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Biomedical subjects

A L Mark

Publications and source records attributed to A L Mark.

At least 91 records · Page 5Linked to original sources
PubMed1989

Effects of alcohol intake on blood pressure and sympathetic nerve activity in normotensive humans: a preliminary report.

Although several epidemiological studies have shown an association between alcohol consumption and high blood pressure, the mechanisms involved in the pressor effect of alcohol are not clear. We hypothesized that alcohol might increase blood pressure at least in part by increasing sympathetic nerve activity. In a double-blind, placebo-controlled study of seven normotensive subjects (mean age +/- s.e.m. 24.0 +/- 1.5 years), we investigated the effects of oral administration of alcohol (0.75 g/kg body weight, diluted in orange juice) or vehicle on arterial blood pressure, heart rate and muscle sympathetic nerve activity, measured directly in the peroneal nerve by microneurography. Plasma ethanol levels increased from 0 (control) to a range of 47.7 +/- 7.6 to 53.3 +/- 5.0 mg/dl 30 min after alcohol intake. This increase in plasma ethanol was accompanied by a significant increase (P less than 0.05) in mean blood pressure, heart rate and sympathetic nerve activity. The vehicle did not affect any of these parameters. Our data suggest that acute oral administration of a moderate dose of alcohol induces a pressure effect through activation of sympathetic nervous outflow.

Adult↗
PubMed1989

Sympathetic outflow to resting muscles during static handgrip and postcontraction muscle ischemia.

Simultaneous microneurographic recordings were made of muscle sympathetic activity (MSA) in the radial and the peroneal nerves of seven healthy subjects during 2-min static handgrip (30% of maximal voluntary contraction) followed by 2 min of forearm ischemia induced by arterial occlusion. At rest sympathetic burst frequency was similar in both nerves, but relative burst strengths differed between the two neurograms, suggesting that sympathetic outflows to arm and leg were not identical. Both radial and peroneal MSA were unchanged during the first minute of handgrip and increased to a similar degree during the second minute. Thus previously reported differences in vascular resistance between forearm and calf during static handgrip cannot be explained by differences in MSA to arm and leg muscles. During forearm ischemia after handgrip, peroneal MSA remained at the same level as during the second minute of handgrip but there was a further increase of radial MSA. This shows that stimulation of chemosensitive endings in forearm muscles induces differentiation of sympathetic neural outflow to muscles in the leg and the contralateral arm.

Adult↗
PubMed1989

Influence of ventilation and hypocapnia on sympathetic nerve responses to hypoxia in normal humans.

The sympathetic response to hypoxia depends on the interaction between chemoreceptor stimulation (CRS) and the associated hyperventilation. We studied this interaction by measuring sympathetic nerve activity (SNA) to muscle in 13 normal subjects, while breathing room air, 14% O2, 10% O2, and 10% O2 with added CO2 to maintain isocapnia. Minute ventilation (VE) and blood pressure (BP) increased significantly more during isocapnic hypoxia (IHO) than hypocapnic hypoxia (HHO). In contrast, SNA increased more during HHO [40 +/- 10% (SE)] than during IHO (25 +/- 19%, P less than 0.05). To determine the reason for the lesser increase in SNA with IHO, 11 subjects underwent voluntary apnea during HHO and IHO. Apnea potentiated the SNA responses to IHO more than to HHO. SNA responses to IHO were 17 +/- 7% during breathing and 173 +/- 47% during apnea whereas SNA responses to HHO were 35 +/- 8% during breathing and 126 +/- 28% during apnea. During ventilation, the sympathoexcitation of IHO (compared with HHO) is suppressed, possibly for two reasons: 1) because of the inhibitory influence of activation of pulmonary afferents as a result of a greater increase in VE, and 2) because of the inhibitory influence of baroreceptor activation due to a greater rise in BP. Thus in humans, the ventilatory response to chemoreceptor stimulation predominates and restrains the sympathetic response. The SNA response to chemoreceptor stimulation represents the net effect of the excitatory influence of the chemoreflex and the inhibitory influence of pulmonary afferents and baroreceptor afferents.

Adult↗
PubMed1989

Contrasting effects of hypoxia and hypercapnia on ventilation and sympathetic activity in humans.

