Attenuated Vasodilator Responses to K+ in Essential Hypertensive Men

Overbeck, Henry W.; Derifield, Randall S.; Pamnani, Motilal B.; Sözen, Tümay

doi:10.1172/jci107605

Cited by 67 publications

(22 citation statements)

References 19 publications

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“…For example, uncomplicated essential hypertensive patients show attenuated vasodilator/ responses to intraarterial infusion of potassium, suggesting suppressed vascular Na + -pump activity. 31 This form of hypertension is not accompanied by volume expansion, on the contrary, most investigators report decreased plasma volume in such patients. 32 -33 Moreover.…”

Section: Discussionmentioning

confidence: 97%

Effect of AV3V lesions on development of DOCA-salt hypertension and vascular Na+-pump activity.

1982

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SUMMARY We studied the effects of anteroventral third ventricle (AV3V) lesions on the vascular Na + -pump activity of deoxycorticosterone acetate-salt (DOCA-salt) treated rats. Blood pressures and Na + -pump activity of the isolated tail arteries, measured as ouabain-sensitive w Rb + -uptake, were determined in untreated control rats, DOCA-salt treated rats, rats with AV3V lesions, and rats with AV3V lesions which were treated with DOCA-salt. Control rats receiving DOCA treatment developed higher blood pressures than rats receiving no DOCA treatment. Placement of AV3V lesions prior to administration of DOCA prevented the increase in blood pressure. Vascular Na + -pump activity in the DOCA-treated group was reduced by 20% compared to all other groups. The AV3V lesions prevented the suppression of Na + -pump activity caused by DOCA treatment. Suppression of vascular Na + -pump activity was due to a humoral substance since Na + -punip activity of tail arteries from control rats incubated in plasma from DOCA-salt treated rats was suppressed by 25% when compared to those incubated in control plasma. Our findings support the hypothesis that a circulating pressor substance is at least partially responsible for the development of DOCA-salt hypertension and that the mechanism by which AV3V lesions prevent DOCA hypertension may be through the interruption of secretion, transport, or synthesis of this factor. (Hypertension 4: 575-580, 1982) KKV WORDS • hypertension • blood pressure • Na + -pump activity • Rb-uptake • tail artery • AV3V lesion

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Section: Discussionmentioning

confidence: 97%

Effect of AV3V lesions on development of DOCA-salt hypertension and vascular Na+-pump activity.

1982

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“…Other evidence suggests that decreases in pump activity are not unique to volumeexpanded forms of hypertension. Overbeck et al 2 found attenuated vasodilatory responses to intraarterial infusions of K + in a significant proportion of patients with uncomplicated essential hypertension. There is little evidence that uncomplicated essential hypertension is accompanied by volume expansion; most investigators report that decreased plasma volume characterizes such patients.…”

Section: Discussionmentioning

confidence: 99%

Sodium pump activity in arteries of Dahl salt-sensitive rats.

Overbeck¹,

Ku²,

Rapp³

1981

Hypertension

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SUMMARY Decreased actirity of the electrogenlc sodium pump of vascular smooth muscle has been reported in several forms of experimental hypertension and may play an important role in basic disease mechanisms. It has been proposed that such pump suppression may characterize volume-expanded forms of hypertension. The present investigation tested this latter hypothesis. Sodium pump activity was assessed in vitro in sodium-loaded tail artery and thoracic aorta freshly excised from Dahl salt-sensitive (S) and saltresistant (R) rats on low (0.4%) or high (8%) NaCI diets for 5 to 7 weeks. Rubidium ( u Rb) uptake in the absence (total uptake) and presence (ouabain-insensitive uptake) of l.OmM ouabain was measured and ouabain-sensitive uptake (nmole/mg dry weight/10 mln) was calculated. In S rats, salt feeding was accompanied by elevation of arterial pressure, cardiac hypertrophy, increases of 20% to 30% in total blood volume, and increases in the ouabain-sensitive, ouabain-insensitive, and total uptakes in the aorta, but no significant change in uptakes in the tail artery. However, ouabaln-sensitire uptake in the tail artery of all S rats exceeded that in R rats. There was no evidence of a decrease in vascular sodium pump activity accompanying hypertension in either artery. Therefore, the results of this study provide no evidence in support of the hypothesis that pump suppression in vascular smooth muscle characterizes volume-expanded forms of hypertension. It is unlikely that the observed increases in vascular pump activity in S rats reflected intracellular sodium concentrations higher than those in the control rats. Rather, increases in the numbers of pump molecules or in their turnover rate are probably involved.

