Orthostatic Stimulation Research Articles

Comparison of plasma renin and prorenin in healthy infants and children as determined with an enzymatic method and a new direct immunoradiometric assay.

We compared plasma active and inactive renin (prorenin) concentrations and activities in infants and children, as measured with a newly available direct immunoradiometric assay kit for active renin and a widely used enzymatic renin assay (plasma renin activity). The study was performed in 57 healthy infants and children under steady-state conditions and in eight subjects after orthostatic stimulation. Our study; (i) reports concentrations for active and inactive renin determined by the immunoradiometric assay in normal infants and children; (ii) confirms, by use of the immunoradiometric assay, the previously described decrease in plasma active and inactive renin, as measured by the enzymatic assay, with increasing age; and (iii) shows close correlations between the results obtained by immunoradiometric and enzymatic assays for active and inactive renin in normal infants and children.

The Influence of Sodium Restriction on Orthostatic Sympathetic Nervous Activity

To evaluate the influence of low-salt diet on the sympathetic nervous system activity, the adaptation to upright posture in five normal subjects was studied during normal salt and 10mEq sodium and 60-mEq potassium diets. On assuming upright posture, there were similar rises in pulse rate and diastolic blood pressure (BP) but a decline in systolic BP, during both diets. A prompt rise in plasma norepinephrine level during low-sodium diet was greater than during normal diet. Orthostatic response of the plasma epinephrine level was small, although significant, but unaffected by the diets. During normal-sodium diet, plasma renin activity response was delayed, but a prompt and enhanced response was observed during low-sodium diet. These data suggest that sodium deprivation enhances the sympathetic nervous system activity and the orthostatic stimulation of renin release.

Choice of control groups in the appraisal of sympathetic nervous activity in essential hypertension.

1. Plasma noradrenaline concentrations were similar in normotensive and hypertensive outpatients, but were significantly lower in laboratory control subjects. 2. Standing plasma noradrenaline concentrations were similar in all three groups. 3. Urinary vanillyl mandelic acid, catecholamines and metanephrines were also similar in the normotensive and hypertensive groups. 4. Laboratory controls, possibly because of familiarity with the techniques of sphygmomanometry and blood sampling, may attain a 'basal' resting level of sympathetic nervous discharge more readily and rapidly than subjects who are unfamiliar with such procedures. 5. After orthostatic stimulation by standing for 2 min, the activity of the sympathetic nervous system, as determined by pulse rate and plasma noradrenaline concentrations, was similar in the three groups, despite the lower starting values in the laboratory staff. 6. The absence of differences in plasma noradrenaline or urinary catecholamine and metabolite concentrations does not support the hypothesis of excessive sympathetic nervous activity in essential hypertension.

Catecholamine responses to orthostatic stimulation in anephric man

Acute experiments on nephrectomized animals suggest inhibition of adrenergic reflexes in the absence of renal humoral factors. That renal failure patients rendered anephric for control of hypertension also have difficulty with blood pressure regulation is confirmed by the blood pressure instability and hemodialysis shock in anephric patients. In the present study, anephric patients were stimulated by passive orthostatic tilting to the 75°, head-up position. Elevated plasma arterial and venous epinephrine and norepinephrine contents were found at rest and after tilting. The relative increase in circulating catecholamines after tilting is consistent with previous studies in normal patients. The resting elevation of catecholamines in these anephric patients suggests either loss of a renal factor restraining adrenergic activity or a chronic stimulus to sympathetic discharge such as hypovolemia.

Plasma renin activity in primary and secondary depression.

Plasma renin activity (PRA), both in supine and standing position, was investigated in primary and secondary depressed patients. After orthostatic stimulation (standing position) primary depressed patients showed PRA values significantly lower than did those with secondary depression. The authors stress the importance of the peripheral sympathetic system in the control of renin release and discuss the data obtained in the light of some evidence in the literature indicating a possible impairment of transmitter turnover in central and peripheral noradrenergic synapses in the pathogenesis of primary depression.

Reinforcement of reflex epinephrine release by angiotensin II.

ARTICLESReinforcement of reflex epinephrine release by angiotensin IITS Harrison, A Birbari, and JF SeatonTS Harrison, A Birbari, and JF SeatonPublished Online:01 Jan 1973https://doi.org/10.1152/ajplegacy.1973.224.1.31MoreSectionsPDF (914 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByNeurohormonal interactions on the renal oxygen delivery and consumption in haemorrhagic shock-induced acute kidney injury12 August 2013 | Acta Physiologica, Vol. 209, No. 1The Early Endocrine Response to InjuryHypovolaemia can potentiate hypoglycaemic stressinduced adrenaline release in the anaesthetized ratNeuroscience Letters, Vol. 112, No. 2-3Renal modulation of electrically stimulated adrenal medullary secretionJournal of Surgical Research, Vol. 36, No. 2Reversal by naloxone of hemorrhagic shock in anephric catsEuropean Journal of Pharmacology, Vol. 65, No. 1Catecholamine responses to orthostatic stimulation in anephric manJournal of Surgical Research, Vol. 26, No. 4Renin-angiotensin mediation of adrenal catecholamine secretion induced by haemorrhageEuropean Journal of Pharmacology, Vol. 44, No. 2 More from this issue > Volume 224Issue 1January 1973Pages 31-34 Copyright & PermissionsCopyright © 1973 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1973.224.1.31PubMed4345738History Published online 1 January 1973 Published in print 1 January 1973 Metrics