We compared the effects of isocapnic hypoxia (IHO) and hyperoxic hypercapnia (HC) on sympathetic nerve activity (SNA) recorded from a peroneal nerve in 13 normal subjects. HC caused greater increases in blood pressure (BP), minute ventilation (VE), and SNA [53 +/- 14% (SE) during HC vs. 21 +/- 7% during IHO; P less than 0.05]. Even at equivalent levels of VE, HC still elicited greater SNA than IHO. However, apnea during HC caused a lesser (P less than 0.05) increase in SNA (91 +/- 26% compared with apnea on room air) than apnea during IHO (173 +/- 50%). Hypercapnic hypoxia resulted in a greater absolute increase in VE (23.6 +/- 2.8 l/min) than the additive increases due to HC alone plus IHO alone (18.0 +/- 1.8 l/min, P less than 0.05). SNA also increased synergistically by 108 +/- 23% with the combined stimulus compared with the additive effect of HC alone plus IHO alone (68 +/- 19%; P less than 0.05). We conclude that 1) HC causes greater increases in VE and SNA than does hypoxia; 2) for the same increase in VE, hypercapnia still causes a greater increase in SNA than hypoxia; however, during apnea, hypoxia causes a much greater increase in SNA than hypercapnia; 3) the inhibitory influence of ventilation on SNA is greater during hypoxia (i.e., predominantly peripheral chemoreceptor stimulation) than hypercapnia (i.e., predominantly central chemoreceptor stimulation); and 4) combined hypoxia and hypercapnia have a synergistic effect on SNA as well as on VE.

Adult↗
PubMed1989

Importance of aortic baroreflex in regulation of sympathetic responses during hypotension. Evidence from direct sympathetic nerve recordings in humans.

Arterial baroreceptors in the carotid sinus and aortic arch regions reflexly regulate heart rate and peripheral vascular responses during changes in arterial pressure. The relative influence of these two arterial baroreflex pathways on the control of these autonomic responses is debatable. Recent studies in our laboratory demonstrate that the aortic baroreflex produces substantial and sustained inhibition of efferent sympathetic nerve activity to muscle (MSNA) during increases in arterial pressure. The regulation of MSNA by these two baroreflexes in humans during hypotension, and particularly the role of the aortic baroreflex, remains undefined. We therefore performed a new series of studies to assess the relative influence of the aortic and carotid baroreflexes on MSNA responses during sustained decreases in arterial pressure. In eight normal male subjects, aged 23 +/- 1 years (mean +/- SEM), we directly measured mean arterial pressure, heart rate, central venous pressure, and MSNA (microneurography) during hypotension (combined aortic and carotid baroreceptor deactivation) produced by intravenous infusion of sodium nitroprusside and during nitroprusside infusion with superimposed application of external neck suction. Neck suction was applied at levels sufficient to maintain transmural carotid sinus pressure above control levels (carotid baroreceptor activation) while the aortic baroreflexes remained deactivated. Central venous pressure was maintained constant with volume infusion. We also studied responses of these same subjects to direct carotid baroreceptor deactivation with the application of external neck pressure. During neck pressure alone, there was a reflex increase in mean arterial pressure; thus, during this portion of the protocol, we achieved carotid baroreceptor deactivation with some aortic baroreceptor activation. Nitroprusside infusion (combined aortic and carotid deactivation) decreased mean arterial pressure from 90.8 +/- 3.1 to 77.8 +/- 1.1 mm Hg (p less than 0.01) with concomitant increases in heart rate from 62.6 +/- 3.0 to 89.7 +/- 6.1 beats/min (p less than 0.001) and in MSNA from 273.8 +/- 43.0 to 950.6 +/- 133.5 units (p less than 0.001). During continued nitroprusside infusion with superimposed neck suction (aortic baroreceptor deactivation and carotid baroreceptor activation), mean arterial pressure decreased to 70.3 +/- 1.9 mm Hg (p less than 0.001 vs. control), heart rate decreased to 82.5 +/- 6.5 beats/min (p less than 0.01 vs. control or vs. nitroprusside alone), but MSNA remained markedly increased at 889.7 +/- 105.1 units (p less than 0.001 vs. control; p = NS vs. nitroprusside alone).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Flow-mediated and reflex changes in large peripheral artery tone in humans.

