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Stimulation of beta-adrenoceptors in the exercising human forearm.

In order to study the effects of local stimulation of beta-adrenoceptors on limb blood flow during exercise and on muscle metabolism, the non-selective beta-adrenoceptor agonist, isoprenaline, was infused intra-arterially into the forearm of six healthy, young subjects. Isoprenaline caused a marked increase in forearm blood flow not only at rest but also during dynamic forearm exercise. The forearm release of lactate increased considerably during drug infusion whereas glucose uptake decreased. The net uptake of free fatty acids during exercise decreased. There were no systemic effects of isoprenaline. These findings suggest that the resistance vessels are responsive to beta-adrenergic vasodilatation also during muscle exercise. The increase in blood flow through the exercising forearm may be secondary to an increased muscle metabolism. The increased lactate release from the exercising muscles indicates an increased muscle glycogen breakdown during beta-adrenoceptor stimulation.

Adult↗

Forearm vascular responses to combined muscle metaboreceptor activation in the upper and lower limbs in humans.

Our previous studies showed that venous occlusion or passive stretch of the lower limb, assuming a mechanical stimulus, attenuates the vasoconstriction in the non-exercised forearm during postexercise muscle ischaemia (PEMI) of the upper limb. In this study, we investigated whether a metabolic stimulus to the lower limb induces a similar response. Eight subjects performed a 2 min static handgrip exercise at 30% maximal voluntary contraction (MVC) followed by 3 min PEMI of the upper limb, concomitant with or without 2 min static ankle dorsiflexion at 30% MVC followed by 2 min PEMI of the lower limb. During PEMI of the upper limb alone, forearm blood flow (FBF) and forearm vascular conductance (FVC) in the non-exercised arm decreased significantly, whereas during combined PEMI of the upper and lower limbs, the decreases in FBF and FVC produced by PEMI of the upper limb was attenuated. Forearm blood flow and FVC were significantly greater during combined PEMI of the upper and lower limbs than during PEMI of the upper limb alone. When PEMI of the lower limb was released after combined PEMI of the upper and lower limbs (only PEMI of the upper limb was maintained continuously), the attenuated decreases in FBF and FVC observed during combined PEMI of the upper and lower limbs was not observed. Thus, forearm vascular responses differ when muscle metaboreceptors are activated in the upper limb and when there is combined activation of muscle metaboreceptors in both the upper and lower limbs.

Adult↗

Early changes in the forearm circulation following transient increase of local external pressure.

1. The pressure at the surface of a segment of forearm enclosed in a plethysmograph was abruptly raised from atmospheric level to +40 mm Hg, held at the new level for 4 sec, and abruptly dropped to atmospheric level.2. Forearm circumference (V(f)) equivalent to the volume of a small segment of forearm, was monitored with a mercury-in-rubber strain gauge. Pressure was measured in the cylinder (P(p)) in veins exposed to external compression (P(v, e)), and in the radial artery exposed to compression (P(ra)).3. Forearm blood flow was measured by venous occlusion plethysmography before, and after, release of external compression. There was, on average, over the 3rd and 4th second after release of pressure, a 2.4-fold increase of inflow, as compared with resting level.4. By the 15th second after release of compression, forearm blood flow had returned to its previous resting level.5. The increase in blood flow after compression appears to be due to active reduction in vascular resistance, for refilling of the arteries and arterioles would be completed before the increased flow was recorded; venous backflow can be excluded, and the pressure difference for flow (arterial minus venous) is virtually unchanged.

Arteries↗

Carotid and cardiopulmonary baroreceptor control of splanchnic and forearm vascular resistance during venous pooling in man.

