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Biomedical subjects

M D Esler

Publications and source records attributed to M D Esler.

At least 127 records · Page 7Linked to original sources
PubMed1986

Effect of changing levels of physical activity on blood-pressure and haemodynamics in essential hypertension.

The long-term effect of exercise on blood-pressure (BP) was assessed in 13 untreated patients with essential hypertension. After a 6-week run-in period the levels of activity studied were sedentary, 45 min bicycling at 60-70% of maximum work capacity (Wmax) three times per week (3/week), and 45 min bicycling seven times per week (7/week), each for 4 weeks. The order differed between subjects in accordance with a Latin square. Supine BP, 48 h after each phase, averaged 148/99 mm Hg in the run-in and 143/96 mm Hg in the sedentary phase; it fell below values in the sedentary phase by 11/9 mm Hg with 3/week exercise, and by 16/11 mm Hg with 7/week exercise (both p less than 0.01). With increasing activity total peripheral resistance fell and the cardiac index rose. Plasma noradrenaline concentration fell below values in the sedentary phase by 21% and 33% after 3/week and 7/week exercise. Bodyweight and 24 h sodium excretion remained constant. Moderate regular exercise lowers BP and seems to be an important non-pharmacological method of treating hypertension.

Adult↗
PubMed1986

Norepinephrine spillover to plasma in patients with congestive heart failure: evidence of increased overall and cardiorenal sympathetic nervous activity.

The analysis of plasma kinetics of the sympathetic neurotransmitter norepinephrine can be used to estimate sympathetic nervous "activity" (integrated nerve firing rate) for the body as a whole and for individual organs. In 12 patients with cardiac failure (left ventricular ejection fraction 10% to 39%), the mean arterial plasma norepinephrine concentration was 557 +/- 68 pg/ml (mean +/- SE) compared with 211 +/- 21 pg/ml in 15 subjects without heart failure (p less than .002). The difference was due to both increased release of norepinephrine to plasma (indicating increased "total" sympathetic activity) and reduced clearance of norepinephrine from plasma. The increase in sympathetic activity did not involve all organs equally. Cardiac (32 +/- 9 vs 5 +/- 1 ng/min; p less than .002) and renal (202 +/- 45 vs 66 +/- 9 ng/min; p = .002) norepinephrine spillover were increased by 540% and 206%, respectively, but norepinephrine spillover from the lungs was normal. Adrenomedullary activity was also increased in the patients with heart failure, whose mean arterial plasma epinephrine concentration was 181 +/- 38 pg/ml compared with 71 +/- 12 pg/ml in control subjects (p less than .02). There is marked regional variation, inapparent from measurements of plasma norepinephrine concentration, in sympathetic nerve activity in patients with congestive heart failure. The finding of increased cardiorenal norepinephrine spillover has important pathophysiologic and therapeutic implications.

Female↗
PubMed1986

Pathogenesis of human primary hypertension: a new approach to the identification of causal factors and to therapy.

In chronic renovascular hypertension the amplifier properties of the hypertrophied heart and vessels contribute considerably more to the maintenance of the elevated blood pressure (BP) than the basic underlying cause. This must also occur in chronic primary hypertension. Accordingly, we hypothesized that after reversal of hypertrophy by antihypertensive medication the cause(s) of hypertension should be easier to detect during the redevelopment of hypertension once medication was stopped, than in the chronic phase of the disorder. We have studied three groups of patients with moderate to severe hypertension in whom BP was controlled for (1) 1 month (2) 1 year and (3) 15 months to 5 years. The rate of subsequent redevelopment of hypertension between the series was inversely related to the duration of therapy, which was mostly with beta-blockers and diuretics. Redevelopment of hypertension was slowest after obtaining regression of both vascular hypertrophy and left ventricular hypertrophy (LVH). Preliminary findings suggest that sympathetic overactivity is present during the redevelopment phase in most patients. Our findings have suggested a new therapeutic strategy, where the effectiveness of non-pharmacological methods of controlling BP is enhanced by first causing regression of cardiovascular hypertrophy by drug treatment. Moderate regular exercise has proved to be an effective non-pharmacological antihypertensive method which has now maintained five patients at normal BP for 1 year, following an initial period of drug treatment.

