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Biomedical subjects

G L Jennings

Publications and source records attributed to G L Jennings.

At least 19 recordsLinked to original sources
PubMed1992

Pet ownership and risk factors for cardiovascular disease.

OBJECTIVE: To compare risk factors for cardiovascular disease in pet owners and non-owners. DESIGN AND PATIENTS: Accepted risk factors for cardiovascular disease were measured in 5741 participants attending a free, screening clinic at the Baker Medical Research Institute in Melbourne. Blood pressure, plasma cholesterol and triglyceride values were compared in pet owners (n = 784) and non-owners (n = 4957). RESULTS: Pet owners had significantly lower systolic blood pressure and plasma triglycerides than non-owners. In men, pet owners had significantly lower systolic but not diastolic blood pressure than non-owners, and significantly lower plasma triglyceride levels, and plasma cholesterol levels. In women over 40 years old, systolic but not diastolic pressure was significantly lower in pet owners and plasma triglycerides also tended to be lower. There were no differences in body mass index and self-reported smoking habits were similar, but pet owners reported that they took significantly more exercise than non-owners, and ate more meat and "take-away" foods. The socioeconomic profile of the pet owners and non-owners appeared to be comparable. CONCLUSIONS: Pet owners in our clinic population had lower levels of accepted risk factors for cardiovascular disease, and this was not explicable on the basis of cigarette smoking, diet, body mass index or socioeconomic profile. The possibility that pet ownership reduces cardiovascular risk factors should therefore be investigated.

Animals↗
PubMed1992

Exercise training reduces the sympathetic component of the blood pressure-heart rate baroreflex in man.

1. Exercise training reduces resting sympathetic activity, but the effects on sympathetic activation or withdrawal during baroreflex responses to blood pressure perturbations are controversial. The purpose of this study was to investigate the effects of training on both the vagal and sympathetic reflex heart rate responses to blood pressure changes. 2. Using 10 healthy males in a randomized cross-over design, we examined the effects of three 30 min cycling sessions at 70% of maximal capacity for 4 weeks on the steady-state reflex heart rate responses to perturbations in mean arterial pressure induced with injections of nitroprusside and phenylephrine. The method provides a sigmoidal relationship between changes in heart rate and blood pressure. The upper plateau (maximum tachycardia in response to blood pressure reduction) and lower plateau (maximum bradycardia in response to blood pressure elevation) are mainly mediated by the cardiac sympathetics and vagus, respectively. The slope of the relationship is a measure of reflex gain. 3. Training, which increased maximal oxygen consumption by 13 +/- 2% (mean +/- standard error of the difference), reduced supine and standing blood pressures by 3 +/- 1/3 +/- 1 mmHg (P less than 0.05) and 4 +/- 1/2 +/- 2 mmHg (P less than 0.05 for systolic), respectively, whereas resting heart rate was lowered by 6 +/- 1 beats/min (P less than 0.05). Reflex sensitivity in the presence of functioning vagus and sympathetics was not altered with training, but the vagal component of sensitivity, as assessed after sympathetic blockade with propranolol, was significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effects of 4 weeks endurance training on cardiac left ventricular structure and function.

1. The effect of 4 weeks of moderate exercise training on cardiac left ventricular structure and function was examined by repeated echocardiographic/Doppler examination in 10 previously sedentary volunteers participating in a single blind, sedentary phase controlled, cross-over study. 2. Left ventricular internal diastolic diameter increased after 4 weeks of training from 4.98 to 5.11 cm with a further increase to 5.24 cm after 2 weeks of detraining (s.e.d. 0.05 cm, P < 0.01). These increases were still significant after adjustment for heart rate which fell from a pretraining average of 67.0-59.9 beats/min after 4 weeks of training. 3. There were no significant changes in systolic diameter or function and left ventricular wall thicknesses were unchanged during training, but were thinned after 2 weeks subsequent detraining. 4. The ratio of early to late transmitral filling velocity (E/A ratio) was significantly increased by training. Although E/A ratio was shown to be heart rate sensitive, training effects were still evident after adjustment for heart rate. 5. These changes in left ventricular volumes and function may contribute to the cardiovascular reflex changes previously shown to be produced by identical training programmes.

Adult↗
PubMed1992

Enhanced contraction to noradrenaline, serotonin and nerve stimulation but normal endothelium-derived relaxing factor response in skin small arteries in human primary hypertension.