1. This study evaluated the contribution of carotid and cardiopulmonary baroreceptors to reflex splanchnic and forearm vascular adjustments during venous pooling in man. We compared (a) responses to lower body suction which produces venous pooling with (b) responses to lower body suction plus simultaneous application of neck suction. The rationale was that simultaneous application of neck suction, which stretches carotid baroreceptors, would minimize the contribution of carotid baroreceptors to circulatory adjustments produced by lower body suction.2. Lower body suction at 40 mmHg decreased central venous pressure and arterial pulse pressure and increased forearm vascular resistance (plethysmography), splanchnic vascular resistance (indocyanine green dye clearance), and heart rate. Simultaneous application of neck suction prevented the tachycardia and most of the splanchnic vasoconstriction during lower body suction, but did not significantly attenuate the forearm vasoconstriction.3. The major findings in this study are first, that the splanchnic vasoconstrictor response during venous pooling is mediated primarily through carotid baroreceptors, and secondly, that carotid and cardiopulmonary baroreceptors produce strikingly contrasting and non-uniform regional vascular responses during venous pooling. Cardiopulmonary baroreceptors exert the predominant influence on forearm vascular resistance, but appear to have only a minor influence on splanchnic vascular resistance. Carotid baroreceptors produce most of the splanchnic vasoconstriction during venous pooling. but have a minor role in the forearm vasoconstriction.

Abdomen↗

Active forearm blood flow adjustments to handgrip exercise in young and older healthy men.

1. Our purpose was to test the hypothesis that ageing impairs the active muscle hyperaemia consequent to dynamic exercise in humans. 2. Eleven young (19-29 years) and eleven older (60-74 years) healthy, non-obese men with similar chronic physical activity levels and forearm size performed two protocols of dynamic handgrip exercise: (a) brief (1 min), incremental loads to exhaustion, and (b) sustained (8 min), submaximal loads. Active forearm blood flow (FBF) was measured at rest and during a brief period of relaxation at the end of each minute of exercise. Arterial blood pressure was recorded to calculate active forearm vascular conductance (FVC). Sustained forearm ischaemia plus handgrip was used to elicit a peak forearm vasodilatatory response. 3. There were no differences in pre-exercise levels of any variable between the young and older men. During exercise, ratings of perceived effort, the peak workload attained, and the ability to sustain submaximal workloads were all similar for the two groups. 4. During brief exercise, both submaximal and peak levels of FBF were similar in the two groups; however, the peak increases in FVC were greater in the older men. During sustained exercise, FBF and FVC were not different in the two groups at the lowest loads, but the increases became relatively greater in the older men with increasing workloads. 5. Peak levels of FBF and FVC in response to the peak vasodilatatory stimulus were similar in the young and older men. 6. These findings fail to support the postulate that ageing results in impaired active muscle hyperaemia and vasodilatation during small-muscle dynamic exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Augmented sympathetic vasoconstriction in exercising forearms of postmenopausal women is reversed by oestrogen therapy.

Sympathetic vasoconstriction is normally attenuated in exercising muscles of young men and women. Recent evidence indicates that such modulation, termed functional sympatholysis, may be impaired in older men. Whether a similar impairment occurs in older women, and what role oestrogen deficiency might play in this impairment, are not known. Based on the strong positive correlation between circulating oestrogen levels and functional sympatholysis previously reported in female rats, we hypothesized that sympatholysis would be impaired in oestrogen-deficient postmenopausal women, and that this impairment would be reversed by oestrogen replacement. To test these hypotheses, we measured vasoconstrictor responses in the forearms of pre- and postmenopausal women using near infrared spectroscopy to detect decreases in muscle oxygenation in response to reflex activation of sympathetic nerves evoked by lower body negative pressure (LBNP). In eight premenopausal women, LBNP decreased muscle oxygenation by 20 +/- 1% in resting forearm, but only by 3 +/- 2% in exercising forearm (P < 0.05). In contrast, in eight postmenopausal women, LBNP decreased muscle oxygenation by 15 +/- 3% in resting forearm, and by 12 +/- 4% in exercising forearm (P > 0.05). After 1 month of transdermal oestradiol replacement in these women, the normal effect of exercise to blunt sympathetic vasoconstriction was restored (rest, -19 +/- 3%; exercise, -2 +/- 3%; P < 0.05). These data indicate that functional sympatholysis is impaired in oestrogen-deficient postmenopausal women. The effect of short-term unopposed oestrogen replacement to correct this impairment implicates a role for oestrogen in the sympathetic neural control of muscle haemodynamics during exercise.

Adult↗

Increased renal and forearm vasoconstriction in response to exercise after heart transplantation.

