The Haemodynamic Response to Salt and Water Loading in Patients with End-Stage Renal Disease and Anephric Man

Kim, K. E.; Onesti, Gaddo; DelGuercio, E T; Greco, James; Fernandes, Michael; Swartz, Charles

doi:10.1042/cs051223s

Cited by 4 publications

(3 citation statements)

References 7 publications

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“…Furthermore, there are several observations that demonstrate that cardiac output does not control the blood pressure. Dialysis patients loaded with saline develop a rise in peripheral resistance without an increase in cardiac output (190), hypertension can occur in a patient with mitral stenosis and a low cardiac output, and after raising the blood pressure of a dog with metapyrone for 6 wk there was no evidence of circulatory autoregulation (372).…”

Section: B Links Between An Inadequate Renal Capacity To Excrete a Hmentioning

confidence: 99%

Links Between Dietary Salt Intake, Renal Salt Handling, Blood Pressure, and Cardiovascular Diseases

Meneton

Jeunemaı̂tre²,

Wardener³

et al. 2005

Physiological Reviews

591

456

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Epidemiological, migration, intervention, and genetic studies in humans and animals provide very strong evidence of a causal link between high salt intake and high blood pressure. The mechanisms by which dietary salt increases arterial pressure are not fully understood, but they seem related to the inability of the kidneys to excrete large amounts of salt. From an evolutionary viewpoint, the human species is adapted to ingest and excrete <1 g of salt per day, at least 10 times less than the average values currently observed in industrialized and urbanized countries. Independent of the rise in blood pressure, dietary salt also increases cardiac left ventricular mass, arterial thickness and stiffness, the incidence of strokes, and the severity of cardiac failure. Thus chronic exposure to a high-salt diet appears to be a major factor involved in the frequent occurrence of hypertension and cardiovascular diseases in human populations.

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Section: B Links Between An Inadequate Renal Capacity To Excrete a Hmentioning

confidence: 99%

Links Between Dietary Salt Intake, Renal Salt Handling, Blood Pressure, and Cardiovascular Diseases

Meneton

Jeunemaı̂tre²,

Wardener³

et al. 2005

Physiological Reviews

591

456

View full text Add to dashboard Cite

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“…This experimental design identified four different patterns of hemodynamic response to salt-and water-loading, which we reported previously as a brief communication. 20 It is the purpose of the present paper to report detailed sequential hemodynamic changes in 10 patients, their blood volume, total exchangeable sodium, plasma renin concentration during volume expansion, and to discuss the mechanisms responsible for BP regulation.…”

Section: H Ypertension In Anephric Patients Andmentioning

confidence: 99%

Sequential hemodynamic changes in end-stage renal disease and the anephric state during volume expansion.

Kim¹,

Onesti²,

DelGuercio³

et al. 1980

Hypertension

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SUMMARYThe sequence of hemodynamic events during periods of salt-and water-loading was studied in anephric patients and those with end-stage kidney disease. The 10 patients studied showed four different sequential hemodynamic patterns: 1) no significant increase in blood pressure (BP) in two patients; 2) increase lit BP associated with an increase in cardiac output and without change in total peripheral resistance in two patients; 3) increase in BP associated with an increase in total peripheral resistance from the beginning without an increase in cardiac output in fire patients; and 4) increase in BP associated with an initial increase in cardiac output followed by an increase in total peripheral resistance in one patient. There was a significant positive correlation between BP and blood volume and between BP and total exchangeable sodium in the patients in whom salt-and water-loading increased the BP. It is concluded that during salt-and water-loading an initial rise in cardiac output is not necessary to increase BP and that a sustained rise in cardiac output does not always increase the total peripheral resistance. Mechanisms other than whole-body autoregulation play a role in increasing BP during salt-and water-loading in patients deprived of renal excretory function. In patients with end-stage kidney disease, the most important factor responsible for this increase in total peripheral resistance are the vasopressor function of the kidneys 1 ' f and the increase in body salt and water.2 " 1 In anephric patients, salt and water balance plays a major role in the regulation of BP.2 -*~8 The final effect of salt-and water-loading in anephric patients has been found to be an increase in total peripheral resistance.2 '" The precise mechanism by which expansion of body fluid increases BP remains uncertain, however. Received January 9, 1979; revision accepted September 24, 1979.In our previous experience with weekly hemodynamic studies, the BP increase induced by salt-and water-loading was associated with an increase in total peripheral resistance.2 Under similar experimental conditions, Coleman and co-workers 8 reported that the initial hemodynamic change observed during saltand water-loading was an increase in cardiac output; an increase in total peripheral resistance followed.' These findings were interpreted as demonstrating that during the development of this hypertension the initial increase in cardiac output results in perfusion of tissues above their metabolic needs, which in turn elicits myogenic constriction of peripheral vessels, thereby producing an increase in total peripheral resistance. 810 According to this theory, the initial increase in cardiac output is the cause of hypertension, and the subsequent rise in total peripheral resistance is the result.8 -10

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“…However, the hypothesis has been subjected to other criticisms over the past few years. For instance, when dialysis patients were loaded with saline in one study (Kim et al, 1976) the accompanying hypertension was associated usually with an increase in peripheral resistance without an initial phase of high cardiac output. In addition, by changing sodium balance in dogs with experimental hypertension, it was possible to increase cardiac output without changing arterial pressure and to produce hypertension without increasing cardiac output (Stephens etal., 1979).…”

Section: Sodium Excretion In Hypertensionmentioning

confidence: 99%

Aetiology of Hypertension

Swales

1984

British Journal of Anaesthesia

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We are still uncertain of the way in which environment and heredity interact to produce increased arterial pressure in patients with essential hypertension. Few indisputable abnormalities can be demonstrated. Of these there is universal agreement that structural vessel hypertrophy is present and this acts probably as a maintenance and perhaps amplifying system resulting from an initial increase in arterial pressure. It cannot of course explain an increase in arterial pressure ab initio. Most of the well defined systems of arterial pressure control do not show any marked abnormality, although there is some evidence for a modest degree of sympathetic nervous system overactivity. Although some of the changes in cation fluxes across erythrocyte and leucocyte membranes are still debatable, there is general agreement that cation handling by erythrocytes and leucocytes is abnormal in many patients with essential hypertension and that some of these abnormalities are shared by the normotensive relatives of hypertensive patients. The most promising approach is that there is an abnormality of the cell membrane vascular smooth muscle which is partly genetically determined and perhaps also involves the autonomic nervous system. This produces an increased pressor response to environmental stimuli which becomes perpetuated and perhaps amplified by structural hypertrophy of the resistance vessels.

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The Haemodynamic Response to Salt and Water Loading in Patients with End-Stage Renal Disease and Anephric Man

Cited by 4 publications

References 7 publications

Links Between Dietary Salt Intake, Renal Salt Handling, Blood Pressure, and Cardiovascular Diseases

Links Between Dietary Salt Intake, Renal Salt Handling, Blood Pressure, and Cardiovascular Diseases

Sequential hemodynamic changes in end-stage renal disease and the anephric state during volume expansion.

Aetiology of Hypertension

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