1. We measured the reactivity of 2 mm long ring segments of human resistance arteries dissected from gluteal skin biopsies and mounted on wires in a Mulvany-Halpern myograph for recording isometric force. Arteries were taken from eight normotensive (N) volunteers (average age 46 years, blood pressure 126/82 mmHg) and eight untreated hypertensives (H; average age 48 years, blood pressure 149/101 mmHg). 2. In small diameter arteries (internal diameter less than 500 microns), the cumulative concentration-response curves to noradrenaline, serotonin and angiotensin II had a greater maximum by 72, 300 and 69%, respectively, in vessels from hypertensive patients than in those from normal volunteers. Nerve stimulation also caused a greater maximum contraction in hypertensive vessels (by 352%). 3. Arteries from H and N patients contracted submaximally by the thromboxane mimetic U46619 were similarly sensitive to the endothelium-dependent relaxing factor (EDRF) acetylcholine, indicating no difference in EDRF release or sensitivity. 4. Morphological measurements of the ratio of wall thickness to lumen radius of the wire-mounted vessels showed no significant difference between H and N vessels. 5. In larger arteries (internal diameter greater than 500 microns), no response to acetylcholine was noted in either H or N arteries. The sensitivity to serotonin and angiotensin II was similar between these arteries but the EC50 to noradrenaline was less in H than in N arteries (delta EC50 = 0.61 -log mol/L). 6. Subcutaneous resistance arteries with an internal diameter less than 500 microns from hypertensive patients show enhanced contractility to noradrenaline, serotonin and nerve stimulation despite a lack of detectable medial hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Muscle glycogen and glucose uptake during exercise in humans.

Six men were studied during 40 min of cycling exercise to examine the relationship between leg glucose uptake and muscle glycogen concentration. Exercise resulted in significant increases in leg glucose uptake, while muscle glycogen and arterial blood glucose concentrations declined. Arterial plasma insulin levels did not change significantly. There was a significant inverse relationship between muscle glycogen concentration and glucose uptake during exercise which suggests a possible regulatory influence of muscle glycogen on glucose uptake in the early stages of exercise in humans.

Adult↗
PubMed1992

Sympathetic nervous function in human heart as assessed by cardiac spillovers of dihydroxyphenylglycol and norepinephrine.

BACKGROUND: Measurement of cardiac norepinephrine spillover may indicate the amount of transmitter at neuroeffector sites but does not distinguish neuronal release or reuptake in determining this amount or provide information about other aspects of sympathetic function. This report examines how cardiac spillover of the norepinephrine metabolite dihydroxyphenylglycol (DHPG) provides additional distinct information about cardiac sympathetic function. METHODS AND RESULTS: Arterial and coronary venous blood samples were taken during cardiac catheterization and intravenous infusion of [3H]norepinephrine in 57 subjects. Subjects were given intravenous yohimbine or underwent mental stress, handgrip exercise, and cycling exercise to activate sympathetic nerves or were given intravenous desipramine to block norepinephrine reuptake. Cardiac DHPG spillover (601 +/- 41 pmol/min) was eightfold greater than norepinephrine spillover (78 +/- 10 pmol/min) at rest and increased during sympathetic activation by 65% of the increase of norepinephrine. This and the desipramine-sensitive cardiac production of [3H]-labeled DHPG from [3H]norepinephrine indicated that 10.5 times more endogenous norepinephrine is recaptured than escapes into plasma; that more than 90% of recaptured norepinephrine is sequestered into storage vesicles; and that under resting conditions, most cardiac spillover of DHPG and turnover of norepinephrine are from metabolism of transmitter leaking from vesicles; the latter process is independent of exocytotic transmitter release with a rate at rest over 100-fold that of norepinephrine spillover and over 10-fold that of norepinephrine reuptake. CONCLUSIONS: Cardiac spillover of DHPG provides information about processes close to or within sympathetic nerve endings that cannot be provided by measurements of norepinephrine spillover alone. This includes quantitative information about the role of neuronal uptake in terminating the actions of norepinephrine at neuroeffector sites and the importance of vesicular-axoplasmic exchange of norepinephrine as a dynamic process contributing to norepinephrine turnover.

Cardiac Output, Low↗
PubMed1992

Increased norepinephrine spillover into the jugular veins in essential hypertension.