OBJECTIVE: To test the hypothesis that the loss of the inhibitory effect of the cardiac ventricular afferent fibres on the vasomotor centre would result in increased vasoconstrictor drive to the forearm and renal vascular beds during supine exercise in heart transplant recipients. DESIGN: Comparison of regional haemodynamic response to exercise in heart transplant recipients and two age matched control groups. SETTING: Regional heart transplant unit. PATIENTS AND METHODS: Orthotopic heart transplant recipients (n = 10), patients with NYHA class II heart failure (n = 10), and normal controls (n = 10) underwent short duration maximal supine bicycle exercise. MAIN OUTCOME MEASURES: Simultaneous measurements were made of heart rate, systemic blood pressure, oxygen consumption (VO2), forearm blood flow, and renal blood flow. Forearm blood flow was measured by forearm plethysmography and renal blood flow by continuous renal vein thermodilution. RESULTS: The peak forearm vascular resistance was significantly greater in the transplant group than in the controls (mean (SEM) 75 (18) v 40 (7) resistance units, p < 0.05). The percentage fall in renal blood flow at peak exercise was significantly greater in heart transplant recipients than in the controls (44% (4%) v 32% (4%), p < 0.05) as was the percentage increase in renal vascular resistance (transplants: 116% (19%) v controls: 78% (17%), p < 0.05). Regional haemodynamics during exercise in the heart failure group were not significantly different from those in the controls. CONCLUSIONS: These findings suggest that surgical division of the cardiac ventricular afferent fibres results in increased vasoconstrictor drive to the kidneys and non-exercising muscle during exercise. This mechanism may contribute to persistent exercise limitation and renal impairment after heart transplantation.

Adult↗

Effects of long-term tennis playing on the muscle-bone relationship in the dominant and nondominant forearms.

The relationship between muscle strength and bone mineral density illustrates the positive effect of mechanical loading on bone. But local and systemic factors may affect both muscle and bone tissues. This study investigated the effects of long-term tennis playing on the relationship between lean tissue mass and bone mineral content in the forearms, taking the body dimensions into account. Fifty-two tennis players (age 24.2 +/- 5.8 yrs, 16.2 +/- 6.1 yrs of practice) were recruited. Lean tissue mass (LTM), bone area, bone mineral content (BMC), and bone mineral density were measured at the forearms from a DXA whole-body scan. Grip strength was assessed with a dynamometer. A marked side-to-side difference (p < 0.0001) was found in favor of the dominant forearm in all parameters. Bone area and BMC correlated with grip strength on both sides (r = 0.81-0.84, p < 0.0001). The correlations were still significant after adjusting for whole-body BMC, body height, or forearm length. This result reinforced the putative role of the muscles in the mechanical loading on bones. In addition, forearm BMC adjusted to LTM or grip strength was higher on the dominant side, suggesting that tennis playing exerts a direct effect on bone.

Absorptiometry, Photon↗

The effect of local heating on blood flow in the finger and the forearm skin.

Blood flow of the finger and the forearm were measured in five male subjects by venous occlusion plethysmography using mercury-in-Silastic strain gauges in either a cool-dry (COOL: 25 degrees C, 40% relative humidity), a hot-dry (WARM: 35 degrees C, 40% relative humidity), or a hot-wet (HOT: 35 degrees C, 80% relative humidity) environment. One hand or forearm was immersed in a water bath, the temperature (Tw) of which was raised every 10 min by steps of 2 degrees C until it reached 41 degrees or 43 degrees C. While the other hand or forearm was kept immersed in a water bath (Tw, 35 degrees C), blood flow in the heated side (BFw) was compared with the corresponding blood flow in the control side (BFc). Under WARM or HOT conditions, finger BFw was significantly lower than finger BFc at a Tw of 39-41 degrees C in the majority of subjects. When Tw was raised to 43 degrees C, however, finger BFw became higher than BFc in nearly half of the subjects. In the COOL state, finger BFw did not decrease but increased steadily when Tw increased from 37 degrees to 43 degrees C. In the forearm, BFw increased steadily with increasing Tw even in WARM-HOT environments. No such heat-induced vasoconstriction was observed in the forearm. From these results we conclude that in hyperthermic subjects, the rise in local temperature to above core temperature produces vasoconstriction in the fingers, an area where no thermal sweating takes place.

