothelin-1 (ET-1) level is increased, resulting in NADPH oxidase activation and superoxide generation. However, the effect of ET-1 on venous superoxide production and its relation to venoconstriction are unknown. The present study tested the hypotheses that ET-1 stimulates venous NADPH oxidase and superoxide via its ET A receptors, resulting in enhanced venoconstriction in DOCA-salt hypertensive rats. Treatment with ET-1 (0.01 to 1 nmol/L), but not the selective ET B receptor agonist sarafotoxin s6c, of vena cavas of normal rats concentration-dependently increased superoxide levels, an effect that was abolished by the selective ET A receptor antagonist ABT-627. Although the ET-1 level was not increased in the vena cava and plasma, both venous NADPH oxidase activity and superoxide levels were significantly higher in DOCA-salt compared with sham rats. Moreover, ET-1 treatment (10 Ϫ9 mol/L, 10 minutes) of isolated vena cavas further elevated superoxide levels in DOCA-salt rats only but not sham rats, an effect that was abrogated by the superoxide scavenger tempol. Similarly, ET-1-induced contractions of isolated vena cavas of DOCA-salt but not sham rats were significantly inhibited by tempol. The NADPH oxidase inhibitor apocynin significantly reduced superoxide levels in vena cavas of DOCA-salt rats and in ET-1-treated vena cavas of normal rats. Finally, in vivo ET A receptor blockade by ABT-627 significantly lowered venous superoxide levels and blood pressure in DOCA-salt but not sham rats. These results suggest that superoxide contributes to ET-1-induced venoconstriction through an elevated venous NADPH oxidase activity in mineralocorticoid hypertension. Ϫ ) contributes to hypertension development in both animals and humans by inactivating nitric oxide (NO) and impairing arterial endothelium-dependent relaxation. 1-3 An increase in venous O 2 Ϫ might also inactivate NO and alter venous functions (eg, impaired relaxation or augmented constriction). However, the role of venous O 2 Ϫ production in hypertension and its effect on venoconstriction are unknown. Because hypertension involves multifactorial hemodynamic alterations, venoconstriction augmented by O 2 Ϫ might contribute to increased blood pressure by enhancing cardiac output and shifting blood from the veins to arteries. 4 -6 Consistent with this notion, endothelin-1 (ET-1) stimulates venous constriction, resulting in significant changes in blood volume distribution, cardiac output, and blood pressure. 5,6 The factors controlling venoconstriction are complex and include both neural and humoral mechanisms. The increased sympathetic nerve activity results in augmented venoconstriction, which predominates in the development of spontaneous hypertension. 4 Various humoral factors, such as angiotensin II (Ang II) and ET-1, also induce venoconstriction. 7 Ang II causes impair...

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Section: Discussionsupporting

confidence: 89%

“…The increased sympathetic nerve activity results in augmented venoconstriction, which predominates in the development of spontaneous hypertension. 4 Various humoral factors, such as angiotensin II (Ang II) and ET-1, also induce venoconstriction. 7 Ang II causes impaired arterial NO-mediated relaxation by increasing O 2 Ϫ in Ang II-induced hypertensive rats.…”

mentioning

confidence: 99%

NADPH Oxidase–Derived Superoxide Augments Endothelin-1–Induced Venoconstriction in Mineralocorticoid Hypertension

Watts

Banes

et al. 2003

Hypertension

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“…1,2 In particular, it has been proposed that attenuated venous elasticity and capacity affect blood volume redistribution in such a manner that blood volume moves from peripheral veins into small arteries 3 or centrally, 2,4 contributing to chronic increases in arterial blood pressure (BP). Supporting this conceptual scheme, previous studies found reduced venous distensibility and blood holding capacity in animals 5,6 and humans [7][8][9] with hypertension. These changes in venous circulation are potentially due to chronic increases in sympathetic autonomic regulation of venous tone.…”