Studies of peripheral blood vessels in humans have focused primarily on regulation of blood flow and vascular resistance, which are thought to reflect small vessel caliber. Recent studies in animals have identified flow-mediated and neurogenic changes in large artery diameter. This study tested for flow-mediated dilatation and reflex constriction of the brachial artery in humans. A dual-crystal pulsed Doppler system was used to measure brachial artery diameter and blood flow proximal to the antecubital fossa. To test for flow-mediated dilatation, flow through the brachial artery was altered by an occluding cuff placed on the forearm distal to the site of brachial artery flow and diameter measurement. Control blood flow was 123 +/- 20 ml/min, and brachial artery diameter was 4.74 +/- 0.17 mm (mean +/- SEM). By inflating the distal occluding cuff (distal circulatory arrest), flow was reduced through the brachial artery to 21 +/- 5 ml/min (p less than 0.005), and brachial artery diameter was reduced to 4.35 +/- 0.20 mm (p less than 0.001). By deflating the distal occluding cuff after 10 minutes (reactive hyperemia), brachial artery flow was increased to 358 +/- 55 ml/min (p less than 0.001), and diameter was increased to 5.6 +/- 0.19 mm (p less than 0.001). These interventions did not change systemic arterial pressure and, as measured in three subjects, caused only small changes in local brachial artery distending pressure. Thus, both increased and decreased brachial artery blood flow produced significant changes in brachial artery diameter without altering arterial distending pressure. These data provide evidence for flow-mediated dilatation in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Evidence for cholinergically mediated vasodilation at the beginning of isometric exercise in humans.

Vasodilation occurs in the nonexercising forearm at the beginning of isometric handgrip despite activation of sympathetic vasoconstrictor reflexes. The mechanism of this response remains unclear. In 33 normal humans, age 24 +/- 1 years (mean +/- SEM), we measured mean arterial pressure, heart rate, and forearm blood flow (plethysmography) in the nonexercising arm during sustained contralateral isometric handgrip at 30% maximal voluntary contraction. Sympathetic nerve activity to calf muscles (microneurography) was also measured in 15 subjects. Handgrip resulted in increases in arterial pressure from 86 +/- 2 to 97 +/- 3 mm Hg (p less than 0.05). Despite increases in nerve activity to calf muscles from 229 +/- 43 to 337 +/- 66 units (p less than 0.005), which would be expected to produce forearm vasoconstriction, forearm vascular resistance in the contralateral resting arm decreased from 20 +/- 3 to 18 +/- 2 units (p less than 0.05). To determine the mechanism of this vasodilatory influence, additional studies were performed with regional autonomic blockade with intra-arterial administration of atropine (0.8 mg, 10 subjects) or propranolol (2.0 mg, eight subjects) into the nonexercising forearm before contraction. Propranolol and vehicle had no effect on forearm vascular responses in the resting arm during SHG in the other arm. In contrast, atropine blocked the vasodilatory response in the resting arm during contraction (delta forearm vascular resistance during contraction, control = -2.1 +/- 0.6 units; postatropine = +0.2 +/- 0.9 units, p less than 0.05). Atropine did not attenuate the vasodilator response to isoproterenol or the vasoconstrictor response to norepinephrine. We conclude 1) a dissociation exists between sympathetic neural and forearm vascular responses to isometric exercise; 2) the vasodilatory response in the nonexercising forearm is not due to sympathetic withdrawal or beta 2-adrenergic-mediated vasodilation; and 3) this response is mediated primarily by cholinergic mechanisms. These studies provide the first direct evidence for active, cholinergically mediated vasodilation during exercise in humans.

Adult↗
PubMed1989

Aggravation of salt-induced hypertension in Dahl rats by 2% supplemental dietary calcium.

There is considerable interest in the antihypertensive potential of supplemental dietary calcium in salt-sensitive hypertension. Previously we reported that very high dietary calcium (4.0% vs. 0.4%) lowers mean arterial pressure in Dahl salt-sensitive (DS) hypertensive rats. However, we have recently observed that more moderate calcium supplementation (2.0% vs. 0.4%) increases mean arterial pressure in DS rats. To further evaluate the pressor action of 2.0% versus 0.4% calcium, we tested for effects of 2.0% calcium in female DS rats fed low (0.2%), moderate (1.0%), and high (2.7%) sodium and in Dahl salt-resistant (DR) rats fed high sodium from 6 to 12 weeks old (n = 10-13 rats per group). At 12 weeks, 2.0% calcium increased mean arterial pressure and the cardiac ventricular weight/body weight ratio in DS rats fed high sodium (p less than 0.05) but not in DS rats fed low or moderate sodium or in DR rats fed high sodium. Ganglionic blockade decreased mean arterial pressure in all groups but failed to abolish or attenuate the difference in mean arterial pressure between high sodium-fed DS rats on 2.0% and 0.4% calcium diets. In the same DS rats fed a high sodium diet, 2.0% calcium increased systemic pressor responsiveness to graded norepinephrine administration after ganglionic blockade. Thus, 2.0% supplemental calcium intake enhances salt-induced hypertension in DS rats. This prohypertensive action of 2.0% calcium is dependent on a critically high level of between 1.0% and 2.7% sodium in the diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Postexercise hypotension and sympathoinhibition in borderline hypertensive men.

