Changes In Plasma Norepinephrine Concentrations Research Articles

The thermic response to food intake in persons with thoracic spinal cord injury.

[Purpose] To investigate the influence of the level of spinal cord injury on the thermic effect of food intake (TEF) in persons with thoracic spinal cord injury. [Subjects and Methods] Seven male subjects with spinal cord injury (SCI; age, 40 ± 6 years) and six able-bodied subjects (AB; age, 37 ± 8 years) volunteered to participate in the present study. The subjects consumed an identical test meal consisting of 7.9 kcal/kg of body weight. Energy expenditure and plasma norepinephrine concentrations were measured over a 3-hour period. [Results] The adjusted TEF at 60 min was almost the same among the three groups [AB, SCI with high thoracic cord (T5–6) injury (HSCI), and SCI with low thoracic cord (T9–12) injury (LSCI)]. Although the LSCI group had almost the same adjusted TEF at 120 min as the AB group, the adjusted TEF at 120 min of the HSCI group was significantly lower than that of the AB group. The changes in plasma norepinephrine concentration and heart rate in response to food intake were similar among the three groups. [Conclusion] SCI at the T5–6 level results in a lower TEF due to sympathetic decentralization.

Subarachnoid hemorrhage induced sympathoexcitation arises due to changes in endothelin and/or nitric oxide activity

The demonstration of the effectiveness of endothelin antagonists and nitric oxide donors in managing vasospasm following subarachnoid hemorrhage is encouraging. Whether such drugs can modify the sympathoexcitation that accompanies this condition remains unknown and was the basis for the present report. Subarachnoid hemorrhage was induced in conscious rats by injecting blood via a catheter placed along the surface of the brain and directed towards the circle of Willis. We combined measurements of arterial plasma catecholamines with the spectral analysis of blood pressure variability in order to examine sympathetic nervous activation following subarachnoid hemorrhage. Experiments were performed in untreated animals and in rats following pretreatment with either bosentan or sodium nitroprusside. Indicative of a pronounced sympathoexcitation, the 0.2-0.6 Hz frequency components of blood pressure were markedly elevated following subarachnoid hemorrhage (2.5 +/- 0.5 vs. 8.9 +/- 2.6 mmHg2, P < 0.01). Parallel changes in plasma norepinephrine concentration were observed (1.0 +/- 0.2 vs. 2.4 +/- 0.4 nmol/l, P < 0.01). The subarachnoid injection of saline did not modify blood pressure variability or plasma norepinephrine concentrations. Pretreatment with either bosentan or sodium nitroprusside completely prevented the subarachnoid hemorrhage induced sympathoexcitation. Experimental subarachnoid hemorrhage is associated with a pronounced activation of the sympathetic nervous system. It would appear that this sympathoexcitation has its roots ensconced in either the release of endothelin or an impairment in nitric oxide mediated vasodilation.

Physiological and psychometric variables for monitoring recovery during tapering for major competition.

This study attempted to identify variables that are useful in monitoring recovery during tapering. Changes in physiological variables, tethered swimming force, mood states, and self-ratings of well-being were measured in 10 elite swimmers from before to after 2 wk of tapering for national championships. Physiological measures included resting heart rate (HR); blood pressure (BP); blood lactate concentration; red blood cell, white blood cell, and differential counts; and plasma cortisol, free testosterone, and catecholamine concentrations. Measures taken after 100-m maximal and 200-m standardized submaximal swims included HR, BP, and blood lactate concentration. Step-down regression analysis showed that changes in plasma norepinephrine concentration, heart rate after maximal effort swimming and confusion as measured by the Profile of Mood States (POMS) predicted the change in swimming time with tapering (r2 = 0.98); the change in plasma norepinephrine concentration predicted the change in swim time with tapering (r2 = 0.82) by itself. These data suggest that recovery after intense training can be monitored during tapering and that an accurate prediction of performance changes may be possible if the changes in a range of physiological and psychological variables are measured.

Role of sympathetic cardiovascular tone in control of arterial pressure in rats with cirrhosis.

