Adrenaline infusion in man increases muscle sympathetic nerve activity and noradrenaline overflow to plasma

This study was conducted to determine if muscle sympathetic nerve activity (MSA) and/or the neuronal release of noradrenaline per impulse are modulated by adrenaline in the physiological plasma concentration range. We gave step-wise infusions of adrenaline (0.05-0.6 nmol/kg per min) to 10 healthy young men and measured: intra-arterial blood pressure; heart rate; central venous pressure (CVP); efferent MSA (microneurography in the peroneal nerve); arterial (brachial artery) and femoral venous plasma concentrations of noradrenaline, and the spillover of noradrenaline to arterial and venous plasma (radiotracer infusion). The infusion of adrenaline caused a fall in diastolic blood pressure and tachycardia, and was associated with increases in MSA and noradrenaline spillover. These observations suggest that part of the adrenaline-induced increase in transmitter release is due to enhanced nerve impulse activity, but such a conclusion rests on the absence of diffusion limitations from the site of noradrenaline infusion into the blood stream. After termination of adrenaline infusion the tachycardia and elevated plasma noradrenaline levels persisted, but these changes were probably due mainly to a profound increase in nerve activity. Concurrently, there was a reduction in CVP which may have triggered the increase in efferent sympathetic nerve activity. Infusions of adrenaline did not influence the clearance of noradrenaline from arterial plasma, but the fractional extraction over the leg was moderately reduced, indicating that more arterial noradrenaline is recovered in venous plasma during adrenaline infusion. The present data suggest that the reasons for the adrenaline-induced increase in noradrenaline release are complex, but they are consistent with the hypothesis that stress levels of adrenaline enhance sympathetic nerve activity, and that circulating adrenaline may modulate both haemodynamic and neural responses to stress.     

Atrial natriuretic peptide attenuates the reflex sympathetic responses to lower body negative pressure

The authors studied the effect of intravenous infusion of atrial natriuretic peptide (ANP) on the plasma catecholamine and forearm vasoconstrictor responses to cardiopulmonary baroreflex deactivation in six normal, male volunteers in order to determine whether ANP influences reflex forearm vasoconstriction in humans. Unloading of low-pressure cardiopulmonary baroreceptors (CPBR) was accomplished by application of low levels (-10 and -20 mm Hg) of lower body negative pressure (LBNP). The authors measured the plasma norepinephrine (NE) and epinephrine, the mean arterial pressure (MAP), and the forearm vascular resistance (FVR) responses to reflex sympathetic activation by LBNP. ANP infusion (0.1 microgram.kg-1.min-1) decreased (p less than 0.01) basal MAP, as well as plasma renin activity and plasma aldosterone levels (p less than 0.05). ANP infusion also reduced (p less than 0.01) plasma NE responses to both levels of LBNP and tended to decrease both epinephrine and FVR during ANP infusion at -20 mm Hg LBNP (p = 0.8). These data suggest that exogenous ANP inhibits the reflex sympathetic responses that occur with CPBR unloading. The blunted plasma NE responses to CPBR unloading parallel the attenuation of FVR response to LBNP during ANP infusion, despite significant LBNP-induced hypotension.     

Antidiuretic Hormone and Atrial Natriuretic Peptide During Lower Body Negative or Positive Pressure in Hypertensive Patients with and Without Left Ventricular Hypertrophy

Aim of the study was to evaluate the effect of cardiopulmonary receptors activation and deactivation on antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) incretion in hypertensive and normotensive subjects.

Twenty-one male subjects, 7 normotensives and 14 mild hypertensives, 7 without and 7 with left ventricular hypertrophy (LVH) were admitted to the study. Each subject underwent selective loading and unloading of cardiopulmonary receptors, by application of a positive (LBPP) or negative (LBNP) pressure to the lower body. Blood samples were taken for measurement of ANP, ADH, PRA, immunoreactive renin, aldosterone, noradrenaline and adrenaline.

ADH plasma concentration increased during cardiopulmonary receptors inhibition, but this increase became statistically significant (p<0.05) at a step of LBNP (-40 mm Hg), in which an involvement of the sinoaortic receptors cannot be excluded.

ANP plasma levels increased progressively during LBPP (p<0.05 at least).

These changes were significantly reduced in hypertensive patients with LVH.     