To determine if there would be a decrease in blood pressure after exercise in patients with borderline hypertension and if this decrease would be accompanied by a decrease in sympathetic nerve activity to muscle, we recorded multifiber postganglionic muscle sympathetic activity from the peroneal nerve at rest in nine men with borderline hypertension (age 25 +/- 1 years, mean +/- SEM) before and 60 minutes after 45 minutes of submaximal treadmill exercise. In addition, responses to a cold pressor test, handgrip, and the Valsalva maneuver were recorded before and after exercise. Four subjects were also studied before and after "sham" exercise. Sham exercise had no effect on blood pressure or sympathetic nerve activity whereas resting systolic blood pressure was lower after treadmill exercise in seven subjects (from 136 +/- 4 before to 123 +/- 2 mm Hg 60 minutes after exercise; p less than 0.01). Sixty minutes after exercise, sympathetic nerve activity was lower in all seven subjects (from 19 +/- 2 to 11 +/- 2 bursts/min, p less than 0.015; or from 27 +/- 3 to 14 +/- 2 bursts/100 heartbeats, p less than 0.005) but was slightly increased in the two subjects without postexercise hypotension. Heart rate and pressor and sympathoneural responses to the cold pressor test, handgrip, and the Valsalva maneuver were not altered by prior exercise. When nitroprusside was infused in five subjects to produce a reduction in systolic blood pressure similar to that seen 60 minutes after exercise, this drug increased sympathetic discharge from 37 +/- 6 to 57 +/- 4 bursts/100 heartbeats (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Elevated sympathetic nerve activity in borderline hypertensive humans. Evidence from direct intraneural recordings.

Reports of elevated plasma catecholamine levels and augmented responses to autonomic blockade suggest increased sympathetic tone in borderline hypertension. It is not known if this reflects greater sympathetic neural outflow. We directly recorded muscle sympathetic nerve activity (microneurography) in 15 normotensive and 12 borderline hypertensive age-matched men to determine whether borderline hypertensive individuals have elevated sympathetic nerve activity. Supine heart rate, blood pressure, plasma norepinephrine, and efferent muscle sympathetic nerve activity (peroneal nerve) were measured after 6 days of both low and high dietary sodium intake (10 and 400 meq sodium/24 hr). Sympathetic nerve activity was elevated significantly in borderline hypertensive individuals on both low (37 +/- 1 in borderline hypertensive individuals vs. 29 +/- 1 bursts/min in normotensive individuals; p less than 0.01) and high (25 + 1 in borderline hypertensive individuals vs. 16 +/- 1 bursts/min in normotensive individuals; p less than 0.01) sodium diets. The borderline hypertensive group had higher systolic (p less than 0.01) and diastolic (p less than 0.05) blood pressures independent of sodium intake. Across both groups, high sodium intake reduced muscle sympathetic nerve activity (p less than 0.001), plasma norepinephrine (p less than 0.001), diastolic blood pressure (p less than 0.02), heart rate (p less than 0.002), and increased weight (p less than 0.005). A significant (p less than 0.05) group-by-diet interaction was observed for plasma norepinephrine levels. Specifically, compared with the normotensive group, plasma norepinephrine levels in the borderline hypertensive group tended to be higher on low sodium diet (p = 0.08) and lower on high sodium diet (p = 0.23).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Differential control of adrenal and renal sympathetic nerve activity during hemorrhagic hypotension in rats.