Although an increase in sympathetic nervous activity has been recognized in cirrhosis, the contribution of this overactivity to the regulation of arterial pressure is unknown. The arterial pressure response to increasing doses of hexamethonium (0.05 to 3.2 mg.kg-1.min-1), a ganglionic blocker that decreases sympathetic cardiovascular tone, was explored in normal rats and in two models of portal hypertension, i.e., rats with cirrhosis and rats with portal vein stenosis. Changes in plasma norepinephrine concentrations were greater in rats with cirrhosis (356 +/- 50 vs 166 +/- 30 pg/ml, p = 0.04) than in normal rats (186 +/- 23 vs 86 +/- 31 pg/ml, p = 0.06) and rats with portal vein stenosis (103 +/- 37 vs 93 +/- 5 pg/ml, p = 0.10). The maximum decrease in arterial pressure was obtained at a dose of 1.6 mg.kg-1.min-1 in each group. However, the decrease in arterial pressure was significantly greater in rats with cirrhosis (-25 +/- 2%) than in normal rats (-11 +/- 1%) and in rats with portal vein stenosis (-13 +/- 2%) (p = 0.04). In conclusion, the results of this study suggest that the sympathetic cardiovascular tone is more important for the maintenance of arterial pressure in rats with cirrhosis than in normal rats and in rats with portal vein stenosis.

Blunted systemic, splanchnic, and renal hemodynamic responses to atrial natriuretic peptide in rats with cirrhosis

Systemic, splanchnic and renal hemodynamic responses to saline, physiological (25 ng.kg-1.min-1) and pharmacological (100, 300 and 600 ng.kg-1.min-1) doses of alpha human atrial natriuretic peptide were measured in normal (n = 7 for saline and 7-8 for each dose of atrial natriuretic peptide) and cirrhotic (n = 7 for saline and 7-8 for each dose of atrial natriuretic peptide), conscious, unrestrained rats. In addition, plasma norepinephrine concentrations were measured in normal and cirrhotic rats, before and following a 300-ng.kg-1.min-1 dose of atrial natriuretic peptide. In cirrhotic rats, splanchnic, renal and systemic hemodynamics were not significantly affected by either physiological or pharmacological doses of atrial natriuretic peptide. In normal rats, a 300 ng.kg-1.min-1 dose of atrial natriuretic peptide significantly decreased cardiac index, portal tributary blood flow and renal blood flow, and significantly increased vascular resistance in the systemic, portal, and renal territories. The other doses of atrial natriuretic peptide did not significantly change regional and systemic hemodynamics. Atrial natriuretic peptide-induced changes in plasma norepinephrine concentrations were significantly higher in normal than in cirrhotic rats (1827 +/- 834 vs. 59 +/- 46 pg/ml, mean +/- S.E., respectively). In conclusion, this study shows that the normal cardiovascular response to a 300 ng.kg-1.min-1 atrial natriuretic peptide infusion is blunted in cirrhotic rats. Moreover, in cirrhotic rats, blunting of vasoconstriction following atrial natriuretic peptide administration seems to be due to a lack of increased sympathetic vascular tone.

Arterial underfilling does not cause sodium retention in cirrhosis

purpose: To test the peripheral arterial vasodilation hypothesis of sodium retention in cirrhosis. This states that sodium retention is triggered by arterial underfilling and predicts that development of sodium retention will be associated with significant and related declines in indices of arterial filling that reverse when sodium retention resolves. design: Longitudinal evaluation of a cohort of patients with alcoholic liver disease. patients and methods: Eighteen men, 8 of whom were studied twice, 3 three times, 2 four times, and 5 five times (40 between-study comparisons). Between 23 studies, the patients were ascites-free (Group NN). Ascites spontaneously disappeared between seven studies (Group YN), appeared between six studies (Group NY), and remained present between four studies (Group YY). Between-study changes in blood volume, arterial blood pressure, cardiac output, systemic vascular resistance, left atrial volume, left ventricular diastolic diameter, aortic root diameter, aortic blood velocity, plasma norepinephrine and atrial natriuretic factor concentrations, plasma renin activity, and urinary sodium excretion were evaluated by paired t-tests. These changes were also compared among groups by analysis of variance. In addition, correlations among the changes were sought. results: Systolic, diastolic, and mean arterial pressures, left ventricular diastolic diameter, aortic root diameter, stroke volume, cardiac output, plasma norepinephrine concentration, and systemic vascular resistance were unchanged between studies. Left atrial volume increased between studies in Group NY. Pulse pressure fell more in Group NY than in Groups NN and YN, principally as a result of a decline in systol ic blood pressure. Plasma norepinephrine concentration, plasma renin activity, and blood volume rose more in Group NY than in Groups NN, YN, and YY. Changes in both systolic and pulse pressures were directly correlated with the change in sodium excretion but unrelated to the change in plasma norepinephrine concentration. Changes in plasma norepinephrine concentration and plasma renin activity were unrelated to changes in blood pressure, systemic vascular resistance, and urinary sodium excretion. conclusions: None of the indices of arterial filling tested except pulse pressure were related to sodium retention. Reduced pulse pressure is inconsistent with arterial underfilling, as peripheral vasodilation instead increases pulse pressure by increasing diastolic run-off. These data do not support the hypothesis that arterial underfilling is the stimulus for sodium retention in alcoholic cirrhosis.