Adult↗

Active and inactive renin in human forearm of hypertensive patients.

Although many in vitro and animal studies indicate the existence of a local renin--angiotensin system, data regarding its physiological role are quite controversial, and moreover, evidence suggesting inactive and active renin release from vascular tissue in vivo is lacking both in animal and humans. The aim of our study was to evaluate whether beta-adrenoceptor stimulation, a well-known stimulus to renin production, through isoproterenol might cause local renin production from vessels of the forearm of hypertensive patients. Drugs were infused into the brachial artery at systemically ineffective rates, while forearm blood flow (FBF, venous plethysmography), mean intra-arterial pressure, and heart rate were monitored throughout. Active and inactive vessel renin production was measured by calculating venous-arterial (V-A) differences by simultaneous sampling from brachial artery and an ipsilateral deep vein. Active renin (PRA) and total renin (Sepharose bound trypsin activation) were measured by radioimmunoassay while inactive renin was calculated as the difference between total and active renin. V-A differences were corrected for FBF to calculate renin extraction or production. In a group of 10 patients, isoproterenol, which was infused at increasing cumulative rates (0.03, 0.1, 0.3 micrograms.100 mL-1 forearm tissue.min-1 for 5 min each), caused a dose-dependent increment in FBF that was blunted by intra-arterial propranolol (n = 5) pretreatment (10 micrograms.100 mL-1 forearm tissue.min-1 for 10 min). beta-Adrenoceptor stimulation caused a dose-dependent outflow of both active and inactive renin, an effect antagonized by propranolol. In conclusion, our data represent the first evidence in humans of tissue active and inactive renin production in the forearm vascular bed.

Female↗

Ultrasonography for the interosseous membrane of the forearm.

The ability to improve the technique for an accurate clinical diagnosis of the injury of interosseous membrane of the forearm (IOM) associated with forearm fractures and dislocations is important for its treatment and prognosis. Ultrasound examination of the IOM in 46 forearms from 18 normal volunteers, five patients with restricted forearm pronation and supination, and two preoperative cases was performed to determine the usefulness and reproductivity of this examination. The intact IOM was observed as a continuous, slightly convex anteriorly and hyperechoic structure between the radius and ulna with both transverse and longitudinal views. IOMs with histories of forearm injuries were distinguished by the findings, which demonstrated a loss of continuity and were seen as hypoechoic traces from the others. This study confirmed that it is possible to trace the entire IOM and to detect differences between intact and disrupted IOMs with transverse and longitudinal views.

Adolescent↗

Influence of puberty on muscle development at the forearm.

Despite its fundamental importance for physical development, the growth of the muscle system has received relatively little consideration. In this study, we analyzed the relationship between cross-sectional area (CSA) of forearm muscles and maximal isometric grip force with age and pubertal stage. The study population comprised 366 children, adolescents, and young adults from 6 to 23 yr of age (185 female) and 107 adults (88 female) aged 29 to 40 yr. By use of peripheral quantitative computed tomography, muscle CSA was determined at the site of the forearm, whose distance to the ulnar styloid process corresponded to 65% of forearm length. Both muscle CSA and grip force were higher in prepubertal boys than in girls. The gender differences decreased until pubertal stage 3 and reincreased thereafter. In girls at pubertal stage 5, muscle CSA no longer increased with age (P > 0.4), whereas there was still some age-related increase in grip force (P = 0.02). In boys at pubertal stage 5, both muscle CSA and grip force continued to increase significantly with age (P < 0.005 each). Specific grip force (grip force per muscle CSA) adjusted for forearm length increased by almost one-half between 6 and 20 yr of age, with no difference between the genders. In conclusion, forearm muscle growth takes a gender-specific course during puberty, indicating that it is influenced by hormonal changes. However, the increase in specific grip force is similar in both genders and thus appears to be independent of sex hormones.

Adolescent↗

Growth hormone acutely stimulates forearm muscle protein synthesis in normal humans.