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“…KC1 has been reported to have both direct and indirect effects on the vascular system. 32 - 33 Intraarterial infusion of KC1 is known to cause arterial vaso- VOL 6, No 2, MARCH-APRIL 1984 dilation, the degree of which is reduced by pretreatment with ouabain. 32 This observation led Overbeck and others 33 to speculate that there might be a defect in Na, K-ATPase in vascular smooth muscle in some patients with essential hypertension whose K vasodilation was attenuated, and that an increase in plasma K would stimulate the Na-K pump, leading to a reduction in blood pressure by vasodilation.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives.

Fujita¹,

Ando²

1984

Hypertension

108

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SUMMARY To clarify the mechanism by which potassium (KC1) protects against the blood pressure rising action of sodium (NaCl), we studied the effects of KC1 loading in patients with idiopathic hypertension who, after a period of NaCl restriction, partook of a high NaCl diet. Eleven patients who had taken the KC1 supplement (96 mEq/day) during the high NaCl period showed lesser mean blood pressure (MAP) rise with changes in NaCl intake from 25 to 250 mEq/day than 12 patients who had not taken the KCI supplement (p < 0.001). With a high NaCl diet, the KCl-supplemented patients retained less NaCl, gained less weight, and showed a lesser increase in plasma volume and cardiac output than the non-KCl-supplemented ones. Overall, the increase in blood pressure levels during the high Na diet correlated directly either with changes in plasma volume (p < 0.05) or with changes in cardiac output (p < 0.01). The results suggest that KCI may prevent a rise in blood pressure with NaCl loads in hypertensive patients by attenuating the increase in cardiac output, mainly as a result of the natriuresis. Furthermore, plasma norepinephrine was measured to estimate the sympathetic activity, since the sympathetic nervous system is known to control urinary NaCl excretion. From the low NaCl diet to Day 3 of the high NaCl diet, plasma norepinephrine was significantly (p < 0.01) decreased in the KCl-supplemented patients, whereas it remained unchanged in the non-KCl-supplemented ones. Concomitantly, urinary Na excretion was significantly greater in the early period of NaCl loading in the KCl-supplemented group as compared to the other group. Taken together, these results suggest that lower levels of norepinephrine measured in the plasma of the KCl-supplemented patients in the early NaCI-loading phases of the study are indicative of reduced adrenergic neural activity, which might be involved not only in the attenuation of increased cardiac output, but also in the responses of the kidney to shift the pressure-natriuresis relationship toward normal, leading to the natriuresis. (Hypertension 6: 184-192, 1984) KEY WORDS • sodium • potassium • norepinephrine • cardiac output N UMEROUS animal studies have presented evidence that the mechanisms by which excess salt (NaCl) intake increases blood pressure may include augmentation of sympathetic nerve activity and release of norepinephrine from adrenergic nerve endings.1 : Studies in humans also suggest that an excess of dietary NaCl may augment not only the vascular responsiveness to catecholamines,-1 but also the sympathetic nerve activity in hypertensive patients. 4 Recently, several investigators found hyperactivity of the sympathetic nervous system in hypertensive patients, who showed a considerable increase in blood pressure with NaCl loads.5 -6 Since sympathetic nerve activity is known to influence urinary Na

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Attenuated Vasodilator Responses to K+ in Essential Hypertensive Men

Abstract: A B S T R A C T

Cited by 67 publications

References 19 publications

Effect of AV3V lesions on development of DOCA-salt hypertension and vascular Na+-pump activity.

Effect of AV3V lesions on development of DOCA-salt hypertension and vascular Na+-pump activity.

Sodium pump activity in arteries of Dahl salt-sensitive rats.

Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives.

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