Ouabain-induced contraction of vascular smooth muscle in spontaneously hypertensive rats and the effect of hydralazine

Morita, Shigeru; Iwasaki, Tadaaki; Nagai, Kazuo; Miyata, Sadao; Kawai, Yoshitaka

doi:10.1016/0014-2999(88)90537-7

Cited by 8 publications

(7 citation statements)

References 35 publications

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“…Ouabaininduced contractions were due to a direct action of the glycoside rather than through release of noradrenaline, because they were unaffected by the a r adrenoceptor an tagonist prazosin. This agrees with previous reports in this vascular preparation [8][9][10], indicating a weak adren ergic innervation in the rat aorta.…”

Section: Discussionsupporting

confidence: 83%

“…as observed by other authors [8][9][10]. The removal of the endothelium modified the contrac tions caused by ouabain on the two strains in different ways.…”

Section: Discussionsupporting

confidence: 68%

“…The ability of ouabain to induce contractile responses has been reported in different vascular preparations [16,21,22], As previously described in the rat aorta [8][9][10], very high concentrations (100 jiM to 1 m l/) were needed to observe clear contractile responses, probably because the rat Na+.K+-ATPase is resistant to blockade by oua bain. For this reason, in most of the experiments only the highest concentrations of ouabain were used.…”

Section: Discussionmentioning

confidence: 77%

“…Indeed, the contractions evoked by a K+-free solution in rat mesenteric arteries [5] and those produced by ouabain in human placental arteries [6] and guinea pig carotid arteries [7] are attenuated when the endothelium is present. The endothelial factor in volved in these effects appears to be nitric oxide (NO) in rat mesenteric arteries [5], but a still unknown factor in human placental and guinea pig carotid arteries [6,7], An increase in the response to ouabain has been reported in the vasculature of spontaneously hypertensive rats (SHR) when compared with that obtained in normotensive Wistar-Kyoto rats (WKY) [8][9][10], These higher responses can be due to enhanced sodium pump activity, higher Na+-Ca2+ exchange or other alterations in mem brane permeability to Na+ and Ca2+ [8][9][10][11]. However, the possible involvement of vascular endothelium has not yet been elucidated although an important endothelial dys function associated with hypertensive disease has been reported [12], Therefore, the aim of the present work was to investi gate any involvement of vascular endothelium in the responses to ouabain in vessels from WKY and SHR, as well as the possible mechanisms involved.…”

Section: Introductionmentioning

confidence: 99%

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Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats

Ponte

Marı́n²,

Arribas³

et al. 1996

J Vasc Res

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The influence of vascular endothelium on ouabain-induced contractions and sodium pump activity in aortic segments of Wistar-Kyoto (WKY) and spontaneously hypertensive rat (SHR) was analyzed. De-endothelialization increased and reduced ouabain-induced contractions in WKY and SHR segments, respectively. The effects of de-endothelialization were not reproduced by pretreatment of the segments with N^G-nitro-L-arginine methyl ester, indo-methacin, or 5, 8, 11, 14-eicosatetraenoic acid, acetyl salicylic acid, dazoxiben, phosphoramidon, BQ-123, or superoxide dismutase. Bioassay experiments suggest that ouabain releases a diffusible factor from endothelial cells that inhibits or facilitates digitalis-induced contractions in WKY and SHR segments, respectively. In a potassium-free solution, potassium-induced relaxation in segments of both strains was abolished by ouabain in de-endothelialized aortas and reduced in intact ones. Ouabain-sensitive ⁸⁶Rb⁺ uptake was significantly reduced by de-endothelialization both in WKY and in SHR. These results suggest that the vascular endothelium of WKY and SHR aortas releases a diffusible factor that stimulates the sodium pump and/or protects it from ouabain blockade. Ouabain also releases a diffusible endothelium-derived factor in SHR aortas that facilitates ouabain-induced contractions.