Attenuation of reflex forearm vasoconstriction by alpha-human atrial natriuretic peptide in men

This study examined whether atrial natriuretic peptide (ANP) modulates reflex forearm vasoconstriction in humans. Synthetic alpha-human ANP (alpha-hANP) was infused at a rate of 0.03 microgram/kg/min in 8 healthy men (mean age 23 +/- 0.7 years, mean +/- SEM). The alpha-hANP decreased systolic blood pressure and central venous pressure (CVP) but did not significantly alter resting heart rate and forearm vascular resistance (FVR). The magnitudes of reflex increases in FVR during lower body negative pressure (LBNP) at -110, -20, and -40 mm Hg were less during infusion of alpha-ANP than those magnitudes during infusion of saline solution. The slope of the regression line relating changes in CVP and those in FVR was less during infusion of alpha-hANP than the slope during infusion of saline solution. Forearm vascular responses to intra-arterial infusion of norepinephrine at doses of 100, 200, and 500 ng/min did not significantly differ during infusion of alpha-hANP and saline solution. These results suggest that alpha-hANP attenuates cardiopulmonary baroreflex control of FVR in normal men.     

Regulation of plasma atrial natriuretic peptide and the cardiopulmonary baroreflex in the rat

To study the physiological regulation of atrial natriuretic peptide (ANP), we examined the effects of volume expansion and depletion and the influence of cardiopulmonary baroreflex on plasma ANP levels in pentobarbital-anesthetized male Wistar rats. The volume expansion by acute intravenous saline infusion (2% of body weight) increased central venous pressure (CVP) and decreased heart rate (HR) in rats with intact baroreflex. The plasma ANP level in the volume expanded group was significantly higher than that in the control rats (453 +/- 100 vs 170 +/- 40 pg/ml, p less than 0.01). Conversely the plasma ANP level decreased from 214 +/- 15 to 125 +/- 13 pg/ml (p less than 0.01) accompanied by a fall in CVP and an increase in HR after nonhypotensive hemorrhage (0.8% of body weight). Hypotensive hemorrhage (2% of body weight) caused a progressive decrease in CVP while plasma ANP did not decrease further (141 +/- 25 pg/ml). Bilateral vagotomy did not modify either the basal plasma ANP level or the plasma ANP responses to volume expansion and depletion, though it inhibited HR response. These results indicate that in the rat, plasma ANP responds not only to volume expansion but also to moderate volume depletion suggesting that ANP may have a physiological role in body fluid homeostasis. The ANP response to changes in blood volume appears to be independent of the cardiopulmonary baroreflex with vagal afferent.     

Resting and volume-stimulated circulating atrial natriuretic peptide in young normotensive men with positive family histories of hypertension.

Normotensive young men (36 +/- 5 years old) with positive family histories of hypertension (n = 11) and age-matched controls (n = 21) with negative family histories of hypertension were examined. The control group was divided into one group matched for body mass index with those subjects with positive family histories (n = 10) and one group with normal body mass index (n = 11). Blood pressure, central venous pressure (CVP), plasma atrial natriuretic peptide (ANP) and serum aldosterone were examined at a baseline and during an acute volume load with 1000 ml saline solution. Subjects with positive family histories and controls matched for body mass index had a higher blood pressure at baseline than controls with normal body mass index. CVP and serum aldosterone did not differ between the three groups, while sodium intake and plasma concentrations of ANP were significantly higher in subjects with positive family histories. During volume loading, CVP increased significantly more in subjects with positive family histories as compared with the two control groups. A blunted response to ANP was observed during volume loading in subjects with positive family histories, while subjects in the two control groups demonstrated comparable and significant increases in circulating ANP. Serum aldosterone, however, decreased during volume loading in all three groups, with no difference between the groups. We conclude that normotensive subjects with positive family histories are characterized by increased basal concentrations of ANP and exhibit a blunted response to an acute volume load.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of digitalis on cardiopulmonary baroreflex in man

We examined whether digitalis augments cardiopulmonary baroreflex control of forearm vascular resistance in normal young men. Cardiopulmonary baroreceptor input was reduced with lower body negative pressure (LBNP) at 10 and 20 mmHg which decreased central venous pressure (CVP) but did not alter blood pressure (BP) or heart rate (HR). Decreases in forearm blood flow and increases in forearm vascular resistance with LBNP were greater after cedilanid than before and the slope of the regression line relating changes in central venous pressure and those in forearm vascular resistance was steeper after cedilanid. Vasoconstrictor responses to a cold pressor test did not differ before and after cedilanid, which suggested that augmented responses to LBNP after cedilanid were not due to a generalized change in reflex control. These results suggest that cedilaniid augments the tonic inhibitory influence of cardiopulmonary baroreceptors in normal men.     