The reflex mechanisms that produce the neurocirculatory adjustments to hemorrhagic hypotension are incompletely understood. The goal of this study was to determine if hemorrhagic hypotension in rats produces differential effects on sympathetic outflow to the adrenal gland and kidney and if the two sympathetic nerve responses are governed by different reflex mechanisms. We performed simultaneous multifiber recordings of adrenal and renal sympathetic nerve activity (SNA) during 8 minutes of sustained hemorrhagic hypotension to a mean arterial pressure of 50 mm Hg in chloralose-anesthetized Sprague-Dawley rats with a) baroreceptors intact, b) cervical vagotomy, c) sinoaortic baroreceptor denervation, and d) combined vagotomy plus sinoaortic denervation. During hemorrhagic hypotension in rats with intact baroreceptors, renal SNA decreased by 31 +/- 10% (mean +/- SEM, p less than 0.05 vs. control) and heart rate decreased from 384 +/- 13 to 365 +/- 16 beats per minute (p less than 0.05), but adrenal SNA increased by 69 +/- 10% over control (p less than 0.05). The decreases in renal SNA and heart rate were reversed by cervical vagotomy but not by atropine, which indicates vagal afferent mediation. In contrast, the increases in adrenal SNA during hemorrhage were not affected by vagotomy alone or by sinoaortic denervation alone but were markedly attenuated by combined sinoaortic denervation and vagotomy, which indicates redundancy in the baroreflex control of adrenal SNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1989

The secret of success.

The new health service will be designed to achieve the benefits of competition. As a consequence, argue Annabelle Mark and Leslie Willcocks, it will lose the benefit of co-operation.

Confidentiality↗
PubMed1989

Renal sympathetic nerves attenuate the natriuretic effects of atrial peptide.

Low frequencies of renal sympathetic nerve stimulation increase renal tubular sodium reabsorption without causing renal hemodynamic changes. We tested the hypothesis that the natriuretic responses to synthetic atrial peptides (atriopeptin III [APIII], 24 amino acids) are modulated by the renal tubular actions of the renal nerves. Responses to intravenous infusions of APIII (0.5 and 2.0 micrograms/kg/min) were examined in three groups of chloralose-anesthetized rats. Bilateral renal function studies were done in all three groups in which the right kidney was denervated and the left kidney was either left innervated (group I, n = 10) or the distal portion of the transected left renal nerves was stimulated at 15 V, 1 msec, and 0.5 Hz (group II, n = 8) or 1.0 Hz (group III, n = 8). In groups I, II, and III, diuretic and natriuretic responses to APIII were significantly (p less than 0.05) less in the kidneys with intact innervation or low-frequency (0.5 and 1.0 Hz) renal nerve stimulation than in the denervated kidneys. In conclusion, renal excretory responses to APIII are substantially modulated by the renal tubular actions resulting from low-frequency renal nerve stimulation. We speculate that the decrease in renal excretory responses to atrial peptides in pathophysiologic states such as congestive heart failure, nephrotic syndrome, and cirrhosis may result in part from an increase in the prevailing level of renal sympathetic nerve activity.

Animals↗
PubMed1988

Serotonergic mechanisms mediate renal sympathoinhibition during severe hemorrhage in rats.

Hemorrhage in rats produces reflex decreases in heart rate (HR) and renal sympathetic nerve activity (RSNA). Because serotonergic antagonists attenuate hemorrhage-induced vagal-mediated bradycardia, we determined whether blockade of serotonin synthesis by p-chlorophenylalanine (PCPA) or of serotonin receptors with methysergide would also abolish the renal sympathoinhibition. Mean arterial pressure (MAP), HR, and RSNA were recorded in chloralose-anesthetized rats pretreated with PCPA (300 mg.kg-1.day-1 X 3 days ip, n = 12) or vehicle (0.3 ml saline, n = 9). During hemorrhage, where MAP was maintained at 50 mmHg for 8 min, vehicle-treated rats decreased HR by 27 +/- 13 beats/min and RSNA by -55 +/- 7%. In PCPA-treated rats, HR and RSNA did not change. Cervical vagotomy abolished the bradycardia and sympathoinhibition during hemorrhage. After acute administration of methysergide (400 micrograms/kg iv, n = 8) hemorrhage produced increases of RSNA, whereas vehicle (0.5 ml saline, n = 7) preserved the renal sympathoinhibition to hemorrhage in conscious rats. Finally, volume expansion (0.88 ml blood/100 g body wt) produced comparable decreases in RSNA in sinoaortic-denervated rats pretreated with PCPA (n = 11) or vehicle (n = 10) (-58 +/- 9 vs. 47 +/- 7%, respectively). We conclude that serotonergic mechanisms are critically involved in vagal afferent inhibition of RSNA during severe hemorrhage in rats.

Animals↗
PubMed1988

Plasma norepinephrine and muscle sympathetic discharge during rhythmic exercise in humans.

