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Biomedical subjects

C Giannattasio

Publications and source records attributed to C Giannattasio.

At least 55 records · Page 3Linked to original sources
PubMed1995

Sympathetic activation and loss of reflex sympathetic control in mild congestive heart failure.

BACKGROUND: Baroreflex control of sympathetic activity is impaired in severe congestive heart failure (CHF), probably causing the marked sympathetic activation typical of this condition. Little information exists, however, as to whether baroreflex impairment and related sympathetic activation also occur in mild CHF. METHODS AND RESULTS: We studied 19 patients (age, 57.5 +/- 2.2 years, mean +/- SEM) with CHF in New York Heart Association (NYHA) class III or IV and with a marked reduction in left ventricular ejection fraction (LVEF, 30.1 +/- 1.5% from echocardiography) and 17 age-matched patients with CHF in NYHA class I or II and with an only slightly reduced LVEF (44.9 +/- 3.3%) that never was < 40%. Seventeen age-matched healthy subjects served as control subjects. Primary measurements included beat-to-beat arterial blood pressure (with the Finapres technique), heart rate (from ECG), and postganglionic muscle sympathetic nerve activity (MSNA, from microneurography at the peroneal nerve). Measurements were performed at baseline and during baroreceptor stimulation (intravenous phenylephrine infusion), baroreceptor deactivation (intravenous nitroprusside infusion), and cold-pressor test. Baseline blood pressure was similar in the three groups, whereas heart rate was progressively greater from control subjects to patients with mild and severe CHF, MSNA (bursts per 100 heart beats) increased significantly and markedly from control subjects to patients with mild and severe CHF (47.1 +/- 2.9 versus 64.4 +/- 6.2 and 82.1 +/- 3.4, P < .05 and P < .01, respectively). Heart rate and MSNA were progressively reduced by phenylephrine infusion and progressively increased by nitroprusside infusion. Compared with control subjects, the responses were strikingly impaired in severe CHF patients, but a marked impairment also was seen in mild CHF patients. On average, baroreflex sensitivity in mild CHF patients was reduced by 59.1 +/- 5.5% (MSNA) and 64.8 +/- 4.8% (heart rate). In contrast, reflex responses to the cold-pressor test were similar in the three groups. CONCLUSIONS: These results demonstrate that in mild CHF patients the baroreceptor inhibitor influence on heart rate and MSNA is already markedly impaired. This impairment may be responsible for the early sympathetic activation that occurs in the course of CHF.

Adult↗
PubMed1995

Alterations of radial artery compliance in patients with congestive heart failure.

Congestive heart failure is accompanied by several hemodynamic alterations. To investigate whether these alterations include reduced arterial compliance, we studied 25 patients (age 57 +/- 2 years, mean +/- SE) with a mild or severe congestive heart failure based on clinical symptoms (New York Heart Association class II vs III or IV) and on echocardiographic alterations of left ventricular diastolic diameter and ejection fraction. Radial artery diameter and blood pressure were continuously measured by Doppler ultrasonography and a finger pressure device, respectively. Compliance was calculated by the Langewouters formula, and compliance values were derived throughout the systolic-diastolic pressure range. The area under the compliance-pressure curve normalized for pulse pressure was used to compare compliance values in the various groups. Data were obtained both in baseline condition and at the release from a 12-minute brachial artery occlusion. Fourteen healthy, age-matched subjects served as controls. Compared with the control group, patients with severe congestive heart failure showed a reduction of baseline compliance index (-48%, p < 0.01). Furthermore, while in control subjects compliance markedly increased after brachial artery occlusion (+43%, p < 0.01), in patients with severe congestive heart failure no increase occurred. No baseline compliance alteration was seen in patients with mild congestive heart failure in whom, however, the postischemic increase in compliance was also significantly blunted (-50% vs controls, p < 0.05). Thus, arterial compliance and arterial compliance modulation are impaired in congestive heart failure. Although more marked in severe congestive heart failure, the impairment is manifest in mild congestive heart failure as well.

Blood Pressure Determination↗
PubMed1995

Structural cardiovascular alterations and blood pressure variability in human hypertension.