Impaired responsiveness of the ventricular sensory receptor in hypertensive patients with left ventricular hypertrophy

We studied the control of forearm vascular resistance (FVR) by cardiopulmonary receptors in seven patients with hypertension and left ventricular hypertrophy (LVH) and in seven normotensive control subjects. Increasing levels of lower body negative pressure (LBNP) (-10 and -40 mm Hg) induced a progressive decrease in central venous pressure (CVP) and an increase in FVR. The changes in these two variables were correlated both in normal subjects and patients with hypertension (slope for normal subjects = -29.9, for patients with hypertension = -40.3, NS). After propranolol, there was a significant reduction in the increase in FVR induced by -40 mm Hg LBNP in normal subjects (+107 +/- 5 vs +129 +/- 15 mm Hg/ml/sec, p less than .05) but not in patients with hypertension. Consequently, the slope of the delta CVP/delta FVR regression was reduced in normal subjects (-20.6, p less than .01) but not in patients with hypertension. In another seven normal subjects and seven patients with hypertension and LVH we assessed the effects of -10 and -40 mm Hg LBNP on left ventricular filling pressure (LVFP). LBNP induced similar changes in CVP, LVFP, and total peripheral resistance both in normal subjects and in patients with hypertension. Propranolol failed to modify the effects of LBNP on CVP and LVFP in both groups and reduced the response of total peripheral resistance to -40 mm Hg LBNP only in normal subjects. Propranolol did not reduce the response of FVR to the cold pressor test and sustained handgrip or the arterial baroreflex response to the injection of phenylephrine and increased neck tissue pressure. Thus, hypertension-induced LVH seems to be associated with a selective impairment of the left ventricular sensory receptors.     

Effect of angiotensin converting enzyme inhibition on cardiovascular regulation during reflex sympathetic activation in sodium-replete patients with essential hypertension

In order to investigate whether angiotensin II (Ang II) may contribute to cardiovascular regulation through facilitation of the adrenergic function, we examined the haemodynamic and humoral effects of the application of lower-body negative pressure (LBNP) in sodium-replete patients with essential hypertension before and after acute and chronic angiotensin converting enzyme (ACE) inhibition. We measured the changes in blood pressure, heart rate, central venous pressure, forearm blood flow, plasma noradrenaline, renin activity and Ang II induced by LBNP of two different magnitudes: a milder one deactivating predominantly the cardiopulmonary receptors (mild LBNP), and a greater one deactivating both the cardiopulmonary and the arterial baroreceptors (strong LBNP). We found that during mild LBNP systemic blood pressure was maintained after acute and chronic ACE inhibition, as in control studies; however, the decrements in forearm blood flow and the increments in forearm vascular resistance caused by LBNP were diminished after ACE inhibition (the latter by 69 and 67%, respectively, in acute and chronic studies), in spite of the fact that the falls in central venous pressure and the increases in noradrenaline (NA) were similar to those observed in control conditions. During strong LBNP, the fall in systemic blood pressure was greater after acute and chronic ACE inhibition than in control conditions and was associated with a reduction in the response of forearm vascular resistance similar to that observed during mild LBNP, while the increments in NA were again superimposable to those seen before ACE inhibition. These alterations in the haemodynamic responses to LBNP induced by ACE inhibition were associated with significant increments in basal plasma renin activity and with marked reductions in Ang II. These findings suggest that even in the sodium-replete state, Ang II exerts a facilitatory action on adrenergic function that is physiologically relevant for the regulation of forearm blood flow and the maintenance of blood pressure during the application of gravitational stresses.     

Baroreflex control of muscle sympathetic nerve activity in borderline hypertension

