Alterations in Cardiac Function and Cardiopulmonary Blood Volume in Chronic Sodium Depletion in Dogs

Lynn, Melvyn; Fouad, Fetnat M.; Cook, Sebastian A.; Napoli, C.; Ferrario, Carlos M.

doi:10.1042/cs059393s

Cited by 8 publications

(6 citation statements)

References 7 publications

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“…A series of correlated studies involving investigation of baroreceptor reflexes, 1 -• cardiac function, 4 and measurements of catecholamines in both plasma and cerebrospinal fluid* support this conclusion. The studies were prompted when the carotid occlusion (CO) reflex was found to be sharply inhibited in dogs subjected to SD of 3 weeks' duration.…”

supporting

confidence: 55%

“…We have shown 1 -4 that the fraction of the blood volume contained in the cardiopulmonary region is proportionally greater in SD animals and that hypovolemia is present 4 while central venous pressure is unchanged. 1 Moreover, ejection fraction was reduced markedly in SD dogs.…”

Section: Figure 4 Comparisons Of Stimulus Response Relations Betweenmentioning

confidence: 97%

“…1 Moreover, ejection fraction was reduced markedly in SD dogs. 4 When assessed collectively, these findings provide insight into the mechanism for the reduced response of renal nerve discharges in SD dogs. If sodium depletion is associated with reduced cardiac function, increased stretch of cardiopulmonary receptors may limit the renal sympathetic response to acute variations in arterial pressure.…”

Section: Figure 4 Comparisons Of Stimulus Response Relations Betweenmentioning

confidence: 99%

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Altered neural control of cardiovascular function in sodium-depleted dogs.

Takishita¹,

Ferrario²

1982

Hypertension

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SUMMARY Sodium restriction affects sympathetic control mechanisms by blunting of the reflex pressor response to carotid sinus hypotension, which is rerersible by section of vagal afferents. To obtain more direct evidence, sympathetic nerre activity was recorded from a renal nerve (RNA) in 16 normal (NS) and 13 sodiumdepleted (SD) dogs anesthetized with morphine-pentobarbital. Integrated RNA was measured during changes in mean arterial pressure (MAP) produced by i.v. infusion of sodium nltroprusslde (100 Mg/kg/min) or phenylephrine (20 Mg/kg/min). The classical inverse relationship between MAP and integrated RNA was found before and after bilateral vagotomy (VAGT) in both NS and SD dogs. However, RNA in SD dogs, expressed as % of maximal neural firing, was significantly less at any blood pressure level when compared to NS dogs. In addition, the critical pressure (point at which RNA ceased) was reduced in SD vs NS dogs (p < 0.002). The decreased sympathetic neural firing in SD dogs was abolished after bilateral VAGT, confirming the pronounced buffering effects of vagal afferents on RNA in salt-depleted dogs. C HRONIC sodium depletion (SD) may produce significant alterations in autonomic nervous system function that do not conform to the usual understanding of the effect of increased blood levels of angiotensin II (All) upon neurogenic drive.1 Although All certainly acts to augment sympathetic efferent activity, in the dog the state of the sodium balance appears to modify significantly, and in an unexpected manner, the expression of the interplay between the renal pressor and the sympathetic nervous systems.A series of correlated studies involving investigation of baroreceptor reflexes, 1 -• cardiac function, 4 and measurements of catecholamines in both plasma and cerebrospinal fluid* support this conclusion. The studies were prompted when the carotid occlusion (CO) reflex was found to be sharply inhibited in dogs subjected to SD of 3 weeks' duration. 1 -* Suppression of the characteristic rises in heart rate and cardiac output persisted even after cholinergic blockade with atropine." However, section of the cervical vagus nerves markedly potentiated the CO reflex to the levels found in normal vagotomized animals..The augmented pressor response was now accompanied by prominent increases in stroke volume and cardiac out- put.' These data suggested that, in the SD state, removal of the inhibitory activity from the carotid sinus barorcceptors during CO was not sufficient to liberate the vasomotor centers from the additional input of vagal afferents probably discharging at rates above their tonic normal influence.The objective of the present study was to determine whether this peculiar effect of SD upon cardiovascular reflexes could be documented more directly by electroneurographic recordings of sympathetic nerve activity both before and after section of the vagus nerves. MethodsExperiments were performed in 29 male mongrel dogs weighing between 17 and 23 kg. Thirteen animals were fed a sodium-restricted diet containi...

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supporting

confidence: 55%

Section: Figure 4 Comparisons Of Stimulus Response Relations Betweenmentioning

confidence: 97%

Section: Figure 4 Comparisons Of Stimulus Response Relations Betweenmentioning

confidence: 99%

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Altered neural control of cardiovascular function in sodium-depleted dogs.