In essential hypertension sympathetic nerve firing is commonly increased. A central nervous system origin has been presumed but not tested directly. To estimate cerebral norepinephrine release in essential hypertension, spillover of norepinephrine into the cerebrovascular circulation was measured by isotope dilution, with high internal jugular venous sampling. Norepinephrine was released into the cerebrovascular circulation in both hypertensive patients and healthy volunteers and was present after administration of the ganglion blocker trimethaphan and in patients with sympathetic nervous failure, indicating that brain neurons and not cerebrovascular sympathetic nerves were the probable source. Although differing among hypertensive patients, norepinephrine spillover on average was higher in the hypertensive patients (153 +/- 41 pmol/min) than in healthy subjects (59 +/- 12 pmol/min; p less than 0.05), and was elevated in six of 17 patients, in whom the accompanying whole body norepinephrine spillover rate was higher than in the remaining 11 patients (p less than 0.01). To test for a possible link between brain norepinephrine release and human sympathetic nervous function, the effect of the tricyclic antidepressant desipramine (0.3 mg/kg i.v.) on both brain and whole body norepinephrine spillover was measured in healthy volunteers. Desipramine lowered the cerebrovascular spillover of norepinephrine, its precursor dihydroxyphenylalanine, and its metabolite dihydroxyphenylglycol by 50-80% and produced a mean fall of 35% in whole body norepinephrine spillover. One interpretation of these results is that human sympathetic nerve firing is dependent on norepinephrine release within the brain and that increased cerebral norepinephrine release may possibly be present in some patients with essential hypertension, underlying their higher sympathetic nerve firing rates.

Cerebrovascular Circulation↗
PubMed1992

Plasma norepinephrine responses to head-up tilt are misleading in autonomic failure.

The failure of plasma norepinephrine to rise during upright posture is accepted as a diagnostic sign of autonomic nervous failure in patients with postural hypotension. Our clinical experience has been that this test is misleading, with an increase in plasma norepinephrine commonly occurring. To test whether this might result from absent reflex postural venous constriction lowering cardiac output and plasma norepinephrine clearance, we measured norepinephrine plasma kinetics during recumbency and 30 degrees head-up tilting in six patients with pure autonomic failure and eight healthy subjects. Mean arterial pressure fell by 54 +/- 8 mm Hg with head-up tilt in the patients with pure autonomic failure. The plasma norepinephrine concentration (arterial sampling) increased 73 +/- 29 pg/ml (mean difference +/- SED, p less than 0.02), solely because of a 36% reduction in the clearance of norepinephrine from plasma (0.78 +/- 0.09 l/min, p less than 0.0001). In normal subjects, plasma norepinephrine concentration rose by 112 +/- 20 pg/ml (p less than 0.001), largely because of a 24% increase in norepinephrine spillover to plasma (190 +/- 20 ng/min, p less than 0.005). When the postural fall in blood pressure and cardiac output in the pure autonomic failure patients was prevented by the selective venoconstrictor dihydroergotamine (10 micrograms/kg i.v.), no fall in plasma clearance or rise in plasma concentration of norepinephrine occurred. Measurement of the change in plasma norepinephrine with postural stimulation in patients with orthostatic hypotension is not a reliable diagnostic test for autonomic failure because elevations can occur in the plasma concentration that are entirely attributable to reduced plasma norepinephrine clearance.

Autonomic Nervous System Diseases↗
PubMed1992

Release of endothelium-derived relaxing factor from resistance arteries in hypertension.

Aortic rings from SHR are reported to have a decreased relaxation response to the endothelium-dependent agent acetylcholine compared with rings from WKY rats. Thus, a reduced EDRF (nitric oxide) response could contribute to hypertension. We found that in mesenteric small resistance arteries (200 microns I.D.) taken from 5- to 50-week old rats and mounted in a Mulvany-Halpern myograph, that the concentration-response curves to acetylcholine were similar in range and sensitivity (EC50) in arteries from SHR and WKY rats at the same age. Similarly, in small resistance arteries from human buttock skin, the relaxation to acetylcholine was not different between vessels from normotensive volunteers (mean BP = 95.2 +/- 1.5 mm Hg) and patients with untreated essential hypertension (mean BP = 116.5 +/- 2.5 mm Hg). In rabbits with chronic renovascular hypertension (cellophane renal wrap), acetylcholine and adenosine infusions into the lower abdominal aorta caused falls in hindquarter resistance that were enhanced in range, but with no change in sensitivity compared with normotensive rabbits. In normotensive rabbits, nitric oxide synthase inhibition with N omega-nitro-L-arginine infusion caused a rise in blood pressure, fall in hindquarter conductance and blockade of the acetylcholine responses. These experiments suggest that at the level of resistance arteries in vivo and in vitro, a defect in the receptor-stimulated response to EDRF associated with hypertension could not be detected. Apparently, basal nitric oxide is important in resting vasodilator tone, but its role in chronic hypertension is still unclear.

