The Second Sir George Pickering Memorial Lecture What Regulates Whole Body Autoregulation? Clinical Observations

Ma, Santos; Aj, Man in't Veld; Gj, Wenting

doi:10.1097/00004872-198504000-00001

Cited by 29 publications

(14 citation statements)

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“…A seminal advance in elucidating the pathophysiology of hypertension was the introduction of the concept of long-term1 “whole body autoregulation” of blood flow [53] and its experimental verification [16, 18, 54, 55]. These studies showed that salt retention and consequent plasma volume expansion initially elevates BP because of an increase in CO. With sustained volume expansion, even for just a few days, however, the CO declines and TPR increases to maintain the elevated BP.…”

Section: Whole Body Autoregulationmentioning

confidence: 99%

“…Thus, relatively normal CO and elevated TPR are routinely observed in established hypertension [11]. Nevertheless, in experimentally-induced hypertension, for example with mineralocorticoids [55] or renal artery clipping [56], a transient initial state of increased CO can often be detected. Failure to observe this high CO stage could be the result of compensatory mechanisms (“autoregulation”) that turn on very shortly after the volume starts to expand.…”

Section: Whole Body Autoregulationmentioning

confidence: 99%

“…This corresponds to a condition of “virtual hypervolemia,” however, because blood volume is still inappropriately high relative to the BP [21]. Importantly, the effects of volume expansion on TPR and BP are rapidly reversed if the stimulus (e.g., the volume load or the mineralocorticoid and salt) is withdrawn [54, 55, 57, 58]. This implies that the (initial) rise in TPR must be functional and not structural, and it must almost certainly be hormonal because this “autoregulation” involves all of the vasculature, veins as well as arteries, and pulmonary as well as systemic vessels [59].…”

Section: Whole Body Autoregulationmentioning

confidence: 99%

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Signaling mechanisms that link salt retention to hypertension: Endogenous ouabain, the Na+ pump, the Na+/Ca2+ exchanger and TRPC proteins

Blaustein

Hamlyn

2010

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Salt retention as a result of chronic, excessive dietary salt intake, is widely accepted as one of the most common causes of hypertension. In a small minority of cases, enhanced Na+ reabsorption by the kidney can be traced to specific genetic defects of salt transport, or pathological conditions of the kidney, adrenal cortex, or pituitary. Far more frequently, however, the salt retention may be the result of minor renal injury or small genetic variation in renal salt transport mechanisms. How the salt retention actually leads to the increase in peripheral vascular resistance (the hallmark of hypertension) and the elevation of blood pressure remain an enigma. Here we review the evidence that endogenous ouabain (an adrenocortical hormone), arterial smooth muscle α2 Na+ pumps, type-1 Na/Ca exchangers, and receptor- and store-operated Ca2+ channels play key roles in the pathway that links salt to hypertension. We discuss cardenolide structure-function relationships in an effort to understand why prolonged administration of ouabain, but not digoxin, induces hypertension, and why digoxin is actually anti-hypertensive. Finally, we summarize recent observations which indicate that ouabain upregulates arterial myocyte Ca2+ signaling mechanisms that promote vasoconstriction, while simultaneously downregulating endothelial vasodilator mechanisms. In sum, the reports reviewed here provide novel insight into the molecular mechanisms by which salt retention leads to hypertension.

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Section: Whole Body Autoregulationmentioning

confidence: 99%

Section: Whole Body Autoregulationmentioning

confidence: 99%

Section: Whole Body Autoregulationmentioning

confidence: 99%

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Signaling mechanisms that link salt retention to hypertension: Endogenous ouabain, the Na+ pump, the Na+/Ca2+ exchanger and TRPC proteins

Blaustein

Hamlyn

2010

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…When supine, patients with autonomic failure often raise their blood pressure, sometimes to hypertensive levels. This increases renal perfusion pressure and probably contributes to recumbency‐induced polyuria (Schalekamp et al. , 1985; Kooner et al.…”

Section: Fluid Depletion and Its Correctionmentioning

confidence: 99%

Water drinking in the management of orthostatic intolerance due to orthostatic hypotension, vasovagal syncope and the postural tachycardia syndrome

Mathias

Young

2004

Euro J of Neurology

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Water drinking recently has been shown to raise blood pressure in normal subjects and in patients with autonomic failure who have orthostatic hypotension. However, in normal young subjects, ingestion of approximately 500 ml has no pressor effect; but in older subjects there is an increase in blood pressure. An even greater rise in blood pressure occurs in cases with autonomic failure. The possible mechanisms responsible for the pressor response to water include neural and humoral factors; fluid redistribution also needs to be considered. This review will concentrate on the water pressor response in normal subjects and different groups of patients with autonomic diseases who have orthostatic intolerance, on the mechanisms that could be involved, and on whether this pressor response may be used in the management of orthostatic hypotension, vasovagal syncope and the postural tachycardia syndrome.

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“…Alternative measures were considered by Mathias et al [9] to reduce fluid loss overnight and improve morning orthostatic hypotension. They were aware that recumbency and restitution of blood pressure, sometimes with a degree of supine hypertension, increased sodium excretion [10]. The antidiuretic hormone vasopressin was a possible choice to reduce nocturnal polyuria, but it also had effects on vasopressin-1 receptors that result in an exaggerated pressor response in patients supersensitive to a variety of vasoactive agents [11].…”

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confidence: 99%

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Young

2003

Clinical Autonomic Research

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The Second Sir George Pickering Memorial Lecture What Regulates Whole Body Autoregulation? Clinical Observations

Cited by 29 publications

References 0 publications

Signaling mechanisms that link salt retention to hypertension: Endogenous ouabain, the Na+ pump, the Na+/Ca2+ exchanger and TRPC proteins

Signaling mechanisms that link salt retention to hypertension: Endogenous ouabain, the Na+ pump, the Na+/Ca2+ exchanger and TRPC proteins

Water drinking in the management of orthostatic intolerance due to orthostatic hypotension, vasovagal syncope and the postural tachycardia syndrome

Plugging the leak

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