AIM: To evaluate the cardiovascular risk of hypertensive patients in relation to left ventricular hypertrophy, arteriolar hypertrophy and blood pressure variability, and the effects of antihypertensive treatment. LEFT VENTRICULAR HYPERTROPHY: In hypertensive subjects with marked left ventricular hypertrophy, cardiovascular problems are about three times more frequent than in hypertensives who do not have left ventricular hypertrophy. The evidence suggests, however, that a moderate degree of left ventricular hypertrophy may be compensatory and that regression of mild hypertrophy should not necessarily be pursued. ARTERIOLAR HYPERTROPHY: An increased wall to lumen ratio leads to an increase in vascular resistance and thus promotes hypertension. Regression of this alteration with antihypertensive treatment appears to be both beneficial and achievable, although it is not clear whether all antihypertensive agents have the same effect. Moreover, there are methodological problems in determining whether a regression has actually been achieved. BLOOD PRESSURE VARIABILITY: There is evidence to suggest that end-organ damage is more frequent and more marked in hypertensives with greater 24 h blood pressure variability. It appears that antihypertensive treatment does not easily reduce this variability, although the intermittent measurements taken by automatic monitoring devices do not fully reflect patterns of blood pressure variation. It may be that hypertensives with a greater degree of blood pressure variability can obtain a reduction in the magnitude of this variability with antihypertensive treatment.

Antihypertensive Agents↗
PubMed1995

Sympathetic activation in obese normotensive subjects.

Human obesity is characterized by profound alterations in the hemodynamic and metabolic states. Whether these alterations involve sympathetic drive is controversial. In 10 young obese subjects (body mass index, 40.5 +/- 1.2 kg/m2, mean +/- SEM) with normal blood pressure and 8 age-matched lean normotensive control subjects, we measured beat-to-beat arterial blood pressure (Finapres technique), heart rate (electrocardiogram), postganglionic muscle sympathetic nerve activity (microneurography at the peroneal nerve), and venous plasma norepinephrine (high-performance liquid chromatography). The measurements were performed in baseline conditions and, with the exception of plasma norepinephrine, during baroreceptor stimulation and deactivation caused by increases and reductions of blood pressure via intravenous infusions of phenylephrine and nitroprusside. Baseline blood pressure and heart rate were similar in obese and control subjects. Plasma norepinephrine was also similar in the two groups. Muscle sympathetic nerve activity, however, was 38.6 +/- 5.1 bursts per minute in obese subjects and less than half that level in control subjects (18.7 +/- 1.3 bursts per minute), the difference being highly statistically significant (P < .02). Muscle sympathetic nerve activity and heart rate were reduced during phenylephrine infusion and increased during nitroprusside infusion, but the changes were about half as great in obese subjects as in control subjects. Thus, even in the absence of any blood pressure alteration, human obesity is characterized by a marked sympathetic activation, possibly because of an impairment of reflex sympathetic restraint. This may be involved in the high rate of hypertension and cardiovascular complications seen in obesity.

Adult↗
PubMed1995

Sympathetic modulation of radial artery compliance in congestive heart failure.

Animal studies have suggested that arterial compliance can be modulated by adrenergic influences. Whether this adrenergic modulation also occurs in humans is still a matter of debate. In the present article we address this issue by examining the relationships between sympathetic tone and arterial compliance in a variety of physiological and pathophysiological conditions. We have found that cigarette smoking, ie, an action that produces a marked sympathetic activation, causes a significant reduction in radial artery compliance, as measured by an echotracking device capable of providing continuous beat-to-beat evaluation of this hemodynamic variable. When expressed as compliance index, ie, as the ratio between the area under the compliance-pressure curve and pulse pressure, the reduction amounted to 35.7 +/- 4.8% (mean +/- SEM) and was independent of the smoking-related blood pressure increase. Furthermore, pharmacological stimulation of adrenergic receptors located in the arterial wall was also shown to affect arterial compliance because the radial artery compliance index was markedly reduced (- 29.5 +/- 3.9%) during phenylephrine infusion in the brachial artery at doses devoid of any systemic blood pressure effect. Evidence was also obtained that the relationship between sympathetic activation and arterial compliance has pathophysiological relevance, because in 17 patients with congestive heart failure (New York Heart Association classes II through IV) there was a significant inverse correlation (r = .62, P < .01) between muscle sympathetic nerve activity (directly measured by microneurography in the peroneal nerve) and radial artery compliance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Angiotensin-converting enzyme inhibition and radial artery compliance in patients with congestive heart failure.