Acetylcholine↗
PubMed1991

Evidence of a selective increase in cardiac sympathetic activity in patients with sustained ventricular arrhythmias.

BACKGROUND: Although enhanced efferent cardiac sympathetic nervous activity has been proposed as an important factor in the genesis of ventricular arrhythmias and sudden cardiac death, direct clinical evidence has been lacking. METHODS: We measured the rates of total and cardiac norepinephrine spillover into the plasma, which reflect respectively overall and cardiac sympathetic nervous activity, in 12 patients who had recovered from a spontaneous, sustained episode of ventricular tachycardia or ventricular fibrillation outside the hospital 4 to 48 days earlier. The results were compared with those from three age-matched reference groups without a history of ventricular arrhythmias: 12 patients with coronary artery disease, 6 patients with chest pain but normal coronary arteries, and 12 healthy, normal subjects. RESULTS: The patients who had had ventricular arrhythmias had reduced left ventricular ejection fractions, as compared with the patients with coronary artery disease or chest pain (mean [+/- SE], 46 +/- 3 percent vs. 58 +/- 4 percent and 69 +/- 5 percent, respectively; P less than 0.003). The rates of total norepinephrine spillover into the plasma were similar in the three reference groups, but 80 percent higher in the patients with ventricular arrhythmias (P less than 0.005). The rate of cardiac norepinephrine spillover was 450 percent higher in these patients (176 +/- 39 pmol per minute, as compared with 32 +/- 8 pmol per minute in the normal subjects; P less than 0.001), a disproportionate increase relative to the increase in total spillover, which indicated selective activation of the cardiac sympathetic outflow. This increase in cardiac norepinephrine spillover was probably caused by a reduction in left ventricular function. CONCLUSIONS: These results suggest that in some patients major ventricular arrhythmias are associated with and perhaps caused by sustained and selective cardiac sympathetic activation. We speculate that depressed ventricular function was present before the ventricular arrhythmia occurred, and that this resulted in reflex cardiac sympathetic activation, which in turn contributed to the genesis of the arrhythmia.

Angina Pectoris↗
PubMed1991

Aortic distensibility in patients with isolated hypercholesterolaemia, coronary artery disease, or cardiac transplant.

The stiffness of the thoracic aorta can be assessed non-invasively. If aortic stiffness can be shown to be related to coronary heart disease, perhaps it can be used to identify which patients with hypercholesterolaemia are most likely to have atheromatous changes and thus to be selected for intensive cholesterol-lowering treatment. Hence the distensibility of the transverse aortic arch was measured by echocardiography of the aortic arch in four groups of patients--symptom-free patients with normal serum cholesterol; symptom-free patients with raised serum cholesterol; patients with coronary heart disease (all with raised serum cholesterol), and post-heart-transplant patients. In all groups distensibility fell with age. The regression slope was steeper (p less than 0.05) for patients with known coronary disease than for either of the disease-free groups, and among cardiac transplant recipients there was also a segregation of distensibility values between those with and without atheroma in their native hearts. The results indicate that aortic distensibility might be an indicator of coronary heart disease and that it might be useful in identifying which symptom-free subjects with modest hypercholesterolaemia should be treated aggressively.

Aging↗
PubMed1991

Biochemical evidence of sympathetic denervation of the heart in pure autonomic failure.

