Plasma Volume After Posture Change in Hypertensive Subjects

Eisenberg, Seymour; Wolf, P

doi:10.1001/archinte.1965.03860130019003

Cited by 29 publications

(2 citation statements)

References 13 publications

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“…Seven additional subjects had plasmapheresis 12 h before and 36 h after administration of etiocholanolone, and their serum was analysed for the present study at hours 6,30 and 54. These time-points were at least 18 h after the last plasmapheresis and at the same time of day (06.00 h) to avoid differences in plasma volume due to postural changes [20].…”

Section: Study Subjects and Protocolmentioning

confidence: 99%

Serum amyloid A and high density lipoproteins during the acute phase response

Bausserman

Bernier

Herbert

1988

Eur J Clin Investigation

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Serum amyloid A and high density lipoprotein (HDL) interrelationships were evaluated in 11 normal men during an acute phase response induced by the inflammatory steroid etiocholanolone. Compared with baseline, HDL-cholesterol levels were significantly elevated at 30 h but not at 50 h (P less than 0.05) after etiocholanolone. A-apoprotein concentrations were unchanged at 30 h but were reduced at 54 h (P less than 0.01). Four subjects were sampled every 6-8 h for 5 days. Two men had peak SAA concentrations of 30 and 33 mg dl-1. Their A-apoprotein levels declined as SAA rose and remained low even after SAA levels had returned to baseline. High density lipoprotein cholesterol levels did not fall, however, when SAA was increasing, and fell only after SAA levels declined. No changes in HDL-cholesterol or protein were observed in two subjects whose peak SAA concentrations were 10 and 12 mg dl-1. These observations suggest that a threshold level of acute phase response is required before HDL reductions occur. Column chromatography of SAA-rich plasma did not demonstrate the presence of either SAA or A-apoproteins that were unassociated with lipoproteins. Serum amyloid A, moreover, demonstrated little capacity to displace A-proteins from HDL at SAA concentrations typically observed during the acute phase response. We infer from these studies that SAA may substitute for the A-apoproteins and temporarily maintain HDL-cholesterol levels; but that low HDL levels during the acute phase response are likely due to reduced A-protein synthesis rather than displacement by SAA.

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Section: Study Subjects and Protocolmentioning

confidence: 99%

Serum amyloid A and high density lipoproteins during the acute phase response

Bausserman

Bernier

Herbert

1988

Eur J Clin Investigation

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“…In this altered regulation, aging cannot be excluded as an important factor, although no significant correlation was calculated between the age of the subjects and their blood pressure response to upright posture. In subjects with essential hypertension, the excessive decrease in upright systolic pressure could be related to an exaggerated decrease in blood volume (24); this possibility could be predominant in subjects with a more severe stable hypertension (group n B ), because a contraction of plasma volume occurs with diastolic pressures over 105 mm Hg (25). In subjects with essential hypertension, the absence of an increase in upright diastolic pressure could be related to a defect in sympathetic response.…”

Section: Discussionmentioning

confidence: 99%

Autonomic Nervous System and Benign Essential Hypertension in Man

Cuche

Küchel

Barbeau

et al. 1974

Circulation Research

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The effect of upright posture as a physiological stimulus of the adrenergic nervous system was studied in 56 subjects with benign essential hypertension. The subjects received a controlled-sodium diet. Blood pressure, heart rate, catecholamines, plasma renin activity, and urinary creatinine, sodium, and potassium excretion were measured in the recumbent and upright positions. We found an alteration in the blood pressure response in subjects with benign essential hypertension; the postural increase in the mean blood pressure in normotensive subjects (3.18 ± 1.35 mm Hg) progressively disappeared and was replaced by a postural decrease in subjects with more severe stable hypertension (-6.71 ± 2.42 mm Hg). The hypertensive subjects also lacked the usual increase in urinary excretion of norepinephrine. A significant increase in plasma renin activity associated with a significant decrease in plasma norepinephrine occurred in subjects with labile hypertension with postural tachycardia. Finally, we found a highly significant correlation between the excretion of sodium and potassium in the recumbent position and the retention of both ions in the upright position. KEY WORDSpostural adaptation plasma renin activity urinary dopamine, norepinephrine, and epinephrine plasma norepinephrine orthostatic antinatriuresis renal clearance of norepinephrine• In a previous paper (1), we described the rationale for and the method in which limits between normotension and labile and stable hypertension were determined in recumbent subjects. In the present investigation, these same subjects were exposed to the stimulus of upright posture. This approach was of interest because the reproducible, physiological stimulus of upright posture normally induces activation of hemodynamic and closely related hormonal mechanisms. Hemodynamic studies of subjects with hypertension have shown that the postural stimulus differentiates between subjects who react by an excessive response and those who have an insufficient postural response (2). Hormonal studies have demonstrated a differentiation between subjects who show a

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