Congestive heart failure is characterized by a clear-cut impairment of arterial compliance of medium-sized arteries, but whether this alteration is irreversible or can be favorably affected by cardiovascular drugs currently used in congestive heart failure treatment is unknown. We studied 9 congestive heart failure patients (New York Heart Association class II; age, [mean +/- SEM] 60.7 +/- 3.3 years) receiving diuretic and digitalis treatment in whom arterial compliance was assessed at the level of the radial artery by an echotracking device capable of measuring the arterial diameter along the entire cardiac cycle. Beat-to-beat arterial blood pressure was concomitantly measured by a Finapres device that allowed diameter-pressure curves and compliance-pressure curves (Langewouters' formula) to be calculated for the entire systolic-diastolic blood pressure range. Arterial compliance was expressed as the area under the compliance-pressure curve normalized for pulse pressure (compliance index). Data were collected before and after 4 and 8 weeks of oral administration of benazepril (10 mg/day). Ten healthy subjects were studied before and after an observational period of 4 weeks (5 subjects) or 8 weeks (5 subjects), and 9 age-matched mildly essential hypertensive subjects studied before and after 4 to 12 weeks of benazepril administration served as control subjects. In congestive heart failure patients, baseline compliance index was significantly less than in normotensive and hypertensive subjects. However, the compliance index showed a marked increase after 4 weeks of benazepril administration (+95.7 +/- 24.9%, P < .05); the increase was also marked after 8 weeks of angiotensin-converting enzyme inhibitor treatment (+77.7 +/- 4.2%, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Radial artery compliance in young, obese, normotensive subjects.

Obesity is characterized by a number of cardiovascular alterations, and whether these alterations involve arterial compliance is unknown. In 12 young, obese, normotensive subjects (age, 23.9 +/- 1.3 years; mean +/- SEM) and 12 age- and sex-matched lean control subjects we measured blood pressure, radial artery diameter, and radial artery compliance continuously over the systodiastolic pressure range with a Finapres device and recently developed echo-tracking device. Measurements were obtained at baseline and after prolonged ischemia, that is, when diameter and compliance are increased. Blood pressure values were normal in both groups (obese subjects: 109.2 +/- 4.9/68.2 +/- 2.7 mm Hg; lean control subjects: 108.2 +/- 4.1/60.7 +/- 3.8 mm Hg), but in addition to a marked increase in body mass index (38.5 +/- 0.8 versus 23.1 +/- 0.9 kg/m2, P < .01), obese subjects showed a slight and nonsignificant increase in heart rate (71.1 +/- 3.2 versus 66.7 +/- 3.3 beats per minute, P = NS), increases in left ventricular wall thickness and left ventricular mass index (121.5 +/- 4.8 versus 103.4 +/- 3.3 kg/m2, P < .01), no changes in plasma renin activity and plasma norepinephrine (compared with normal values), and a marked reduction in total body glucose uptake (glucose clamp technique). Obese subjects showed radial artery diameter and compliance values that were greater than those seen in control subjects throughout the systodiastolic pressure range. The differences were 13% (P < .05) and 96% (P < .01), respectively, and both diameter and compliance remained higher in obese than lean subjects after forearm ischemia. In obese and lean subjects baseline radial artery diameter values correlated highly with body weight, body surface area, and body mass index.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Cardiac and vascular structural changes in normotensive subjects with parental hypertension.

OBJECTIVE: To evaluate whether a predisposition to hypertension is associated with early cardiac and vascular alterations. SUBJECTS: Twenty-five normotensive subjects with both parents hypertensive (group 1) and 28 age- and sex-matched control subjects with both parents normotensive (group 2). METHODS: In the two groups the measurements included: clinic blood pressure; left ventricular end-diastolic diameter, septal wall thickness and posterior wall thickness (by echocardiography); minimal forearm and calf vascular resistances (i.e. resistance assessed immediately after prolonged ischaemia, which depends on arteriolar wall thickness); and baseline and postischaemic radial artery compliance-pressure curves over the systolodiastolic pressure range (by echotracking device and finger blood pressure). RESULTS: Group 1 had a slightly higher clinic blood pressure, and septal and posterior wall thickness, than group 2. Minimal forearm vascular resistance was clearly greater in group 1 than in group 2, whereas minimal calf vascular resistance was not significantly different in the two groups. Radial artery compliance was also similar in the two groups. CONCLUSIONS: Parental predisposition to hypertension is accompanied by cardiac and arteriolar structural changes qualitatively similar to those found in hypertensive patients, although arteriolar structural changes do not involve all vascular beds. Arterial compliance is not altered in this condition. Vascular changes may be determined by mechanisms other than blood pressure elevation.