Primary autonomic failure is a heterogenous group of diseases with evidence for lesions in both the central and peripheral elements of the autonomic nervous system. We determined the extent of peripheral sympathetic dysfunction in six patients with primary autonomic failure without clinical evidence of central nervous system involvement (pure autonomic failure) using biochemical methods for studying regional noradrenaline spillover and removal. The results were compared with those from 14 age-matched normal subjects, seven of whom were studied before and after pharmacological neuronal uptake-blockade with desipramine. Total, cardiac and renal noradrenaline spillover to plasma were 78%, 98% and 66% lower respectively in pure autonomic failure than in normal subjects (p less than 0.001). Total noradrenaline plasma clearance was 20% lower in pure autonomic failure (p less than 0.005) than in normal subjects and similar to the level observed in normal subjects following neuronal noradrenaline uptake-blockade with desipramine, mean transcardiac extraction of tritiated noradrenaline was 74% in normal subjects and 20% in pure autonomic failure, identical to the value post-desipramine in normal subjects. Cardiac spillover of the noradrenaline precursor, dihydroxyphenylanine, and the primary intra-neuronal metabolite dihydroxyphenylglycol, were 78% and 94% lower respectively in pure autonomic failure than in normal subjects (p less than 0.001). These data indicate a marked reduction in the apparent release rate and neuronal uptake of noradrenaline in the hearts of patients with pure autonomic failure, and provide biochemical evidence of almost total postganglionic sympathetic denervation in this condition.

Aged↗
PubMed1991

Direct determination of homovanillic acid release from the human brain, an indicator of central dopaminergic activity.

The plasma concentration of the dopamine (DA) metabolite, homovanillic acid (HVA), is used as an indicator of central nervous system dopaminergic activity. Using percutaneously inserted catheters we were able to obtain blood samples simultaneously from the right and left internal jugular veins. Veno-arterial HVA plasma concentration differences combined with adjusted organ plasma flows were used, according to the Fick Principle, to determine the HVA overflow from the brain. The HVA overflow from the liver was also measured. HVA overflow from the brain represented 12% of the total body HVA production. A similar amount was released from the liver, illustrating the limited validity of peripheral plasma HVA measurements as an indicator of central dopaminergic activity. HVA release from the human brain displayed a degree of asymmetry, the overflow into the left internal jugular vein being 36% greater than that into the right. Cerebral venous blood flow scans indicated that cortical cerebral regions drained preferentially into the right internal jugular; by inference the higher HVA overflow on the left originated from dopamine-rich subcortical brain areas. Since HVA in plasma may arise from the metabolism of DA existing either as a neurotransmitter or a norepinephrine (NE) precursor we measured the internal jugular vein plasma concentrations of NE, and its metabolite dihydroxyphenylglycol (DHPG), to determine whether they displayed a similar pattern of release to HVA. The overflow of both NE and DHPG into the right internal jugular vein was approximately double that on the left. Since the overflow of HVA did not parallel that of NE and DHPG it may be inferred that the origin of much of the subcortically produced HVA is from dopaminergic neurons and not from the metabolism of precursor DA in noradrenergic neurones or cerebrovascular sympathetic nerves.

Adolescent↗
PubMed1991

Amplifier function of resistance vessels and the left ventricle in hypertension.

We have recently modeled the structural factors responsible for the increased slope of the dose-vascular resistance response curves in the hindquarter bed under both in vitro and in vivo conditions. Slope increases when the ratio of wall thickness to internal radius (ri) increases and when ri decreases, but the slope decreases with greater wall stiffness. Enhanced slope is an indicator of the vascular amplifier properties. Resistance at maximum vasodilation in hypertension is also structurally determined converting enzyme inhibitors in spontaneously hypertensive rats (SHR) suggest that the reduction in ri can be reversed, suggesting that it is due to vascular hypertrophy. The concentrically hypertrophied left ventricle is an amplifier of stroke volume. Together, the vascular and left ventricular amplifiers contribute about 70% to the elevated total peripheral resistance in renovascular hypertension. In SHR, the vascular amplifier is present early in postnatal life before the onset of hypertension, which occurs in parallel with left ventricular hypertrophy (LVH). The development of the vascular amplifiers appears to be under the control of the renin-angiotensin system, whilst LVH appears to be under sympathoadrenal control, acting through cardiac alpha-adrenoceptors. Early immunosympathectomy plus prazosin treatment specifically prevents development of LVH in SHR and also prevents hypertension. In human hypertension, cardiac hypertrophy also plays an important role; after a period of prolonged therapy, the rate of redevelopment of hypertension when the drugs are stopped depends on the degree of regression of LVH during treatment. We conclude that the early development of vascular and cardiac amplifiers in primary hypertension appears to be genetically determined and the role of the heart in pathogenesis appears to be greater than previously thought.