The purpose of this study was to examine the relationship between plasma norepinephrine concentrations (PNE) and efferent muscle sympathetic nerve activity to noncontracting muscle (MSNA) during graded, rhythmic exercise in humans. In the initial study, six healthy men (ages 20-30 yr) performed 2-min bouts of two-arm cycling exercise at power outputs of 0, 10, 20, 40, 60 (n = 6), and 80 (n = 3) W. Heart rate (HR) was recorded and intraneural measurements of MSNA (right peroneal nerve) were made continuously for 2 min before (control) and during exercise at each work load. At least 2 wk later, subjects performed the same exercise bouts at which time HR was measured and a venous (forearm) blood sample was obtained for the subsequent determination of PNE by high-performance liquid chromatography. During exercise, HR increased progressively from 0 to 80 W. Neither MSNA nor PNE increased above control in response to arm cycling at 0, 10, and 20 W [0-16 +/- 1% (SE) of peak work load], but both variables increased progressively at the 40-, 60-, and 80-W (33 +/- 1 to 67 +/- 2% of peak work load) levels (all P less than 0.05). The individual MSNA and PNE responses (% change from control) over the six work loads were directly related (r = 0.80, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes.

Arterial baroreceptors in the carotid sinus (CBR) and aortic arch (ABR) regions exert important control over heart rate and peripheral vascular responses to changes in arterial pressure. The relative roles of these two baroreflex pathways on control of sympathetic nerve activity during sustained elevation of arterial pressure in man is unknown. We therefore studied the relative contributions of the carotid versus the aortic baroreflexes on the control of muscle sympathetic nerve activity (MSNA) during elevation of arterial pressure in normal human subjects. In eight normal men (group I), we measured MSNA (microneurography) during sustained elevation of arterial pressure produced by intravenous infusion of phenylephrine (PE) alone (combined ABR and CBR activation) versus during PE infusion with superimposed application of sustained external neck pressure (NP). NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone. Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency X amplitude) and expressed as units. Infusion of PE (ABR and CBR activation) increased mean arterial pressure from 87.2 +/- 2.8 to 94.9 +/- 2.9 mm Hg (+/- SE, p less than .001). This was accompanied by a decrease in heart rate from 65.8 +/- 3.4 to 56.1 +/- 3.3 beats/min (p less than .001) and a decrease in MSNA from 236.2 +/- 47.5 to 84.5 +/- 19.3 units (p less than .001). During infusion of PE with superimposed NP (ABR activation alone), mean arterial pressure increased further to 101.2 +/- 2.9 mm Hg (p less than .001 versus control or PE alone), and heart rate returned to control levels of 62.9 +/- 2.0 beats/min (p = NS vs control; p less than .01 PE vs PE plus NP), but MSNA remained reduced at 48.6 +/- 9.2 units (p less than .01 vs control; p = NS vs PE alone). Thus, combined activation of ABR and CBR resulted in a 65 +/- 5% attenution of MSNA, while activation of ABR alone resulted in a 73 +/- 7% attenuation of MSNA. In a separate series of experiments in seven subjects (group II) we used sustained external neck suction alone to activate the CBR (leaving the ABR either unchanged or minimally deactivated) and studied the MSNA responses to this CBR activation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Dietary salt produces abnormal renal vasoconstrictor responses to upright posture in borderline hypertensive subjects.

We studied the effect of high and low NaCl diets in normotensive and borderline hypertensive subjects to determine if a high NaCl diet produces abnormal renal vasoconstriction during the stress of upright posture in borderline hypertensive subjects. We studied 13 normotensive young men with diastolic blood pressures below 85 mm Hg and nine borderline hypertensive young men defined by diastolic blood pressures intermittently above 90 mm Hg. The subjects achieved comparable sodium balance during 6 days of low NaCl (10 mEq Na, 40 mEq Cl, 100 mEq K) and high NaCl (400 mEq Na, 400 mEq Cl, 100 mEq K) diets. In the normotensive subjects, standing for 30 minutes resulted in a tendency for diastolic blood pressure to fall during both diets. In contrast, during standing borderline hypertensive subjects showed no change in diastolic blood pressure during the low salt diet and a tendency for diastolic blood pressure to increase after the high salt diet. Standing reduced renal plasma flow in both groups during both diets. However, only during the high NaCl diet did the absolute decrease and percent decrease in renal plasma flow during standing differ significantly (p less than 0.05 and p less than 0.01, respectively) between the borderline hypertensive (-151 +/- 24 ml/min/1.73m2; -29 +/- 4%) and normotensive subjects (-79 +/- 17 ml/min/1.73m2; -15 +/- 3%). The resultant increase in the renal vascular resistance index with standing did not differ between the two groups during the low NaCl diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