Contribution of the sympathetic nervous system to the hypertensive effect of a high sodium diet in stroke-prone spontaneously hypertensive rats.

Dietz, Rainer; Schömig, Albert; Rascher, Wolfgang; Strasser, Ruth H.; Lüth, J. B.; Ganten, Ursula; Kübler, W.

doi:10.1161/01.hyp.4.6.773

Cited by 45 publications

(19 citation statements)

References 36 publications

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“…24 -" Elevation of the plasma level of norepinephrine has been reported in the former, 26 and intracerebroventricular administration of 6-hydroxydopamine prevented the DOCAinduced hypertension and increase in plasma norepinephrine. 27 On the contrary, our observations are consistent with reports of no increase in norepinephrine in saline-loaded Wistar rats 28 and of a decrease in norepinephrine in metyraponeinduced hypertensive dogs. 8 The discrepancy between these findings may be due to differences in the species used and the rapidity of volume expansion.…”

Section: Figure 4 Relationship Between Change In Pressor Response Tosupporting

confidence: 92%

Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs.

et al. 1988

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SUMMARY In a search for factors contributing to the sustained Mood pressure (BP) elevation in acutely volume-loaded animals, dextran dissolved in lactated Ringer's solution (20 ml/kg) was infused into 34 mongrel dogs over a period of 1 hour under pentobarbital anesthesia and changes in bemodynamic and humoral variables were monitored during its infusion and for 3 hours after its infusion. BP elevation during volume loading (from 114 ± 3 to 128 ± 3 [SEM] mm Hg) was attributed to an increase in cardiac output. After volume loading, some dogs maintained BP elevation whereas others did not. The former group showed an increase in total peripheral resistance, demonstrating a transformation of cardiac output to total peripheral resistance as a responsible factor in maintenance of the elevated BP. The plasma levels of norepinephrine, vasopressin, and plasma renin activity were not elevated, indicating that these vasoactive factors were not responsible for elevation of the BP or total peripheral resistance. The changes in the hematocrit, atrial natriuretk factor, urine volume, and urinary sodium excretion were identical in the two groups, and natrluresis was not prominent when total peripheral resistance was high. Pressor responses to norepinephrine and angiotensm n were potentiated 3 hours after stopping Infusion in both groups, but this potentiation was not correlated with the Increase hi total peripheral resistance or mean BP. Thus, acute volume expansion produced resistance-dependent hypertension following the initial volume-dependent hypertension. It is unlikely that a vascular sensitizing natriuretk factor plays a role in the resistance-dependent BP elevation. The mechanism and physiological importance of hypersensitivity to vasoactive substances remain to be elucidated.

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Section: Figure 4 Relationship Between Change In Pressor Response Tosupporting

confidence: 92%

Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs.

et al. 1988

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“…Potassium might interfere with a number of mechanisms that have been implicated in the adverse effects of high sodium intake in SHRSP. Such mechanisms include changes in extracellular fluid volume, 7 activation of central or autonomic nervous system, 8 " 10 enhanced vascular reactivity to pressor agents, 11 Previous research from our laboratory has defined the effects of dietary potassium deprivation and administration on plasma renin activity (PRA) in both animals 18 and human subjects. 19 We also detected a positive correlation between PRA and the development of stroke and heart attack in humans.…”

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confidence: 99%

Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats.

et al. 1990

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We studied the effects of regular diet (035% NaCl/1.1% potassium), high sodium diet (4% NaCl/0.75% potassium), or high sodium and high potassium diet (4% NaQ/2.11% potassium) on blood pressure, plasma renin activity, renal and cerebrovascular lesions, and incidence of stroke and mortality in male stroke-prone spontaneously hypertensive rats (SHRSP). In the first 4 weeks, the rise in blood pressure was higher hi high NaQ than in high NaCI/high potassium or regular diet groups. However, by 8 and 12 weeks, the blood pressure in all three groups was similar. After 4 weeks of diet, plasma renin activity was similar in the three groups (3.4±0.8, 4.1±0.9, and 52±1.6 ng/ml/hr, in high NaO, high NaCI/high potassium, and regular diet groups, respectively) and were not related to sodium excretion. After 8 weeks, plasma renin activity was significantly increased only in the high NaQ group (13.7±3.7 ng/ml/hr), and by 12 weeks plasma renin activity was significantly higher in the high NaCl group (253 ±3.6 ng/ml/hr) than in the high NaCI/high potassium (11.1±2.9 ng/ml/hr) or in the regular diet (7.8±4.6 ng/ml/hr) groups. Moderate to severe renal vascular lesions were first detected in the high NaQ group by 8 weeks of diet At 12 weeks, renal vascular damage index (RVDI), estimated hlstologically, was significantly higher in the high NaCl group (RVDI=79±14) than hi the high NaCI/high potassium (RVDI=40±ll) and regular diet (RVDI=7.8±4.6) groups. At this time, incidence of stroke was 81% in high NaCl, 24.5% in high NaCI/high potassium, and 7.7% in regular diet groups. Hie data demonstrate that: 1) the increase in mortality, stroke, and renal and cerebrovascular lesions in SHRSP fed a high sodium diet is associated with a paradoxical rise in plasma renin activity; 2) the protective effect of high potassium hi SHRSP fed a high potassium diet is related to a lower blood pressure at 2 -4 weeks and a lower plasma renin activity, but not a lower blood pressure at 8-12 weeks; 3) this rise in plasma renin activity demonstrates that a high potassium diet suppresses or delays a primary or secondary paradoxical rise hi plasma renin activity and thus, angiotensin JJ in the rats fed a high sodium diet This action together with possible direct effects of potassium hi the vasculature contributes to the protective effect on end organ damage and stroke hi SHRSP. {Hypertension 1990;15:318-326)

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“…8 "" Although the precise mechanism of the antihypertensive action of KCI remains controversial, its natriuretic properties are thought to play an important role. 10 ' 2 13 Moreover, recent reports have indicated that dietary KCI supplementation decreased plasma norepinephrine concentration in NaCl-loaded hypertensive rats 14 and improved baroreceptor function in hypertensive rats 15 and humans. 16 Taken together, there is a considerable possibility that KCI may change the sympathetic nerve activity, leading in turn to the natriuresis and resultant attenuation of the rise in blood pressure with NaCl loads in hypertensive patients.…”

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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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Contribution of the sympathetic nervous system to the hypertensive effect of a high sodium diet in stroke-prone spontaneously hypertensive rats.

Cited by 45 publications

References 36 publications

Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs.

Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs.

Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats.

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

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