本態性高血圧患者における運動負荷時の心血行動態に及ぼすａｍｌｏｄｉｐｉｎｅの影響

The effects of amlodipine, a Ca2+-channel blockade, on hemodynamic and hormonal responses to exercise were evaluated in patients with essential hypertension. In 7 patients (WHO stage, I, II), the exercise by bicycle ergometer was done before and after amlodipine treatment (5mg/day, 2-4wk). The hemodynamic responses to exercise were evaluated by changes in systolic and diastolic blood pressure, heart rate, cardiac output measured by UCG, and total peripheral resistance. In addition, plasma norepinephrine concentration (PNE) and renin activity (PRA) were measured at rest and peak exercise. A significant rise in systolic and diastolic blood pressure associated with tachycardia was observed during exercise. An increase in cardiac output was also observed, but the total peripheral resistance decreased by exercise. The PNE and PRA were increased by exercise. Amlodipine reduced both basal blood pressure and exercise-induced rise in blood pressure. On the other hand, the basal heart rate and exercise-induced increase in heart rate were not affected by amlodipine treatment. These changes were similar to those in pretreatment of amlodipine. Amlodipine did not produce any significant changes in PNE both at rest and during exercise. Although the PRA at rest was increased by amlodipine treatment, the increase in PRA induced by exercise was unaffected by amlodipine. These findings indicate that amlodipine might have some different effects on hemodynamics and hormones compared with the other Ca2+-channel blockades which produce an enhanced response of hemodynamics and hormonal system to exercise.

A study of some potential correlates of the hypotensive effects of prolonged submaximal exercise in normotensive men.

This study was undertaken (1) to examine the relation of plasma catecholamine and insulin levels to the blood pressure response during and after submaximal exercise, (2) to verify whether the blood pressure response to an epinephrine infusion is associated with the blood pressure response to a prolonged submaximal exercise, and (3) to study some potential correlates of the hypotensive effect of prolonged aerobic exercise. Nine normotensive young men (mean age 22.0 +/- 1.4 years) were subjected to a 1-h epinephrine infusion protocol and a 1-h submaximal exercise test on a cycle ergometer. The two tests were performed 1 week apart. The physiological and hormonal responses observed during the submaximal exercise test were generally greater than those observed during the epinephrine infusion test. Blood pressure responses in both tests showed no significant association with changes in plasma insulin levels. Changes in plasma norepinephrine concentration were positively correlated with changes in systolic blood pressure during the submaximal exercise test but not during the epinephrine infusion. Results also showed that the blood pressure response to epinephrine infusion was not correlated with the blood pressure response to submaximal exercise. However, post-exercise and post-infusion systolic blood pressure responses (differences between "post-test" and "resting" values) were significantly associated (r = 0.81, p less than 0.01). In addition, a significant hypotensive effect of submaximal exercise was observed for both systolic and diastolic blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular responses to bicuculline in the paraventricular nucleus of the rat.

The present study was undertaken to determine whether gamma-aminobutyric acid in the paraventricular nucleus contributes to the regulation of cardiovascular function. Blood pressure and heart rate were recorded and plasma catecholamines were measured in conscious rats receiving microinfusions of either artificial cerebrospinal fluid or a gamma-aminobutyric acid antagonist, bicuculline methiodide, bilaterally into the paraventricular nucleus. Artificial cerebrospinal fluid had no effect on any of the recorded variables. In contrast, infusion of bicuculline into the region of the paraventricular nucleus produced increases in blood pressure (20 +/- 2 mm Hg), heart rate (110 +/- 11 beats/min), and plasma concentrations of norepinephrine (640 +/- 107 pg/ml) and epinephrine (1,266 +/- 267 pg/ml). Pretreatment with a ganglionic blocking agent abolished both the blood pressure (-1 +/- 2 mm Hg) and heart rate (5 +/- 18 beats/min) effects. Bilateral adrenal medullectomy reduced the changes in plasma norepinephrine concentrations (81 +/- 14 pg/ml) significantly and abolished the changes in plasma epinephrine concentrations (5 +/- 4 pg/ml). Conversely, adrenal medullectomy reduced the pressor effects (18 +/- 2 mm Hg) only slightly while the heart rate responses were attenuated (42 +/- 9 beats/min) by approximately 50%. These results suggest that an endogenous gamma-aminobutyric acid system exerts a tonic inhibitory effect on the sympathetic nervous system at the level of the paraventricular nucleus of the hypothalamus.