Patients with borderline hypertension have exaggerated vascular responses to orthostatic stress produced by tilt or lower body negative pressure (LBNP). It has been suggested that 1) in the supine position, these patients have augmented activity of cardiopulmonary baroreceptors that exerts an increased restraint on sympathetic vasoconstrictor tone; 2) withdrawal of this augmented inhibitory baroreceptor activity during orthostatic stress elicits augmented reflex sympathetic vasoconstrictor outflow; and 3) augmented cardiopulmonary baroreceptor activity may be secondary to impaired arterial baroreflex mechanisms. To test these hypotheses, we recorded muscle sympathetic nerve activity from the peroneal nerve in seven borderline hypertensive subjects and seven age-, sex-, and weight-matched normotensive subjects during three levels of nonhypotensive LBNP and infusions of phenylephrine and nitroprusside. During LBNP, reductions of central venous pressure were similar in borderline hypertensive and normotensive subjects, and arterial pressure and heart rate values were unchanged. Increases of sympathetic nerve activity, however, were significantly greater in borderline hypertensive than in normotensive subjects at each level of LBNP, indicating an augmented gain of the cardiopulmonary baroreflex. To determine whether this augmentation is related to impairment of arterial baroreflexes, we measured changes of sympathetic nerve activity during increases and decreases of arterial pressure produced with infusions of intravenous phenylephrine and nitroprusside. Central venous pressure was held at control levels by LBNP during phenylephrine and saline infusion during nitroprusside. Changes of sympathetic nerve activity during alterations of arterial pressure were similar in borderline hypertensive and normotensive subjects. These data show that cardiopulmonary baroreflex control of SNA is augmented in borderline hypertensive subjects and that this augmentation does not result from an attenuation of the arterial baroreflex.     

Effects of lower-body negative pressure on sympathetic nerve responses to static exercise in humans. Microneurographic evidence against cardiac baroreflex modulation of the exercise pressor reflex

Although previous studies in both animals and humans have suggested that cardiac baroreceptors modulate reflex sympathetic vasoconstriction during exercise, more recent studies in conscious animals have not supported this view. To further test this concept in humans, we measured sympathetic nerve discharge with intraneural microelectrodes while we used static handgrip to activate the exercise pressor reflex and nonhypotensive lower-body negative pressure (LBNP) to selectively unload the cardiac baroreflex. In nine healthy subjects, we measured blood pressure, heart rate, central venous pressure, and muscle sympathetic nerve activity (MSNA) from the peroneal nerve (resting leg) during 2 minutes of static handgrip at 20% and 30% of maximal voluntary contraction (MVC) alone and in combination with LBNP at -5 mm Hg. Handgrip alone (exercise reflex) at 20% and 30% MVC caused graded increases in MSNA. LBNP alone (cardiac reflex) did not alter blood pressure or heart rate but decreased central venous pressure by 2.5 +/- 0.1 mm Hg (mean +/- SEM, p less than 0.05) and increased MSNA by 92 +/- 22% over the control value. Most important, handgrip performed during LBNP (interaction of reflexes) caused increases in MSNA that were comparable with the increases during handgrip alone: +114 +/- 32% versus +175 +/- 89% at 20% MVC and +328 +/- 101% versus +431 +/- 110% at 30% MVC (handgrip plus LBNP vs. handgrip alone, p greater than 0.1). Pressor and heart rate responses to handgrip also were unaffected by LBNP. In five additional experiments, comparable findings were obtained when the LBNP was superimposed on handgrip rather than handgrip being superimposed on LBNP. In conclusion, this study provides direct evidence in humans that nonhypotensive LBNP does not augment muscle sympathetic outflow during static handgrip and challenges the concept of an important interaction between cardiac baroreceptor and exercise pressor reflexes during this form of exercise.     

Different effects of α-human atrial natriuretic peptide and nitroglycerin on cardiac dimensions in humans

Summary This study aimed to examine whether-human atrial natriuretic peptide (-hANP) alters cardiac dimensions in humans. Left atrial (LA) and left ventricular diastolic (LV) diameters were measured by echocardiography at control and with lower body negative pressure (LBNP) at –10 and –20 mmHg during intravenous (IV) infusion of saline or-hANP at a dose of 0.03–0.04 µg/kg per minute (n=8). Studies were also done during IV infusion of saline or nitroglycerin (NG) at a dose of 10–15 µg/kg per minute in another group of subjects (n=6). LBNP decreased central venous pressure (CVP) and the LA and LV diameter.-hANP lowered CVP at rest and with LBNP at –10 and –20 mmHg compared with corresponding values during saline infusion; NG produced comparable decreases in CVP, which suggests that decreases in venous return caused by the two drugs were similar. However, NG decreased, but-hANP did not alter the LA and LV diameter at rest or with LBNP. In another group of subjects (n=4), we observed that-hANP caused comparable decreases in CVP and pulmonary capillary wedge pressure. These data suggest that ANP may dilate the cardiac chambers in humans.     