Adult↗
PubMed1995

[Changes in the compliance of the radial artery in normotensive subjects with familial hypercholesterolemia].

BACKGROUND: Recent studies have shown that in normotensive hypercholesterolemic subjects endothelial dependent dilatation of arterioles is impaired. METHODS: We studied the effects of hypercholesterolemia on arterial compliance in normotensive subjects of both sexes, with a normal serum cholesterol (n = 8, total serum cholesterol = 209 +/- 7 mg/dl, means +/- SEM), an elevated serum cholesterol (n = 8, 285 +/- 8 mg/dl) and familial hypercholesterolemia (n = 8, 393 +/- 20 mg/dl). All subjects were normotensive and devoid of clinical and laboratory evidence of atherosclerotic lesions. The mean age of the 3 groups was 46.7 +/- 2.5, 51.5 +/- 2.9 and 49.8 +/- 2.9 years respectively. In hypercholesterolemic subjects use of hypolipidemic drugs was stopped 2 months before the study. Arterial compliance was measured from the radial artery by an echo-tracking device capable of providing radial artery diameter and, with the addition of a Finapres device, diameter/pressure and compliance/pressure curves continuously over the systolic-diastolic blood pressure range. RESULTS: Mean arterial pressure was similar in the three groups (84.5 +/- 6.1, 79.8 +/- 2.4 and 73.1 +/- 4.4 mm Hg). Arterial compliance was similar in normocholesterolemic and non familial hypercholesterolemic subjects but it was strikingly reduced (50%) in familial hypercholesterolemic subjects. The reduction was even more evident following prolonged local ischemia because while in the first two groups arterial compliance increased after ischemia, in familial hypercholesterolemia no increase occurred. CONCLUSIONS: Thus, familial hypercholesterolemia is accompanied by a striking CONCLUSIONS: Thus, familial hypercholesterolemia is accompanied by a striking reduction in radial artery compliance, i.e. a marked increase in arterial wall stiffness. This may increase the traumatic effect of blood pressure on the arterial wall, favouring atherosclerosis. The lack of compliance alterations in non familial hypercholesterolemia suggests that this hemodynamic disturbance either occurs when serum cholesterol is more markedly increased or it has a genetic origin.

Analysis of Variance↗
PubMed1995

Reproducibility of ultrasound assessment of common carotid and femoral artery compliance and distensibility in the anesthetized rat.

OBJECTIVE: To validate ultrasound assessment of common carotid and femoral artery compliance and distensibility in the anesthetized rat. MATERIALS AND METHODS: A reproducibility study was performed by taking measurements twice on two different days in anesthetized Wistar-Kyoto (WKY) rats. The common carotid or femoral arterial diameter on one side and the contralateral arterial blood pressure were measured using a 10-MHz probe echo-Doppler device and an arterial catheter, respectively. The pressure and diameter data were stored in a computer programmed to calculate the arterial compliance and distensibility coefficients (Reneman formulas) and compliance and distensibility indices (arctangent model of Langewouters). A second experimental session was repeated 1 day later, and mean values, day-to-day mean differences and repeatability coefficients were calculated for each parameter. RESULTS: For both the common carotid and the femoral artery, the mean values for heart rate, mean arterial pressure, arterial diameter, arterial compliance and arterial distensibility were similar on the first and second days; mean day-to-day differences were small and repeatability coefficients were in the range 5-10% of the mean value for diameter and mean arterial pressure and 10-20% of the mean value for compliance and distensibility. CONCLUSIONS: In the anesthetized rat, ultrasound evaluation of the mechanical properties of the common carotid and femoral arteries is a reliable and reproducible technique.

Anesthesia, General↗
PubMed1994

Mechanisms responsible for sympathetic activation by cigarette smoking in humans.

