Extracellular calcium and altered vascular responsiveness in the deoxycorticosterone acetate-salt rat.

Soltis, Edward E.; Field, F P

doi:10.1161/01.hyp.8.6.526

Cited by 22 publications

(17 citation statements)

References 17 publications

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“…Hypertensive rats showed not only more hypertrophy of vascular tissue and the adrenal gland, but also increasing thickness of media, compared to the normotensive rats. A number of studies have corroborated the results of our present study 6,7) . Growth of vascular wall thickness was verified as a coincident tendency in the primary hypertension animal model, and this result is considered to be highly significant 21) .…”

Section: Discussionsupporting

confidence: 91%

“…This is especially true in the case of forceful hyperplasia or the action of catecholamine which is known to have an adverse effect on the mechanism pain induction, especially in hypertension, because it is likely to aggravate the excessive tension in the vascular smooth muscle cells that occurs in this disease 3,19) . Studies by Dahl and others have reported that the saltdependent hypertension and the DOCA-salt hypertension animal models are important models for experiments in hypertension research 4,6,20) . There is a direct correlation between the secondary hypertension of Korean adults and the DOCA-salt hypertension animal model.…”

Section: Discussionmentioning

confidence: 99%

“…This is now receiving proper medical attention because there is a direct correlation between these factors and hypertension 3) . Furthermore, the creation and aggravation of hypertension is closely related to the increased peripheral resistance that is caused by elongation of blood vessel wall or other factors, giving rise to change in the blood vessel wall's reaction, and an increase in transmural pressure induced by norepinephrine 4,6) . In clinical findings, myotonic and structural changes of the blood vessel wall, especially, are directly connected with cardiovascular disorders such as hypertension, cerebral hemorrhage and angina 4,7) .…”

Section: Introductionmentioning

confidence: 99%

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Noxiousness of Hypertension-related Norepinephrine and Upregulation of Norepinephrine Induced by High Intensity Electrical Stimulation in Healthy Volunteers

et al. 2012

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Abstract.[Purpose] The purpose of the present study was to assist the design of future experiments on pain therapeutics and to establish the reliability and understanding of animal models of neurotransmitters of sympathetic nerves.[Subjects] The subjects were fifty-five male rats and ten female volunteers. [Methods] In vitro testing of experimental animals, measuring blood pressure, muscle tension, histological changes, intracellular Ca 2+ , and enzymatic activity. We also induced hypertension-related sympathetic effects by physical therapy with high intensity electrical stimulation as evidenced by 24-hour urine analysis of norepinephrine. [Results] In isometric tension and histological analyse, norepinephrine-induced tension and collagen fibers were significantly increased in muscle strips from hypertensive rat aorta. In [Ca 2+ ] i analysis, norepinephrine-induced change of [Ca 2+ ] i in muscle strips from normotensive and hypertensive rat aorta was observed. Analysis by western blotting with anti-phosphorylated antibodies showed that the phosphorylation of ERK1/2 (extracellular signal-regulated protein kinase 1 and 2) and p38 MAPK (p38 mitogen-activated protein kinase) were significantly increased in the norepinephrine-induced state in the rats. Furthermore, high intensity electrical stimulation significantly increased pain-related concentration of norepinephrine in the healthy volunteers.[Conclusion] These results suggest that the application of norepinephrine to aorta muscle strips is associated with changed muscle tension, [Ca 2+ ] i , and phosphorylation of MAPK, and that the increased responsiveness of norepinephrine to high intensity electrical stimulation may be, in part, related to the increase of sympathetic effects.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Noxiousness of Hypertension-related Norepinephrine and Upregulation of Norepinephrine Induced by High Intensity Electrical Stimulation in Healthy Volunteers

et al. 2012

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“…Soltis and Field (27) observed that femoral arteries from DOCA rats exhibit an increased reactivity to KCl and to norepinephrine only in the presence of normal extracellular Ca 2+ concentration, but not in the presence of low extracellular Ca 2+ . These authors suggested that the increased reactivity to KCl in arteries from hypertensive rats is related to an increased sensitivity to extracellular Ca 2+ .…”