Responses of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP) to hypertonic saline infusion in essential hypertensive patients and normotensive subjects]

The demonstration that exogenous atrial natriuretic polypeptide (ANP) has markedly lowered plasma antidiuretic hormone (ADH) suggests a possible negative control of endogenous ANP on the secretion of ADH from the posterior hypophysis. To test this possibility and to clarify the role of ADH and ANP in the pathophysiology of essential hypertension (EHT), the responses of ADH and ANP to a hypertonic saline infusion were investigated in EHT patients and normotensive subjects (NT). Twenty inpatients with EHT (10 males and 10 females; 50.5 +/- 6.5y) and 10 NT subjects (5 males and 5 females; 50.6 +/- 7.8y) underwent a 20 min intravenous infusion of hypertonic saline (2.5% NaCl; 0.25ml/kg/min) in a fasting state. Blood samples were drawn before and 10, 20, 30, 45 and 60 min after the infusion and analyzed for ADH and ANP as well as plasma osmolarity (Posm), Na and albumin. Basal levels of ADH and ANP were not significantly different between NT and EHT. ADH was rapidly increased by the infusion in both groups; however, its percent increase was much higher in EHT than in NT during and after the infusion. Surprisingly, a highly significant negative correlation between ADH and ANP was found before and after the infusion in both groups. Although blood pressure was not changed significantly, the enhanced response of ADH to a sodium and volume load may play a role in part in the pathophysiology of EHT. In addition, it has been suggested that a possible suppression by ANP on the secretion of ADH may be one of the mechanisms of the diuretic action of ANP.     

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.     

Reduction of serum parathyroid hormone levels during sympathetic stimulation in man

The parathyroid glands contain sympathetic nerve endings and the parathyroid cells are endowed with beta-adrenergic receptors. The physiological role of the sympathoadrenal system for the secretion of parathyroid hormone (PTH) has, however, not been clarified. Using the technique of lower body negative pressure (LBNP), which is an established method to achieve sympathetic nerve activation, it was found in 17 healthy subjects that the venous serum levels of PTH were reduced by 7% within 20 min [from 0.79 +/- 0.12 (SD) to 0.74 +/- 0.11 arbU/l, p less than 0.01, paired t test]. The reduction corresponds to 30% of the maximal suppressibility of PTH by induced hypercalcemia or following parathyroidectomy when studied with the same PTH assay and with the short time period involved. After cessation of LBNP the PTH levels returned to baseline within 20 min. There were no concomitant changes of the plasma ionized calcium concentrations. The findings are compatible with a role for the sympathetic nervous system in the physiologic regulation of the secretion of PTH.     

Cardiovascular responses to lower body negative pressure in the elderly: role of reduced leg compliance

BACKGROUND: It is warranted to test the hypothesis that the orthostatic tolerance does not diminish in the aging process per se in healthy individuals. OBJECTIVE: The purpose of the present study was to examine the effects of aging on cardiovascular response and baroreflex sensitivity during lower body negative pressure (LBNP) with a special reference to leg compliance. METHODS: Fifteen healthy old male subjects [mean age 68.2 +/- (SE) 0.8 years] and 22 young male subjects [mean age 21.4 +/- (SE) 0.3 years] underwent a 21-min bout of ramped LBNP (from 0 to -60 mm Hg, 10 mm Hg each for 3 min). Heart rate (HR), blood pressure, stroke volume (SV), forearm blood flow, and leg volume were measured throughout the experimental period. The arterial baroreflex sensitivity was calculated from spontaneous changes in beat-to-beat arterial pressure and HR during LBNP. RESULTS: The leg compliance was lower, and the orthostatic tolerance index was higher in old than in young participants. The LBNP-associated increases in leg volume and HR and the decreases in SV were lower in old subjects, suggesting that the reduction of venous return was less in magnitude in old subjects during LBNP. The baseline value of baroreflex sensitivity evaluated by the sequence analysis was smaller, and no LBNP-related change was observed in old subjects, whereas a gradual LBNP-related reduction was observed in young subjects. The slope of regression between DeltaSV and change in forearm vascular resistance during LBNP was identical in both age groups. CONCLUSIONS: We conclude that: (1) aging per se does not increase the intolerance to orthostatic stress induced by LBNP; (2) a low magnitude of venous return reduction during LBNP contributes to a higher tolerance in the old because of lower leg compliance, and (3) the sensitivity of baroreflex control of the HR is attenuated in the old; however, there is no deterioration of the sensitivity of the peripheral vasoconstriction during LBNP.     

Plasma atrial natriuretic peptide concentrations in patients weaning from positive-pressure ventilation.