BACKGROUND: The pressor and tachycardic effects of cigarette smoking are associated with an increase in plasma catecholamines, suggesting the dependence of these effects on adrenergic stimulation. Whether the stimulation occurs at a central or a peripheral level and whether reflex mechanisms are involved is unknown. METHODS AND RESULTS: In nine normotensive healthy subjects (age, 33.0 +/- 3.5 years, mean +/- SEM), we measured blood pressure (Finapres device), heart rate (ECG), calf blood flow and vascular resistance (venous occlusion plethysmography), plasma norepinephrine and epinephrine (high-performance liquid chromatography assay), and postganglionic muscle sympathetic nerve activity (microneurography from the peroneal nerve) while subjects were smoking a filter cigarette (nicotine content, 1.1 mg) or were in control condition. Cigarette smoking (which raised plasma nicotine measured by high-performance liquid chromatography from 1.0 +/- 0.9 to 44.2 +/- 7.1 ng/mL) markedly and significantly increased mean arterial pressure (+13.2 +/- 2.3%), heart rate (+30.3 +/- 4.7%), calf vascular resistance (+12.1 +/- 4.9%), plasma norepinephrine (+34.8 +/- 7.0%), and plasma epinephrine (+90.5 +/- 39.0%). In contrast, muscle sympathetic nerve activity showed a marked reduction (integrated activity -31.8 +/- 5.1%, P < .01). The reduction was inversely related to the increase in mean arterial pressure (r = -.67, P < .05), but the slope of the relation was markedly less (-54.1 +/- 7.5%, P < .05) than that obtained by intravenous infusion of phenylephrine in absence of smoking. The hemodynamic and neurohumoral changes were still visible 30 minutes after smoking and occurred again on smoking a second cigarette. Sham smoking was devoid of any hemodynamic and neurohumoral effect. CONCLUSIONS: These data support the hypothesis that in humans the sympathetic activation induced by smoking depends on an increased release and/or a reduced clearance of catecholamines at the neuroeffector junctions. Central sympathetic activity is inhibited by smoking, presumably via a baroreceptor stimulation triggered by the smoking-related pressor response. The baroreflex is impaired by smoking, however, indicating that partial inability to reflexly counteract the effect of sympathetic activation is also responsible for the pressor response.

Adult↗
PubMed1994

[Hemodynamics and pressure variability in isolated systolic hypertension].

Isolated systolic hypertension is a common feature in aged individuals and it has been associated with an increased cardiovascular mortality and morbidity. More recently it has been shown that this condition is characterized by peculiar abnormalities of arterial vessels. For example isolated systolic hypertension is associated with a reduction in arterial compliance evident both in muscle arteries, like the radial one, and in elastic arteries, like the carotid one. On the other side cardiovascular homeostasis is markedly deranged and blood pressure variability more marked than in age matched normotensive subjects. Finally, 24-hour blood pressure monitoring has allowed to exclude that isolated systolic hypertension might be merely linked to an exaggerated alarm reaction, showing that blood pressure is elevated along the whole 24-hour blood pressure profile.

Hemodynamics↗
PubMed1994

Alterations in neural cardiovascular control mechanisms with ageing.

AGEING AND MECHANISMS OF BLOOD PRESSURE CONTROL: Ageing is associated with functional and structural alterations to the cardiovascular system. Evidence is accumulating, however, that ageing also determines major changes in the effectiveness of mechanisms involved in blood pressure control and that this represents an important determinant of the cardiovascular changes that can be observed in the elderly. DIFFERENCES SEEN IN ELDERLY SUBJECTS: It has been observed that compared to young subjects, in the elderly (1) baroreceptor control of the heart rate and cardiac function is impaired; (2) baroreceptor modulation of the sympathetic drive to the peripheral circulation is impaired, particularly the speed of reflex adjustments to normal and abnormal stimuli; and (3) cardiopulmonary stretch receptors, which tonically inhibit sympathetic tone, the renal release of renin and vasopressin secretion, are impaired. These three factors may account, at least in part, for the raised blood pressure and sympathetic activity in the elderly. They certainly explain the reduced ability of elderly people to maintain blood pressure and blood volume homeostasis, and their increased blood pressure variability over 24 h. ASSOCIATION WITH HYPERTENSION: All these problems are exacerbated if ageing is associated with hypertension, and are highly relevant to antihypertensive treatment. Care should be taken that any antihypertensive drugs selected for treatment in the elderly do not aggravate these basic homeostatic problems.