Animals↗
PubMed1991

Significance of cardiovascular hypertrophy in the development and maintenance of hypertension.

The amplifier properties associated with the structural changes in the heart and resistance vessels in chronic hypertension together play a major role in maintaining the elevated blood pressure (BP) in chronic hypertension, which is greater than that of the initiating cause. In patients with primary hypertension, long-term antihypertensive drug therapy causes substantial regression of the structural changes, as assessed by normalization of the total peripheral resistance (including the nonautonomic component) and of the left ventricular (LV) mass. Reversal of LV hypertrophy (LVH) took considerably longer than reversal of the vascular changes and the more complete the reversal of LVH, the slower the rate of redevelopment of hypertension upon cessation of treatment. We observed no change in sympathetic activity or in renin-angiotensin-aldosterone levels during the redevelopment phase and we hypothesized that the cardiovascular amplifiers played a role in pathogenesis. This hypothesis was examined in spontaneously hypertensive rats (SHRs), where the vascular amplifier properties were developed substantially by 4 weeks of age, i.e., before the development of hypertension, whereas LVH occurred pari passu the rise in BP. When young SHRs were treated with enalapril for brief periods, there was almost complete long-term regression of vascular amplifier properties, but attenuation of LVH and hypertension were both smaller and more transient. In 4-week-old SHRs, complete abolition of sympathetic activity had a minimal effect on vascular amplifier properties, but affected LVH. Our findings suggest that LVH is as important in both the development and maintenance of hypertension as the structurally determined amplifier properties of the resistance vessels.

Animals↗
PubMed1991

Measuring blood cholesterol outside the pathology laboratory: issues of accuracy and reliability.

Desk-top analysers that are simple to use, portable and free from technical requirements are now widely used for blood cholesterol measurement outside the traditional pathology laboratory setting. Test accuracy and reliability are essential if these portable desk-top analysers are to be of value in the assessment and management of elevated blood cholesterol. To determine their accuracy and reliability we compared the results obtained from four different desk-top analysers with those from a teaching hospital's routine laboratory method. The desk-top analysers assessed were the Ames Minilab, the Kodak DT60, the Boehringer Reflotron and the Abbott Vision. The precision of each desk-top analyser was within acceptable limits, defined as a coefficient of variation less than 5 per cent. The results from the Vision, Reflotron and DT60 related closely to those from routine laboratory method, with least squares linear regression slopes ranging from 0.92 to 1.06 and intra-class correlation coefficients from 0.95 to 0.99. The Minilab showed least agreement with the routine laboratory method and caution should be taken in the interpretation of cholesterol estimations made with this device.

Blood Chemical Analysis↗
PubMed1991

Exercise training lowers resting renal but not cardiac sympathetic activity in humans.

Endurance exercise training has previously been shown to reduce the plasma concentration of norepinephrine. Whether reduction in sympathetic activity is responsible for the blood pressure-lowering effects of exercise training is unknown. Using a radiotracer technique, we measured resting total, cardiac, and renal norepinephrine spillover to plasma in eight habitually sedentary healthy normotensive men (aged 36 +/- 3 years, mean +/- SEM) after 1 month of regular exercise and 1 month of sedentary activity, performed in a randomized order. One month of bicycle exercise 3 times/wk (40 minutes at 60-70% maximum work capacity) reduced resting blood pressure by 8/5 mm Hg (p less than 0.01) and increased maximum oxygen consumption by 15% (p less than 0.05). The fall in blood pressure was attributable to a 12.1% increase in total peripheral conductance. Total norepinephrine spillover to plasma was reduced by 24% from a mean of 438.8 ng/min (p less than 0.05). Renal norepinephrine spillover fell by an average of 41% from 169.4 ng/min with bicycle training (p less than 0.05), accounting for the majority (66%) of the fall in total norepinephrine spillover. Renal vascular conductance was increased by 10% (p less than 0.05), but this constituted only 18% of the increase in total peripheral conductance. There was no change in cardiac norepinephrine spillover. The reduction in resting sympathetic activity with regular endurance exercise is largely confined to the kidney. The magnitude of the fall in renal vascular resistance, however, is insufficient to directly account for the blood pressure-lowering effect of exercise, although other effects of inhibition of the renal sympathetic outflow may be important.

Adult↗