Actions of sodium and potassium ions on baroreceptors of normotensive and spontaneously hypertensive rats.

Saum, William R.; Ayachi, S; Brown, Alison

doi:10.1161/01.res.41.6.768

Cited by 43 publications

(26 citation statements)

References 33 publications

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“…Ouabain would minimize this hyperpolarization by reducing sodium pumping, thereby enhancing sensitivity. [23][24][25][26][27][28][29] The effects of perfusing the carotid sinus with a low-potassium-ion solution were somewhat different from the effects of ouabain. Although there was no significant change in the peak slope or maximal discharge rate during perfusion with a lowpotassium-ion solution in either normal or heartfailure dogs, threshold pressure was significantly reduced only in the heart-failure dogs, and there was a tendency for the curves to be shifted to the left in the heart-failure dogs.…”

Section: Discussion Liameter Inmentioning

confidence: 99%

Carotid sinus baroreceptor sensitivity in experimental heart failure.

Wang¹,

Chen²,

Zucker³

1990

Circulation

136

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Single-unit carotid sinus baroreceptor activity was recorded in normal and heart-failure (pacing-induced) dogs. The sensitivity of these units was compared between the two groups of dogs. After development of clinical heart failure, the animals were anesthetized, and the left carotid sinus was vascularly isolated and perfused with oxygenated Krebs-Henseleit solution. Single-unit baroreceptor discharge was recorded from the carotid sinus nerve in response to stepwise increases in carotid sinus pressure (CSP). In addition, the carotid sinus diameter was measured with sonomicrometer crystals. In this way, both CSP-discharge and CSP-diameter curves were constructed for both normal and heart-failure dogs. Analysis of these curves demonstrated that the heart-failure group exhibited a significant decrease in peak discharge (48.1±3.0 vs. 22.2±+ 2.2 spikes/sec; p<0.001) and a significant elevation in threshold pressure compared with the normal animals (91.0 +5.0 vs. 119.1±+4.4 mm Hg; p<0.001). The peak slope of the CSP-discharge curve was also significantly lower in the heart-failure group (0.63 ±0.06 vs. 0.40 ±0.09 spikes/sec/mm Hg; p <0.05). In the heart-failure group, perfusion of the carotid sinus with ouabain (0.01 ,ug/ml) caused a significant decrease in threshold pressure and a significant increase in peak discharge frequency, as well as an increase in slope of the CSP-discharge curve. There were no changes in CSP-diameter relations in response to ouabain. This dose of ouabain had no effect on pressure-discharge relations or carotid sinus diameters in normal dogs. Perfusion of the isolated carotid sinus with a Krebs-Henseleit solution with 50% of the normal potassium ion concentration had no effect on peak discharge or slope, but this perfusion protocol significantly reduced threshold pressure in heart-failure dogs. Low potassium ion concentration had no effect in the normal dogs. From these data, we conclude that there is attenuation of the carotid sinus baroreceptor discharge sensitivity in this model of low-output heart failure. The data are consistent with the view that there is an augmentation of Na+,K+-ATPase activity in the carotid sinus baroreceptor. (Circulation 1990;81:1959-1966 T he reflex control of the circulation is clearly abnormal in heart failure.1-8 The arterial baroreflex is abnormal in both low-and high-output heart failure in humans3'4 and in animals.5-8 The mechanisms for this reflex abnormality are not completely understood. Derangements in any part of the reflex arc could be responsible for the depression in baroreflex sensitivity that has been observed in heart failure.Clearly, data indicate that the efferent components of the baroreflex control of heart rate are abnormal,2'4 and it has also been shown that both catecholamine synthesis and responsiveness are depressed in heart failure. both systemic norepinephrine clearance and spillover are abnormal in heart failure.1" Evidence from this laboratory also suggests that both carotid and aortic baroreceptor discharge sensitivities are depres...

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Section: Discussion Liameter Inmentioning

confidence: 99%

Carotid sinus baroreceptor sensitivity in experimental heart failure.

Wang¹,

Chen²,

Zucker³

1990

Circulation

136

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“…Improvement of baroreceptor function with high KC1 intake has been observed in humans 16 and animals. 15 Also, the increased extracellular K concentration could decrease the nerve-evoked release of norepinephrine from the nerve ending, in vitro. 30 Finally, KC1 supplementation could decrease plasma norepinephrine concentration in NaCl-loaded stroke-prone spontaneously hypertensive rats.…”

Section: Discussionmentioning

confidence: 99%

“…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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“…From a functional point of view, distinction between receptor and axon is not crucial. A consideration of the contribution of Na + to the receptor potential of mechanoreceptors using constant field theory (Hodgkin and Katz, 1949;Saum et al, 1977) led to the prediction that a reduction in extracellular sodium ion concentration, [Na + ],,, should reset baroreceptors and reduce their sensitivity to changes in suprathreshold pressures; this was found to be the case Kunze and Brown, 1978;Kunze et al, 1977) (Fig. 4A) (Fig.…”

Section: Ionic Sensitivity Of Baroreceptorsmentioning

confidence: 99%