The short-term effects of growth hormone (GH) on skeletal muscle protein synthesis and degradation in normal humans are unknown. We studied seven postabsorptive healthy men (age 18-23 yr) who received GH (0.014 micrograms.kg-1.min-1) via intrabrachial artery infusion for 6 h. The effects of GH on forearm amino acid and glucose balances and on forearm amino acid kinetics [( 3H]Phe and [14C]Leu) were determined after 3 and 6 h of the GH infusion. Forearm deep vein GH rose to 35 +/- 6 ng/ml in response to GH, whereas systemic levels of GH, insulin, and insulin-like growth factor I (IGF-I) were unchanged. Forearm glucose uptake did not change during the study. After 6 h, GH suppressed forearm net release (3 vs. 6 h) of Phe (P less than 0.05), Leu (P less than 0.01), total branched-chain amino acids (P less than 0.025), and essential neutral amino acids (0.05 less than P less than 0.1). The effect on the net balance of Phe and Leu was due to an increase in the tissue uptake for Phe (71%, P less than 0.05) and Leu (37%, P less than 0.005) in the absence of any significant change in release of Phe or Leu from tissue. In the absence of any change in systemic GH, IGF-I, or insulin, these findings suggest that locally infused GH stimulates skeletal muscle protein synthesis. These findings have important physiological implications for both the role of daily GH pulses and the mechanisms through which GH can promote protein anabolism.

Adult↗

Forearm vasodilator mechanisms during mental stress: possible roles for epinephrine and ANP.

The contribution of epinephrine (Epi) to forearm vasodilator responses to mental stress was evaluated in 12 healthy men by comparing hemodynamic and plasma catecholamine responses to mental stress and to intravenous and intra-arterial infusions of epinephrine. Mental stress decreased forearm vascular resistance (FVR) by 45%, increased arterial Epi from 0.23 to 0.44 nmol/l in arterial plasma, and increased forearm norepinephrine overflow. Intra-arterial Epi infusion decreased FVR concentration dependently by up to 43%. Intravenous Epi infusion decreased diastolic arterial pressure and increased heart rate and systolic blood pressure dose dependently. FVR decreased by up to 39% at 4.60 nmol/l Epi in arterial plasma. The average Epi contribution to forearm vasodilation during mental stress was calculated to be between 9 and 30%, depending on if responses to stress were compared with intravenous or intra-arterial Epi infusion. Arterial atrial natriuretic peptide immunoreactivity increased by 23% during stress, supporting a vasodilator influence, whereas vasopressin immunoreactivity was unaffected. Thus secretion of Epi explains only part of the stress-induced forearm vasodilation. Intravenous infusion of Epi appears to activate sympathetic counterregulation.

Adult↗

Inhibition of vascular ATP-sensitive K+ channels does not affect reactive hyperemia in human forearm.

The extent to which ATP-sensitive K(+) channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K(+) channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced (n = 9). The contribution of vascular ATP-sensitive K(+) channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K(+) channel inhibitor (n = 12). To document ATP-sensitive K(+) channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K(+) channel opener, was undertaken (n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K(+) channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.

Adenosine Triphosphate↗

Impact of combined NO and PG blockade on rapid vasodilation in a forearm mild-to-moderate exercise transition in humans.

We tested the hypothesis that nitric oxide (NO) and prostaglandins (PGs) contribute to the rapid vasodilation that accompanies a transition from mild to moderate exercise. Nine healthy volunteers (2 women and 7 men) lay supine with forearm at heart level. Subjects were instrumented for continuous brachial artery infusion of saline (control condition) or combined infusion of N(G)-nitro-L-arginine methyl ester (L-NAME) and ketorolac (drug condition) to inhibit NO synthase and cyclooxygenase, respectively. A step increase from 5 min of steady-state mild (5.4 kg) rhythmic, dynamic forearm handgrip exercise (1 s of contraction followed by 2 s of relaxation) to moderate (10.9 kg) exercise for 30 s was performed. Steady-state forearm blood flow (FBF; Doppler ultrasound) and forearm vascular conductance (FVC) were attenuated in drug compared with saline (control) treatment: FBF = 196.8 +/- 30.8 vs. 281.4 +/- 34.3 ml/min and FVC = 179.3 +/- 29.4 vs. 277.8 +/- 34.8 ml.min(-1).100 mmHg(-1) (both P < 0.01). FBF and FVC increased from steady state after release of the initial contraction at the higher workload in saline and drug conditions: DeltaFBF = 72.4 +/- 8.7 and 52.9 +/- 7.8 ml/min, respectively, and DeltaFVC = 66.3 +/- 7.3 and 44.1 +/- 7.0 ml.min(-1).100 mmHg(-1), respectively (all P < 0.05). The percent DeltaFBF and DeltaFVC were not different during saline infusion or combined inhibition of NO and PGs: DeltaFBF = 27.2 +/- 3.1 and 28.1 +/- 3.8%, respectively (P = 0.78) and DeltaFVC = 25.7 +/- 3.2 and 26.0 +/- 4.0%, respectively (P = 0.94). The data suggest that NO and vasodilatory PGs are not obligatory for rapid vasodilation at the onset of a step increase from mild- to moderate-intensity forearm exercise. Additional vasodilatory mechanisms not dependent on NO and PG release contribute to the immediate and early increase in blood flow in an exercise-to-exercise transition.