Sympathoinhibitory effects of atrial natriuretic factor in normal humans.

In rats, atrial natriuretic factor (ANF) reduces sympathetic nerve activity (SNA) reflexively by sensitizing cardiac mechanoreceptors with inhibitory vagal afferents. We performed three series of experiments in 26 normal young men to document whether ANF inhibits SNA in humans and if so, to determine potential mechanisms for this phenomenon. First, we recorded muscle SNA before and during brief infusions of ANF, vehicle (saline solution), and sodium nitroprusside, titrated to achieve reductions similar to those produced by ANF in diastolic pressure and central venous pressure, and we also assessed the effect of ANF on sympathetic nerve responses to a cold pressor test (CPT). Second, we determined the effect of ANF on Doppler-derived measurements of cardiac output and responses to hypotensive (-40 mm Hg) lower-body negative pressure (LBNP) and its sudden cessation. Third, we applied nonhypotensive (-15 mm Hg) LBNP to selectively unload cardiopulmonary baroreceptors, and we released LBNP to stimulate these inhibitory afferents during sequential infusions of nitroglycerin, vehicle (saline solution), and ANF. Our key findings were that 1) reductions in arterial and central venous pressures during ANF infusion were not accompanied by anticipated reflex increases in muscle SNA; 2) ANF blunted the increase in SNA with CPT; 3) ANF increased stroke volume and cardiac output; and 4) sympathoneural responses to both the application and the sudden cessation of nonhypotensive LBNP were attenuated, not augmented, by ANF. Changes in plasma norepinephrine concentrations reflected these sympathetic nerve responses to ANF. These results do not support the concept that ANF inhibits sympathetic outflow reflexively in humans by increasing discharge from cardiac mechanoreceptors with inhibitory vagal afferents but are consistent with either a central or a ganglionic sympathoinhibitory action of ANF. ANF could facilitate hypotension and natriuresis in humans by attenuating the reflex sympathetic response to baroreceptor deactivation.

Relation between plasma norepinephrine and response to medical therapy in men with congestive heart failure secondary to coronary artery disease or idiopathic dilated cardiomyopathy

This study examines the relation between the change in clinical status and the change in plasma norepinephrine concentration in patients with congestive heart failure (CHF) receiving standard medical therapy. Hemodynamic measurements in 11 patients with CHF (ejection fraction 19 ± 4%) were obtained before and immediately after the administration of digoxin and angiotensin-converting enzyme inhibitors. Patients were then followed for 1 year. Clinical status was determined using the Boston Clinical Heart Failure scoring system. Of the 11 patients, 6 demonstrated significant clinical improvement after therapy, based on the Boston score, over a 1-year period. Five patients did not respond to therapy: 4 died and the remaining patient had worsening CHF. There was no difference between responders and nonresponders in either baseline hemodynamics or acute response to the administration of digoxin and an angiotensin-converting enzyme inhibitor. In the patients who improved, plasma norepinephrine decreased from 706 ± 235 to 545 ± 223 pg/ml (p = 0.08) after 1 year of medical therapy. In patients whose CHF worsened or who died, plasma norepinephrine increased from 715 ± 275 at baseline to 1,237 ± 671 pg/ml at their last measurement (p = 0.06). Although at baseline the plasma norepinephrine levels were similar in both groups of patients, a significant difference between responders and nonresponders was observed at final follow-up (p < 0.002). Change in plasma norepinephrine correlated with change in CHF score (r = 0.79, p < 0.004). Thus, in patients with CHF, serial measurements of plasma norepinephrine correlate with changes in cynical status.