Section: Abnormalities Of Vascular Function Vs Ca 2+ Handlingmentioning

confidence: 99%

Calcium handling by vascular myocytes in hypertension

Tostes¹,

Wilde²,

Bendhack³

et al. 1997

Braz J Med Biol Res

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Calcium ions (Ca 2+ ) trigger the contraction of vascular myocytes and the level of free intracellular Ca 2+ within the myocyte is precisely regulated by sequestration and extrusion mechanisms. Extensive evidence indicates that a defect in the regulation of intracellular Ca 2+ plays a role in the augmented vascular reactivity characteristic of clinical and experimental hypertension. For example, arteries from spontaneously hypertensive rats (SHR) have an increased contractile sensitivity to extracellular Ca 2+ and intracellular Ca 2+ levels are elevated in aortic smooth muscle cells of SHR. We hypothesize that these changes are due to an increase in membrane Ca 2+ channel density and possibly function in vascular myocytes from hypertensive animals. Several observations using various experimental approaches support this hypothesis: 1) the contractile activity in response to depolarizing stimuli is increased in arteries from hypertensive animals demonstrating increased voltage-dependent Ca 2+ channel activity in hypertension; 2) Ca 2+ channel agonists such as Bay K 8644 produce contractions in isolated arterial segments from hypertensive rats and minimal contraction in those from normotensive rats; 3) intracellular Ca 2+ concentration is abnormally increased in vascular myocytes from hypertensive animals following treatment with Ca 2+ channel agonists and depolarizing interventions, and 4) using the voltage-clamp technique, the inward Ca 2+ current in arterial myocytes from hypertensive rats is nearly twice as large as that from myocytes of normotensive rats. We suggest that an alteration in Ca 2+ channel function and/or an increase in Ca 2+ channel density, resulting from increased channel synthesis or reduced turnover, underlies the increased vascular reactivity characteristic of hypertension.

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“…Furthermore, Soltis and Field (37) reported an increased reactivity to KCl and to norepinephrine in femoral arteries from DOCA rats, which was related to increased sensitivity to extracellular Ca 2+ , supporting the suggestion of an augmented membrane permeability to Ca 2+ . While an increased membrane permeability to Ca 2+ in DOCA aortic cells can account for the alterations observed, alternative mechanisms must be considered.…”

Section: µM Serotoninmentioning

confidence: 60%

The effects of cyclopiazonic acid on intracellular Ca2+ in aortic smooth muscle cells from DOCA-hypertensive rats

Tostes¹,

Wilde²,

Bendhack

et al. 1997

Braz J Med Biol Res

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We tested the hypothesis that cyclopiazonic acid (CPA), an inhibitor of the sarcoplasmic reticulum (SR) Ca 2+ -ATPase, increases intracellular Ca 2+ concentration ([Ca 2+ ] i ) in aortic myocytes and that the increase in [Ca 2+ ] i is higher in aortic cells from deoxycorticosterone acetate (DOCA)-hypertensive rats. Male Sprague-Dawley rats, 250-300 g, underwent uninephrectomy, received a silastic implant containing DOCA (200 mg/kg) and had free access to water supplemented with 1.0% NaCl and 0.2% KCl. Control rats were also uninephrectomized, received normal tap water, but no implant. Intracellular Ca 2+ measurements were performed in aortic myocytes isolated from normotensive (Systolic blood pressure = 120 ± 3 mmHg; body weight = 478 ± 7 g, N = 7) and DOCA-hypertensive rats (195 ± 10 mmHg; 358 ± 16

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Extracellular calcium and altered vascular responsiveness in the deoxycorticosterone acetate-salt rat.

Cited by 22 publications

References 17 publications

Noxiousness of Hypertension-related Norepinephrine and Upregulation of Norepinephrine Induced by High Intensity Electrical Stimulation in Healthy Volunteers

Noxiousness of Hypertension-related Norepinephrine and Upregulation of Norepinephrine Induced by High Intensity Electrical Stimulation in Healthy Volunteers

Calcium handling by vascular myocytes in hypertension

The effects of cyclopiazonic acid on intracellular Ca2+ in aortic smooth muscle cells from DOCA-hypertensive rats

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