Adult↗

Acute changes in forearm venous volume and tone using radionuclide plethysmography.

In this investigation blood pool scintigraphy was validated as a method to study acute changes in human forearm veins. Changes in regional forearm vascular volume (capacity) and the occluding pressure-volume (P-V) relationship induced by sublingual nifedipine (NIF) and nitroglycerin (GTN) were recorded in 16 patients with simultaneous data collection by the radionuclide and the mercury-in-rubber strain-gauge techniques. The standard error of estimate (Syx) between successive control measurements using the radionuclide method was 3.1% compared with 3.2% for the strain-gauge method. The venous P-V curves were highly reproducible using both techniques. Strain gauge and radionuclide measurements of acute changes in forearm venous volume correlated well (r = 0.86; Syx = 7%, n = 156). After 20 mg of NIF or 0.6 mg of GTN, mean heart rate increased from 71 +/- 10 to 77 +/- 9 and from 68 +/- 10 to 75 +/- 11 beats/min, respectively, and group systolic blood pressure decreased from 128 +/- 22 to 120 +/- 19 and from 136 +/- 18 to 126 +/- 23 mmHg, respectively (P less than 0.05). At venous occluding pressures of 0 and 30 mmHg, the forearm vascular volume did not change after NIF (2 +/- 4 and -1 +/- 4%; P greater than 0.05), whereas it increased after GTN (8 +/- 5 and 12 +/- 7%; P less than 0.001). The forearm venous P-V relationship did not change after NIF, whereas a significant rightward shift (venodilation, with an increase in unstressed volume) occurred after GTN.(ABSTRACT TRUNCATED AT 250 WORDS)

Forearm↗

Atrial natriuretic peptide augments forearm capillary filtration in humans.

Low-dose infusions of atrial natriuretic peptide (ANP) into humans reduce cardiac filling pressures without enhancing renal excretion or producing vasodilation. The present human study was undertaken to seek an effect of ANP on capillary filtration in humans and to determine its relationship to reductions in cardiac filling pressures. Heart rate (electrocardiogram), blood pressure (cuff method), and renal excretion of salt and water were determined, and central venous pressure (jugular vein cannulation, strain-gauge transducer) and forearm venous compliance and capillary filtration coefficient (strain-gauge plethysmography) were derived by computer. Forearm girth and venous pressure (peripheral vein catheter) measurements were obtained while the arm was elevated above heart level, and an upper arm blood pressure cuff was intermittently inflated to venous occluding pressures of 20, 30, and 40 mmHg. Forearm measurements, hematocrit, plasma proteins, albumin and plasma levels of ANP were determined from euvolemic volunteers before and during 60 min intravenous infusions of ANP (5 ng.kg-1.min-1, n = 9) or placebo (isotonic saline, n = 7). ANP infusions produced physiological increases (4- to 5-fold) in plasma ANP (from a base line 35 +/- 6 pg/ml) (P less than 0.05). Hemodynamic responses to ANP consisted of a reduction in central venous pressure (P less than 0.05) and no change in heart rate, mean arterial pressure, or renal excretory parameters. ANP increased forearm capillary filtration between 37 and 63% (P less than 0.05) from base line but did not significantly alter forearm compliance measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