Takishita¹,

Ferrario²

1982

Hypertension

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“…Ferrario et al , n Szilagyi et al , 15 Brosnihan et al, 10 and Lynn et al, 24 have shown that sodium depletion, as carried out in the present experiments, is associated with important changes in neuroendocrine function as reflected by reduced peripheral sympathetic nerve activity, 15 -23 alterations in the norepinephrine concentration of both CSF and medulla oblongata consonant with increased central noradrenergic turnover, 10 and resetting of the interaction between high and low pressor baroreceptor reflexes. 15 n - 24 The present finding of reduced activity of the brain renin angiotensin system, at least as judged by the decreased activity of the brain iso-enzyme, is congruent with the possibility that the brain angiotensinergic system has a facilitative influence upon the sympathetic system.…”

Section: Figure 1 Renin Activity In Brain Regions and Spinal Cord Ofmentioning

confidence: 77%

“…10 -15U - 24 The experiments of Ganten et al in young and old dogs 18 and Sen et al 22 in rats treated with an angiotensin antagonist provided evidence toward the possible existence of a negative feedback between the kidney and brain angiotensin systems. The experiments of Ganten 18 were not entirely conclusive, however, because their methodology did not eliminate the participation of other proteases which could generate angiotensin I at a lower pH.…”

Section: Figure 1 Renin Activity In Brain Regions and Spinal Cord Ofmentioning

confidence: 99%

Effects of chronic sodium depletion on canine brain renin and cathepsin D activities.

Brosnihan¹,

Smeby²,

Ferrario³

1982

Hypertension

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SUMMARYThe activities of brain renin and cathepsin D were measured in brain regions of 10 dogs on a normal sodium intake (65 mEq Na + /day) and 10 other dogs placed on a low sodium diet (< 4 mEq Na + /day) for 21 days and given a diuretic. The purpose of this study was twofold: to assess the effect of sodium depletion on brain renin activity; and to assess in the same regions alterations in brain renin and cathepsin D activities. Sodium depletion caused a ninefold increase in plasma renin activity, hemoconcentration, and hyponatremia. In the presence of marked hyperreninemia, the average cerebral renin activity was reduced significantly; the most pronounced changes occurred in the upper and lower brain-stem regions. Cerebrospinal fluid renin was increased by 30%, but this change was not significant in sodiumdepleted dogs. There were no significant alterations in cathepsin D activity whether assessed in total or regional brain areas. These observations support the view that there is an inverse relationship between plasma and brain renin activity in chronically sodium-depleted dogs. Additionally, evidence is provided that brain renin activity is modified independently from cathepsin D activity. this peptide system may function in the brain to regulate blood pressure via a presumed action upon central adrenergic neurons. Severs 2 and Phillips 3 suggest that brain renin affects the intake and excretion of water and sodium via activation of thirst, sodium appetite, and vasopressin release. A unifying hypothesis has been proposed by Ferrario et al. 4 They suggest that the kidney and brain renin angiotensin systems function in a cooperative manner to exert total integration of central and peripheral autonomic nervous system function and sodium and water metabolism. Before 1979, a welter of conflicting observations raised doubts about the existence of renin in the brain and handicapped efforts to establish its physiological significance. The ability of brain homogenates to generate angiotensin I was attributed to an acid protease (cathepsin D) normally present in lysosomes.5 -6 Thus, in vivo this enzyme would be forced to exert its functions separated from renin substrate and at an unfavorable pH. Further, any angiotensin I formed by cathepsin D might be rendered inactive by this enzyme before it could have an action outside the cell. Using two different chromatographic procedures, Osman et al.,7 Smeby et al. , 8 and Hirose et al. 9 independently showed that cathepsin D could be separated from brain renin and that the latter had the ability to form angiotensin I at a neutral pH. This discovery permitted us to evaluate the possible existence of an interplay between the brain and kidney renin angiotensin systems by inducing a stage of prolonged hyperreninemia due to sodium restriction. Both renin and cathepsin D activities were determined in subdivisions of the brain to ascertain if the protein that acted enzymatically to cleave angiotensin I from its substrate was modified independently of the acid protease.

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Chronic sodium depletion suppresses the area postrema pressor pathway

Szilagyi

Ferrario

1987

Life Sciences

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Alterations in Cardiac Function and Cardiopulmonary Blood Volume in Chronic Sodium Depletion in Dogs

Cited by 8 publications

References 7 publications

Altered neural control of cardiovascular function in sodium-depleted dogs.

Altered neural control of cardiovascular function in sodium-depleted dogs.

Effects of chronic sodium depletion on canine brain renin and cathepsin D activities.

Chronic sodium depletion suppresses the area postrema pressor pathway

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