Factors determining sodium chloride sensitivity of patients with essential hypertension

Factors which determine sodium chloride sensitivity, defined as the difference between the mean blood pressure after 1 week of a low sodium chloride diet (3 g/day) and that after 1 week of a high sodium chloride diet (20 g/day), were studied in 60 inpatients with essential hypertension using a multivariate analysis. The sodium chloride sensitivity was independently correlated with the change in erythrocyte sodium concentration (r = 0.47) and with the change in plasma renin activity (r = 0.29); but it was not related to basal blood pressure, the change in plasma volume of the change in plasma norepinephrine concentration. These data suggest that both intracellular sodium accumulation and inadequate suppression of the renin-angiotensin system may be independently involved in the elevation of blood pressure after sodium chloride loading. We could not find the independent importance of volume retention, hyperadrenergic activity or basal blood pressure in the sodium chloride sensitivity.

The Effect of General and Regional Anesthesia on Tourniquet-Induced Blood Pressure Elevation

This study was undertaken to determine if blood pressure elevation associated with the use of a pneumatic tourniquet during lower extremity surgery is related to the type of anesthesia used. A possible hormonal cause for the blood pressure elevation was also sought. Thirty patients undergoing operation on the leg requiring use of a tourniquet were divided into three equal groups. Each group received either general, spinal, or epidural anesthesia. A blood sample was collected before induction of anesthesia, immediately before inflation of the tourniquet, 30 minutes after inflation, and 5 minutes after deflation of the tourniquet. Plasma concentrations of norepinephrine, epinephrine, cortisol, and glucose were assayed. Systolic, diastolic, and mean blood pressures and pulse rate were recorded every minute during induction of anesthesia and then at 5-minute intervals using an automated blood pressure monitor. Thirty minutes after inflation of the tourniquet, mean blood pressure rose only in the general anesthesia group. No change in plasma norepinephrine concentration was observed in any group. A fall in plasma epinephrine concentration occurred after the induction of spinal anesthesia. Five minutes after the tourniquet was released, plasma cortisol concentration rose in the general anesthesia group as did norepinephrine concentration in the epidural group. The cause of the blood pressure elevation during general anesthesia could not be ascribed to activation of the hypophyseal-adrenal axis. Other possibilities are discussed.

Preferential inhibitory effect of nifedipine on angiotensin II-induced renal vasoconstriction.

The inhibitory effects of nifedipine on renal vasoconstrictor response to angiotensin II, norepinephrine, or renal nerve stimulation were tested in anesthetized dogs. Intrarenal infusions of nifedipine (0.3, 1, and 3 micrograms/min) dose-dependently suppressed the renal vasoconstriction induced by intrarenal injections of angiotension II (0.03, 0.05, and 0.1 microgram) or norepinephrine (0.3-1 micrograms) but not that by renal nerve stimulation (4-7 Hz). However, the inhibitory effect of nifedipine on angiotensin II-induced vasoconstriction was greater than its effect on norepinephrine-induced or renal nerve stimulation-induced vasoconstriction (i.e., 50% reduction in renal blood flow). Furthermore, a greater renal vasodilation induced by intrarenal bolus injections of nifedipine (1,3, and 10 micrograms) but not by acetylcholine (0.1 and 0.3 microgram) was observed during the reduction in the perfusion pressure of the contralateral kidney to approximately 50 mm Hg, which resulted in an increase in plasma renin activity and plasma angiotensin II concentration but no change in plasma norepinephrine concentration. There was a significant positive correlation between plasma renin activity and plasma angiotensin II concentration before nifedipine injections and the subsequent increase in renal blood flow produced by each dose of nifedipine. These results indicate that nifedipine has a relatively preferential inhibitory effect on the renal vasoconstriction produced by both exogenous and endogenous angiotensin II in canine renal vasculature.

Captopril modifies the hemodynamic and neuroendocrine responses to sodium nitroprusside in hypertensive patients.