Aged↗
PubMed1994

Acute effects of smoking on radial artery compliance in humans.

OBJECTIVE: To clarify whether the acute and marked increase in blood pressure associated with smoking is accompanied by an alteration in arterial compliance. DESIGN: Arterial compliance was measured in 13 subjects before and after smoking a cigarette with a nicotine content of 1.2 mg, or before and after sham smoking. Measurements were obtained with the subjects at rest and after prolonged brachial artery occlusion (12 min). METHODS: Compliance was measured using an echo-tracking system capable of continuously providing (300 readings/s) radial diameter data and, with the addition of a photoplesythmographic device, blood pressure measurement. RESULTS: Acute cigarette smoking caused a pressor and tachycardic response, and decreased markedly both resting radial artery diameter and compliance, at blood pressure values identical to those before smoking. The marked increase in radial artery diameter and compliance brought about by local ischaemia was unaffected by smoking, and no changes were observed both at rest and after ischaemia as a result of sham smoking. CONCLUSIONS: Smoking causes a marked reduction in radial artery compliance, and the effect is independent of the increase in blood pressure. However, the marked increase in compliance due to ischaemia is not modified by smoking.

Adult↗
PubMed1993

Vascular effects of lacidipine: a review of animal and human data.

AIM: To compare the vascular effects of lacidipine with those of other calcium antagonists. METHODS: A review of published studies. RESULTS: Experimental studies have shown that for a similar fall in blood pressure, lacidipine increased cardiac contractility while verapamil decreased cardiac contractility. In the rat aorta, the dose of lacidipine required to reduce a calcium-induced contraction by 50% was lower than that of all other calcium antagonists tested except nisoldipine. In human studies, especially, there are inherent limitations in the techniques available to measure regional blood flows under physiological conditions, making it difficult to compare the effects of different antihypertensive drugs. A recent study showed that renal blood flow was increased by lacidipine without any reduction in renal function. As in animals, vital organ perfusion was either preserved or increased. Further, maximal coronary vasodilation was associated with lower coronary resistance values during lacidipine treatment compared with pretreatment values. Another lacidipine study showed increased brachial artery compliance, while a study on the radial artery showed that lacidipine increased the compliance of this artery also. CONCLUSIONS: Lacidipine has vascular selectivity. Although regional blood flows are difficult to measure, due to inherent limitations in the techniques available, the evidence suggests that lacidipine produces vasodilation in essential hypertensive subjects while maintaining or even increasing vital organ perfusion. This appears to be due to a regression of the structural changes that characterize hypertension.

Animals↗
PubMed1993

Reflex vasopressin and renin modulation by cardiac receptors in humans.

Animal studies have shown that vasopressin secretion is modulated by arterial baroreceptors and cardiopulmonary volume receptors. Whether this is the case also in humans is controversial, however. To determine whether vasopressin is reflexly modulated by cardiac volume receptors, we studied the effect on plasma vasopressin (venous blood, radioimmunoassay) of reducing venous return and left ventricular end-diastolic diameter (echocardiography) by producing a 20-minute lower body negative pressure in 14 healthy subjects (aged 49.3 +/- 3.8 years, mean +/- SEM). The data were compared with those of 14 age-matched heart-transplant recipients, i.e., subjects with cardiac denervation. In healthy subjects, lower body negative pressure at -15 mm Hg caused a modest reduction in left ventricular end-diastolic diameter (-5 +/- 3.4%) and no change in vasopressin, whereas lower body negative pressure at -37.5 mm Hg caused a more marked reduction in left ventricular end-diastolic diameter (-12 +/- 2.5%) and a small, variable, but overall statistically significant (p < 0.05) increase in vasopressin (+145 +/- 46%, p < 0.01). The left ventricular end-diastolic diameter changes induced by the two lower body negative pressure stimuli were similar in heart-transplant recipients, but the vasopressin increase seen with the lower body negative pressure at -37.5 mm Hg was abolished. The marked increase in plasma renin activity and forearm vascular resistance induced by lower body negative pressure in healthy subjects was also abolished or drastically attenuated in heart-transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