Effect of ouabain on arteriolar responses to norepinephrine in chronic, benign, volume-expanded hypertension.

Overbeck, H W

doi:10.1161/01.hyp.6.2_pt_2.i82

Cited by 8 publications

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“…Previous reports have demonstrated that higher doses of ouabain sensitize the contractile response to a-adrenergic agonists and to KCl in 1K1C rats (21,22). The same occurs with DOCA-salt rats in which ouabain treatment increased even more the pressor responses (23).…”

Section: Discussionmentioning

confidence: 57%

Effects of small doses of ouabain on the arterial blood pressure of anesthetized hypertensive and normotensive rats

Rossoni

Pinto

Vassallo

2001

Braz J Med Biol Res

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Ouabain increases vascular resistance and may induce hypertension by inhibiting the Na + pump. The effects of 0.18 and 18 µg/kg, and 1.8 mg/ kg ouabain pretreatment on the phenylephrine (PHE; 0.1, 0.25 and 0.5 µg, in bolus)-evoked pressor responses were investigated using anesthetized normotensive (control and uninephrectomized) and hypertensive (1K1C and DOCA-salt treated) rats. Treatment with 18 µg/kg ouabain increased systolic and diastolic blood pressure in all groups studied. However, the magnitude of this increase was larger for the hypertensive 1K1C and DOCA-salt rats than for normotensive animals, while the pressor effect of 0.18 µg/kg ouabain was greater only in DOCA-salt rats. A very large dose (1.8 mg/kg) produced toxic effects on the normotensive control but not on uninephrectomized or 1K1C rats. Rat tail vascular beds were perfused to analyze the effects of 10 nM ouabain on the pressor response to PHE. In all animals, 10 nM ouabain increased the PHE pressor response, but this increase was larger in hypertensive DOCA-salt rats than in normotensive and 1K1C rats. Results suggested that a) increases in diastolic blood pressure induced by 18 µg/kg ouabain were larger in hypertensive than normotensive rats; b) in DOCA-salt rats, smaller ouabain doses had a stronger effect than in other groups; c) hypertensive and uninephrectomized rats were less sensitive to toxic doses of ouabain, and d) after treatment with 10 nM ouabain isolated tail vascular beds from DOCA-salt rats were more sensitive to the pressor effect of PHE than those from normotensive and 1K1C hypertensive rats. These data suggest that very small doses of ouabain, which might produce nanomolar plasma concentrations, enhance pressor reactivity in DOCA-salt hypertensive rats, supporting the idea that endogenous ouabain may contribute to the increase and maintenance of vascular tone in hypertension. Correspondence

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Section: Discussionmentioning

confidence: 57%

Effects of small doses of ouabain on the arterial blood pressure of anesthetized hypertensive and normotensive rats

Rossoni

Pinto

Vassallo

2001

Braz J Med Biol Res

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“…The ouabain-like substance has received attention because of its diuretic and vasoconstrictive action mediated by the inhibitory action against Na+-K+-ATPase. In spite of many reports suggesting the existence of this substance, its physiologial role remains controversial (19)(20)(21). Pedrinelli (21) examined the pressor response to exogenous ouabain in patients with primary hyperaldosteronism and low renin essential hypertension, who are reported to have an increased level of the ouabain-like substance and found no differnce in the blood pressure response compared with normal renin essential hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…Pedrinelli (21) examined the pressor response to exogenous ouabain in patients with primary hyperaldosteronism and low renin essential hypertension, who are reported to have an increased level of the ouabain-like substance and found no differnce in the blood pressure response compared with normal renin essential hypertension. Overbeck (19,20) also reported no evidence for the physiological role of this substance in the pathogenesis or maintenance in early and chronic stages of Goldblatt hypertension models.…”

Section: Discussionmentioning

confidence: 99%

“…We showed previously (18) that an acute volume expansion produced a rise in blood pressure associated with vasoconstriction of various degrees, and decreases in the level of plasma catecholamines, plasma renin activity, and vasopressin. If the vasoconstriction produced by volume expansion was due to the increase in the endogenous Na*-K+-ATPase inhibitor, blunted response to exogenous Na+-K+-ATPase inhibitor would be observed (19,20). To test this hypothesis we infused ouabain after volume expansion and evaluated the relationship between the response to volume expansion and the response to ouabain administration.…”

Section: Introductionmentioning

confidence: 99%

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Effect of ouabain on hemodynamics in acute volume expanded hypertensive dogs

et al. 1989

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To evaluate possible roles of endogenous Na+-K+-ATPase inhibitors in vasoconstricted blood pressure elevation produced by acute volume expansion, we administered ouabain (Na+-K+-ATPase inhibitor) intravenously (30 micrograms/kg) for 10 min to dogs, 3 h after volume expansion with dextran in lactated Ringer's solution (20 ml/kg, for 1 h). Acute volume expansion resulted in the elevation of blood pressure associated with an increase in cardiac output. In some dogs the blood pressure remained elevated with gradual increase in total peripheral resistance (Group I) or with sustained high cardiac output (Group II), and in other dogs (Group III) it returned to the control level. Ouabain administration elevated the blood pressure and total peripheral resistance in these groups and sham dogs which did not have volume expansion. And these effects of ouabain were not correlated with the degree of blood pressure or vasoconstriction produced by volume expansion. Thus, it is not likely that endogenous Na+-K+-ATPase inhibitors increased to produce vasoconstricted hypertension after acute volume expansion.

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“…Such differences have important and complex influences on vascular responses to norepinephrine, 14 influences that make data interpretation difficult. In some rats we used adenosine injections and then infusions to evoke and maintain maximal vasodilation.…”

Section: S Everal Laboratories Have Provided Evidencementioning

confidence: 99%

The vascular Na+-K+ pump in experimental hypertension.

Overbeck

1987

Hypertension

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SUMMARYWe assessed the role of putative circulating ouabainlike factor(s) on in vivo arteriolar function in rats with very early (<7 days; mean, 3 days) and chronic (> 4 weeks) benign, one-kidney, one clip (1K1C) hypertension. Thus, we measured vascular responses in vasodilated (nitroprusside or adenosine), vascularly isolated, innervated hindlimb vascular beds of chloralose-anesthetized 1K1C rats perfused with their own blood at 1 ml/min. Complete norepinephrine dose-response curves in 8 rats with chronic and 28 with early 1K1C hypertension, compared with appropriate normotensive control rats, showed unchanged thresholds and ED M values. Magnitude of ouabain-induced leftward shifts of the norepinephrine dose-response curve in 18 rats with chronic and 21 with early IK1C hypertension, compared with appropriate normotensive control rats, was unchanged. Blockade of neural uptake of norepinephrine by desimipramine (10~7 M) in 81K1C rats did not alter these results. These findings provide no evidence in this form and these stages of hypertension that humoral ouabainlike inhibitors of the Na + -K + pump evoke physiologically significant inotropic effects in arterioles in vivo. It is possible, however, that induction of vascular Na + ,K + -adenosine triphosphatase by circulating inhibitors modified the vascular responses to norepinephrine and ouabain in these rats.

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Effect of ouabain on arteriolar responses to norepinephrine in chronic, benign, volume-expanded hypertension.

Cited by 8 publications

References 0 publications

Effects of small doses of ouabain on the arterial blood pressure of anesthetized hypertensive and normotensive rats

Effects of small doses of ouabain on the arterial blood pressure of anesthetized hypertensive and normotensive rats

Effect of ouabain on hemodynamics in acute volume expanded hypertensive dogs

The vascular Na+-K+ pump in experimental hypertension.

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