To determine if clinically effective doses of the antihypertensive agent captopril affected the neuronal release of norepinephrine or baroreflex sensitivity, changes in plasma norepinephrine concentration and heart rate were related to the changes in mean arterial pressure seen during the intravenous infusion of stepwise incremental doses of sodium nitroprusside before and during captopril treatment in eight hypertensive men with normal or low plasma renin activity. At all times, significant linear correlations were found between the decrease in mean arterial pressure and the dose of sodium nitroprusside, the increase in heart rate and the decrease in mean arterial pressure, and the increase in plasma norepinephrine concentration and the decrease in mean arterial pressure. When the subjects were treated with captopril (25 mg t.i.d.) for 2 to 4 weeks, supine mean arterial pressure decreased from 130 to 114 mm Hg (-12%; p less than 0.05), heart rate did not change, supine and upright plasma renin activity increased, while supine plasma norepinephrine and epinephrine concentration decreased slightly. Therapy with captopril (25 mg t.i.d.) increased baroreflex sensitivity, as assessed by the slope of the regression line relating the increase in heart rate to the decrease in mean arterial pressure, and increased the responsiveness of the sympathetic nervous system, as assessed by the slope of the regression line relating the increase in plasma norepinephrine concentration to the decrease in mean arterial pressure. These increases were accompanied by a decrease in the slope of the regression line relating the decrease in mean arterial pressure to the dose of sodium nitroprusside and thus were associated with a decreased sensitivity to the vasodepressor effects of sodium nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma norepinephrine concentration reflects pharmacological alteration of sympathetic activity in the conscious cat

This study (1) provides the first comprehensive set of basal values for hemodynamic variables, plasma norepinephrine (NE) and epinephrine concentrations and plasma renin activity in the conscious cat and (2) demonstrates that changes in plasma NE concentration in the conscious cat accurately reflect the alterations in sympathetic discharge caused by hydralazine, yohimbine, chlorisondamine and clonidine.

Increased circulating plasma norepinephrine concentrations in noncardiac causes of pulmonary hypertension.

Sympathetic nervous system (SNS) activity and circulating norepinephrine (NE) levels may play roles in the elevated pulmonary vascular resistance (PVR) found in patients with pulmonary hypertension. To study the relationship between plasma NE levels, pulmonary NE metabolism, and pulmonary hypertension, we studied 9 patients, suspected of having noncardiac causes of pulmonary hypertension, before and after vasodilator therapy with phentolamine, nitroglycerin, isoproterenol, or hydralazine. Patients were admitted to the ICU and studied using pulmonary artery thermodilution catheters. Seven of 9 patients had noncardiogenic pulmonary hypertension whereas 2 patients did not have hemodynamic evidence of pulmonary hypertension. Simultaneous pulmonary and radial artery samples were analyzed for plasma NE and epinephrine (EPI) content before and after various vasodilator agents. Baseline pulmonary artery (PA) and radial artery NE concentrations correlated (r = .72) with PVR, PA pressures, and PA minus pulmonary capillary wedge (WP) pressures and were increased compared to the 2 patients with normal pulmonary pressures (p less than .01). The normal pulmonary extraction of circulating NE was absent in the 7 patients with pulmonary hypertension. PVR decreased significantly in all 7 patients with each vasodilator (p less than .05); however, the decrease was independent of any change in plasma NE concentration and therapy had no effect on the pulmonary extraction of circulating NE. These data indicate that elevations in plasma NE are coincident with the presence of noncardiogenic pulmonary hypertension and that acute pharmacologic reduction of PVR does not normalize the loss of pulmonary NE metabolism.

Cardiovascular, Humoral, and Renal Effects of Phenoxybenzamine in Hypertension

We examined the effects of alpha adrenergic receptor blockade with phenoxybenzamine on various parameters related to blood pressure regulation in 10 normotensive and 12 essential hypertensive subjects. The responses were observed before and after phenoxybenzamine treatment during standardized maneuvers of volume expansion with saline infusion and volume contraction with a diuretic. Alpha adrenergic blockade produced a significantly greater (P less than 0.02) reduction in blood pressure in the hypertensive group than in the normotensive subjects. The baroreceptor response, evaluated by comparing the change in plasma norepinephrine concentration in relation to the change in blood pressure, was significantly reduced (P less than 0.05) in hypertensives compared to normal subjects. Plasma and urinary norepinephrine concentration, which were similar in the two groups, increased in both during phenoxybenzamine treatment. There was no significant change in the mean levels of plasma renin activity or plasma aldosterone concentration in either group after phenoxybenzamine treatment. However, the relationship between plasma renin activity and plasma aldosterone levels, as judged by linear regression analysis, was significantly altered (P less than 0.05) by phenoxybenzamine therapy in both groups. The latter may reflect an effect of phenoxybenzamine on the metabolism or secretion of aldosterone. These results, utilizing an alpha adrenergic antagonist, confirm the enhanced vascular reactivity and diminished baroreceptor function in essential hypertension; no evidence for an alpha adrenergic effect on plasma renin activity could be demonstrated in normotensive or hypertensive subjects.