Section: Introductionsupporting

confidence: 56%

“…These changes in venous circulation are potentially due to chronic increases in sympathetic autonomic regulation of venous tone. 6 In addition to chronic influences on vascular tone, the sympathetic nervous system modulates cardiovascular adjustments to short-term physiological perturbations, ensuring blood pressure homeostasis and preserving blood flow. Yet, animals and humans with hypertension often present with altered autonomic modulation and, as a result, they exhibit abnormal cardiovascular responses to short-term physiological stressors.…”

Section: Introductionmentioning

confidence: 99%

“…It was hypothesized that calf venous compliance and capacitance responses to lower body negative pressure (LBNP) would be impaired in subjects with HBP compared with agematched NT controls. Previous studies suggested that the contribution of the venous system to hypertension may be instrumental at the beginning of the hypertensive process; 1,6,9 thus, we studied non-medicated subjects with prehypertension and stage-1 hypertension.…”

Section: Introductionmentioning

confidence: 99%

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Limb venous compliance responses to lower body negative pressure in humans with high blood pressure

et al. 2011

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This study tested the hypothesis that limb venous responses to baroreceptor unloading are altered in individuals with high blood pressure (HBP) compared with normotensive (NT) controls. Calf venous compliance was assessed in 20 subjects with prehypertension and stage-1 hypertension (mean arterial pressure, MAP: 104 ± 1 mm Hg) and 13 NT controls (MAP: 86 ± 2 mm Hg) at baseline and during lower body negative pressure (LBNP), using venous occlusion plethysmography. Baroreflex sensitivity (BRS) was measured using the sequence technique and total peripheral resistance (TPR) was estimated from finger plethysmography. Baseline venous compliance was not different between groups, but the HBP group had lower baseline lnBRS (2.22±0.14 vs 2.7±0.18 ms mm Hg À1) and greater baseline TPR (3828 ± 138 vs 3250 ± 111 dyn sec À1 cm À5 m 2 , Po0.05). Calf venous compliance was reduced in response to LBNP only in the NT group (Po0.05). The HBP group had a greater increase in TPR (DTPR) compared with the NT group ( þ 1649 ± 335 vs þ 718 ± 196 dyn sec À1 cm À5 m 2 , Po0.05). In conclusion, the early stages of hypertension are characterized by an attenuated venoconstrictor response to baroreceptor unloading, which may compensate for an exaggerated vasoconstrictor response and protect against further increases in blood pressure.

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Impaired in vivo venous constriction in conscious obese Zucker rats with metabolic syndrome

Song

Hutchings

Pang

2006

Naunyn-Schmied Arch Pharmacol

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The venous system plays a crucial role in regulating cardiac output and blood pressure. Although the relationship between obesity and hypertension is well recognized, little is known about the effect of obesity on venous function. We examined if 16-week-old obese Zucker rats, relative to age-matched lean Zucker rats, had altered in vivo venoconstriction to noradrenaline. The obese rats, compared to the controls, had higher mean arterial pressure (MAP), body weight, and plasma insulin and triglycerides, but reduced pressor and mean circulatory filling pressure (MCFP, index of venous tone) responses to noradrenaline (2.5-30x10(-9) mol/kg/min, i.v.). N(G)-nitro-L-arginine methyl ester (L-NAME, 8 mg/kg, i.v., non-selective inhibitor of nitric oxide synthase) did not alter MCFP in either group, but increased MAP of both groups, though the increase was markedly less in the obese than lean rats. Therefore, obese Zucker rats had increased baseline MAP, but impaired in vivo pressor and MCFP responses to noradrenaline, and reduced pressor response to L-NAME. The increased baseline MAP in the obese rats was not due to increased arterial and venous constriction to noradrenaline but rather to reduced influence of the nitric oxide/L-arginine system.

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Venous Tone in the Developmental Stages of Spontaneous Hypertension

Cited by 46 publications

References 32 publications

NADPH Oxidase–Derived Superoxide Augments Endothelin-1–Induced Venoconstriction in Mineralocorticoid Hypertension

NADPH Oxidase–Derived Superoxide Augments Endothelin-1–Induced Venoconstriction in Mineralocorticoid Hypertension

Limb venous compliance responses to lower body negative pressure in humans with high blood pressure

Impaired in vivo venous constriction in conscious obese Zucker rats with metabolic syndrome

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