The effect of positive-pressure ventilation on plasma atrial natriuretic peptide (ANP) concentrations was investigated in sixteen patients weaning from the ventilator. During spontaneous ventilation plasma ANP concentrations rose significantly from 59 (16-270) to 67 (13-320) pg/ml (median and range, P less than 0.05) and mean arterial blood pressure rose from 84 +/- 3 to 92 +/- 3 mmHg (mean +/- SEM, P less than 0.05) if compared with periods of positive-pressure ventilation. This increase in plasma ANP concentrations occurred irrespective of the underlying disease and the wide scatter of the ANP plasma levels found in individual patients. As right atrial stretch is the major stimulus for the release of the ANP the data indicate a decrease in cardiac output during positive-pressure ventilation following an impaired central venous return to the heart.     

Impaired adaptation of cardiopulmonary receptors to western diet in normotensive black immigrants

A blood pressure increase was reported in black immigrants from Africa to Western countries. The present study was undertaken to evaluate whether an impairment of the cardiopulmonary reflex might make blacks unable to adapt peripheral vascular resistance to increased sodium intake.Ten normotensive clinically healthy blacks (aged 38 ± 6 years) who had recently migrated from Mogadishu, Somalia to Florence and 10 age- and gender-matched healthy white subjects were investigated. Cardiopulmonary baroreceptor reflex was studied after 7 days of normal (108 mEq) and low (30 mEq) sodium intake by assessing forearm vascular resistance (FVR) and central venous pressure (CVP) during the application of lower body negative pressure (LBNP) at −10 and −20 mm Hg.With a normal sodium diet the gain in cardiopulmonary baroreceptor reflex, expressed as the FVR increase per mm Hg of CVP reduction, was significantly lower in blacks than in white subjects (2.6 ± 1.1 v 5.1 ± 1.1 U per mm Hg of CVP, P < .001). Differences between the groups disappeared with a low-sodium diet because the reduction of the efficiency of the cardiopulmonary baroreceptor reflex was lower in blacks than in whites (2.4 ± 0.7 v 3.3 ± 0.7 U per mm Hg of CVP, P = .09).In conclusion, the efficiency of the cardiopulmonary reflex is lower in normotensive black immigrants than in whites. The lower adaptation of the cardiovascular system to the Western sodium diet could contribute to reported long-term blood pressure increase.     

Digitalis-induced augmentation of cardiopulmonary baroreflex control of forearm vascular resistance

We sought to determine whether digitalis augments cardiopulmonary baroreflex control of forearm vascular resistance in normal young men. Cardiopulmonary baroreceptor input was reduced with lower body negative pressure (LBNP) at 10 and 20 mm Hg, which decreased central venous pressure but did not alter blood pressure or heart rate. Decreases in forearm blood flow and increases in forearm vascular resistance with LBNP were greater after administration of lanatoside C (Cedilanid) than before, and the slope of the regression line relating changes in central venous pressure and those in forearm vascular resistance was steeper after lanatoside C. Vasoconstrictor responses to the cold pressor test did not differ before and after lanatoside C, which suggested that augmented responses to LBNP after the drug were not caused by a generalized change in reflex control. These results suggest that lanatoside C augments the tonic inhibitory influence of cardiopulmonary baroreceptors in normal men.     

Changes of circulating atrial natriuretic peptide and antidiuretic hormone in obstructive sleep apnea syndrome.

Patients with obstructive sleep apnea (OSA) syndrome are known to exhibit nocturnal natriuresis/diuresis. We studied plasma and urinary levels of atrial natriuretic peptide (ANP), a potent natriuretic hormone released from the heart, and plasma antidiuretic hormone (ADH) levels in patients with OSA during awake and sleeping periods, to compare with those of normal subjects. Seven patients with OSA and 6 normal subjects were studied. Arterial blood samples were drawn during the awake and the sleeping period, while in patients with OSA, blood samples were obtained during the apneic period. Urine samples were collected over two 12-hour periods (9 a.m.-9 p.m. and 9 p.m.-9 a.m.) In patients with OSA, plasma ANP as well as urinary ANP excretion increased during the apneic period compared with the awake period. There was a significant negative correlation between plasma levels of ANP and ADH in patients with OSA. On the other hand, normal subjects had no apparent differences in plasma and urinary ANP levels between the two periods. It is suggested that nocturnal increase in ANP and decrease in ADH are responsible for the nocturnal diuresis and natriuresis associated with OSA.