Ion transport defects and hypertension. Where is the link?

Ives, Harlan E.

doi:10.1161/01.hyp.14.6.590

Cited by 49 publications

(16 citation statements)

References 76 publications

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“…Defects in one or more of these transport systems have been proposed to play an important role in the pathogenesis of hypertension. 22 The results from the present study have shown that 10% ethanol intake leads to an increase in systolic blood pressure with an increase in platelet cytosolic [Ca 2+ ],. Platelets were chosen for this study because, besides being an easily accessible tissue, they likely represent abnormalities in calcium handling similar to those described in vascular tissue, which share many common intracellular features with platelets, including a calcium-dependent contraction-coupling process.…”

Section: In Vitro Effects Of Ethanol Onsupporting

confidence: 50%

Platelet-free calcium and vascular calcium uptake in ethanol-induced hypertensive rats.

Vasdev¹,

Sampson²,

Prabhakaran³

1991

Hypertension

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This study examined the effect of moderate ethanol intake on systolic blood pressure, platelet cytosolic free calcium, aortic calcium, and rubidium-86 uptake in Wistar-Kyoto rats. Twelve Wistar-Kyoto rats, aged 6 weeks, were given 5% ethanol in drinking water the first week followed by 10% ethanol in drinking water for the next 6 weeks. Twelve control animals were given regular tap water. Systolic blood pressure in the ethanol-treated rats was significantly higher (p<0.05) than that in controls after 1 week and remained higher throughout the study. At 13 weeks of age, platelet cytosolic free calcium and calcium uptake by aortas were significantly higher (p< 0.001) in ethanol-treated animals as compared with those in controls. Ethanol intake did not affect aortic ouabain-sensitive 6 -8 However, the mechanisms by which ethanol intake elevates blood pressure is not known.Abnormal contractile activity of the vascular smooth muscle is considered to be one cause for the development of hypertension.9 The contractile activity of vascular smooth muscle is regulated by the level of intracellular free calcium ions ([Ca 2+ ]j). "12 It has been suggested that factors leading to an increased [Ca 2+ ]i within the vascular smooth muscle cell may be responsible for the increased contraction of the smooth muscle and the development of hypertension. Such factors may be an increased entry of calcium ions through the cell membrane via calcium channels or an increased release of calcium ions within the smooth muscle cells. Calcium influx through cell surface calcium channels is a major contributing factor to cytosolic free calcium. 1314 In the present study, we investigated the effect of an oral intake of 10% ethanol in drinking water on systolic blood pressure, platelet cytosolic free calcium and aortic calcium, and ^Rb* uptake in Wistar-Kyoto rats. Methods Animals, Diet, and Administration of EthanolMale WKY rats from Charles River, Quebec, Canada were used in this study. All rats were given standard rat chow throughout the study and had free access to water or water/ethanol mixture. At 6 weeks of age, rats were divided into two groups: a control group (12 rats) and an ethanol group (12 rats). Animals in the control group were given regular drinking water from the tap, and the ethanol group was given 5% vol/vol ethanol in tap water in the first week and 10% ethanol in tap water from the second through the

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Section: In Vitro Effects Of Ethanol Onsupporting

confidence: 50%

Platelet-free calcium and vascular calcium uptake in ethanol-induced hypertensive rats.

Vasdev¹,

Sampson²,

Prabhakaran³

1991

Hypertension

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“…This subject has recently been reviewed in this journal. 18 Also the exact role of C1-HCO 3 exchange (or of any other HCO 3 -dependent transport system) in regulating smooth muscle cell pH is still unknown. However, the examples given above are intended to illustrate the point that if intracellular sodium, cell pH, or sodium-hydrogen exchange activity is to be implicated as a critical component in the development of essential hypertension, then HCCydependent transport processes cannot be ignored.…”

mentioning

confidence: 99%

Potential role of Cl-HCO3 exchange in regulating vascular tone.

Karniski

1990

Hypertension

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“…primary defects in renal ion regulation [13][14][15] , and congenital 16 and acquired 17,18 reduction in the number of nephrons or in the filtration surface area per glomerulus, and abnormalities in the renin-angiotensin system 19,20 . Experiments with SHR-SP have revealed that development of hypertension correlates with abnormalities of the renin-angiotensinaldosterone system with increased plasma concentrations of aldosterone detected in prehypertensive animals 21,22 .…”

Section: Fig 6-2mentioning

confidence: 99%

Protective and Ameliorative Effects of Benidipine Hydrochloride Against Renal Damage in the Stroke-prone Spontaneously Hypertensive Rat(SHR-SP).

Kakuni¹,

Takeda²,

Ueno³

et al. 2001

J Toxicol Pathol

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Abstract:The potential of benidipine hydrochloride (BH), a 1,4-dihydropyridine calcium antagonist and a possible vasodilator, to protect against renal damage in the stroke-prone spontaneously hypertensive rat (SHR-SP) was examined using fifty-five males (10 weeks old). The animals were allotted into experiments 1 and 2, in each case subdivided into three groups (control and BH at doses of 3 and 10 mg/kg). Administration of BH was initiated before identification of clinical stroke in Experiment 1 and after its onset in Experiment 2. Measurement of body weight (BW) and systolic blood pressure (SBP) indicated that treatment of BH was associated with increased BW gain and reduced blood pressure in both experiments. Histopathological assessment revealed significant and dose-dependent decrease in the degree of fibrinoid necrosis in renal blood vessels, sclerosis, hyalinization, edematous thickening and Bowman's space dilatation in glomeruli, as well as protein casts, dilated or regenerative tubules, and interstitial inflammatory infiltration with fibrosis in tubulointerstitium in the BH treated groups as compared with the control group. These results indicated that BH exerts vasodilative effects on the kidney with improvement of regional blood flow, then preventing and ameliorating renal damage. (J Toxicol Pathol 2001; 14: 179-186)

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Ion transport defects and hypertension. Where is the link?

Cited by 49 publications

References 76 publications

Platelet-free calcium and vascular calcium uptake in ethanol-induced hypertensive rats.

Platelet-free calcium and vascular calcium uptake in ethanol-induced hypertensive rats.

Potential role of Cl-HCO3 exchange in regulating vascular tone.

Protective and Ameliorative Effects of Benidipine Hydrochloride Against Renal Damage in the Stroke-prone Spontaneously Hypertensive Rat(SHR-SP).

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