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Section: Discussionsupporting

confidence: 83%

“…as observed by other authors [8][9][10]. The removal of the endothelium modified the contrac tions caused by ouabain on the two strains in different ways.…”

Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats

Ponte

Marı́n²,

Arribas³

et al. 1996

J Vasc Res

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show abstract

“…146,147 In addition, increased Ca 2ϩ entry through L-type channels is also responsible for augmented contraction of SHRSP arteries due to membrane depolarization after Na ϩ -K ϩ pump inhibition. 148 This abnormality is already present in the prehypertensive stage 149 and cosegregated with BP of SHRSP ϫ WKY F 2 hybrids. 150 On the contrary, cosegregation studies performed with platelets did not reveal a significant association between BP and [Ca 2ϩ ] i , in SHR ϫ Donryu F 2 hybrids 151 or LH ϫ Lewis F 2 hybrids (Zicha et al, unpublished data).…”

Section: Cell Calcium Handlingmentioning

confidence: 99%

Abnormalities of membrane function and lipid metabolism in hypertension A review

Zicha

Kuneš

Devynck

1999

American Journal of Hypertension

211

175

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Hypertension, which is characterized by multiple alterations in the structure and function of the cell membrane, is often associated with important metabolic abnormalities including those concerning lipid metabolism. Dyslipidemia accompanying essential hypertension consists of elevated plasma triglycerides, low HDL cholesterol, and increased levels of atherogenic LDL cholesterol particles. The altered membrane microviscosity seen in hypertensive subjects reflects the changes of membrane lipid composition resulting from intensive exchange between circulating and membrane lipids, as well as from abnormal cellular lipid synthesis and metabolism. The changes of membrane microviscosity are known to modulate the activity of proteins involved in ion transport, signal transduction, cell Ca 2؉ handling, intracellular pH regulation, etc. Alterations in plasma or membrane lipids are indeed closely associated with ion transport abnormalities as well as with impaired control of cytosolic Ca 2؉ T here is no doubt that essential hypertension is associated with multiple membrane alterations, including changes in membrane microviscosity, receptor function, signal transduction, ion transport, calcium mobilization, intracellular pH regulation, and so on. Lipids, as an integral part of the cell membrane, play a decisive role in the modulation of the membrane properties mentioned. Specific lipid-lipid and lipid-protein interactions result in a highly dynamic but precisely controlled architecture of membrane components. Major regulators of membrane architecture are membrane potential, intracellular Ca 2ϩ and pH, lipid composition, cell-to-cell contact, and membrane coupling with the cytoskeleton or extracellular matrix. Intermolecular associations in the membrane and at the membrane-cytoskeleton interface are further selectively controlled by specific phosphorylation and dephosphorylation cascades involving both proteins and lipids. This is regulated by the extracellular matrix as well as by the binding of growth factors and hormones to their specific receptors. 1,2The aim of this review is to outline some interrelationships between abnormal lipid metabolism and altered membrane structure or function in human and experimental hypertension, and to evaluate whether abnormal lipid metabolism, which is responsible for a great part of membrane abnormalities found in hypertension, might be an integral part of its pathogenetic mechanisms. BLOOD PRESSUREMultiple metabolic abnormalities often accompany essential hypertension. Decreased high-density lipoproteins (HDL) together with increased plasma levels of low-density (LDL) and very low-density lipoproteins (VLDL), as well as hypertriglyceridemia, hypercholesterolemia, and insulin resistance, were found in many hypertensive patients. 3,4 There is increasing evidence for a genetic basis for the association of hypertension with insulin resistance and dyslipidemia. The genetic locus associated with dyslipidemia accompanying hypertension or diabetes seems to be closely linked to the LDL recept...

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Regional specificity of long-term regulation of tyrosine hydroxylase in some catecholaminergic rat brainstem areas. II. Effect of a chronic dihydralazine treatment

et al. 1993

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Ouabain-induced contraction of vascular smooth muscle in spontaneously hypertensive rats and the effect of hydralazine

Cited by 8 publications

References 35 publications

Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats

Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats

Abnormalities of membrane function and lipid metabolism in hypertension A review

Regional specificity of long-term regulation of tyrosine hydroxylase in some catecholaminergic rat brainstem areas. II. Effect of a chronic dihydralazine treatment

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