Adrenergic beta-Antagonists↗
PubMed1985

Blunted norepinephrine responsiveness to changing energy states in obese subjects.

We have previously reported in lean subjects a significant relationship between plasma norepinephrine metabolism and energy state. The present study has examined in six obese men the response in plasma norepinephrine flux to ten day periods of overeating (+ 1000 kcal/m2 above isocaloric requirements) or undereating (400 kcal/d). Despite significant gains or losses in body weight, norepinephrine flux, measured during constant infusions of 3H-l-norepinephrine, failed to change significantly. Measurements of glucose utilization during constant infusions of insulin, showed significant changes with changing energy state, falling with overeating and rising with undereating. Insulin sensitivity was not correlated with plasma norepinephrine metabolism.

Adolescent↗
PubMed1985

Noradrenaline release and sympathetic nervous system activity.

Measurements of the plasma concentration of noradrenaline, or more specifically the rate at which noradrenaline enters plasma, provide a useful guide to sympathetic nervous system function in humans. The overall rate of release of noradrenaline to plasma gives an overview of sympathetic nervous system activity (integrated nerve firing rate), detecting generalized changes, whether occurring as a reflex response, produced by drugs, or accompanying disease processes. The pattern of sympathetic nervous activation, however, is not delineated, only the net change in neurotransmitter release. Measurement of regional rates of noradrenaline release allows the clinical assessment of organ-specific sympathetic nervous tone, and consequently more penetrating analysis of sympathetic nervous system pathophysiology in disease states. The major problem in interpreting regional noradrenaline spillover measurements lies in the difficulty in differentiating those changes in noradrenaline spillover due to altered nerve firing, from those due to extraneous factors which might also affect spillover, such as the possible influence of blood flow on noradrenaline washout.

Adrenergic Fibers↗
PubMed1984

Estimation of 'total' renal, cardiac and splanchnic sympathetic nervous tone in essential hypertension from measurements of noradrenaline release.

The overall rate of release of noradrenaline to plasma was increased in 31 patients with essential hypertension; the median value was 32% (526 pmol/min) higher than in 22 subjects with normal blood pressure. To ascertain the pattern of sympathetic nervous system activation underlying this abnormality, regional sympathetic nervous activity was estimated, from radiotracer-derived estimates of organ-specific noradrenaline release to plasma, in the kidneys, heart and hepatomesenteric circulation. Renal sympathetic nervous tone was preferentially increased in essential hypertension, especially in young patients with hypersecretion of renin. Cardiac noradrenaline release (and possibly cardiac sympathetic tone) was also higher in hypertensive patients; the difficulty in interpretation here arises because left ventricular mass is also increased in essential hypertension. Approximately half of the surfeit in total noradrenaline release to plasma noted in hypertensive patients was accounted for by the increased cardio-renal noradrenaline release. The balance comes from undetermined sites, but not from the splanchnic circulation, in which sympathetic nervous activity was not increased.

Adult↗
PubMed1984

Effects of changes in physical activity on blood pressure and sympathetic tone.

We investigated the relationship between the level of physical activity and blood pressure (BP). Twelve sedentary normotensive subjects were studied after consecutive one-month periods at four different levels of daily activity. These were minimal activity; usual sedentary activities; exercise three times weekly for 45 min at 60-70% maximum capacity (Wmax) on a bicycle ergometer and similar exercise performed daily. The order of the various levels of physical activity were randomised according to a Latin square. As expected there was a progressive increase in Wmax, maximum oxygen consumption and fall in resting and exercise heart rate with increasing activity. Supine blood pressure averaged 133/69 mmHg at the end of the sedentary period and fell by 10/8 mmHg after one month of exercise three times weekly and 12/8 mmHg after daily exercise (both P less than 0.001). The fall in resting BP with increased activity was due to lowering of total peripheral resistance. These haemodynamic changes were associated with biochemical evidence of marked reduction in overall sympathetic tone in 10/12 subjects especially after the period of daily exercise. Increased physical activity for one month lowers blood pressure in normotensive subjects. The fall with daily exercise is similar to that after some centrally-acting antihypertensive drugs, and may be due to a reduction in sympathetic nervous activity.

Blood Pressure↗
PubMed1984

How hypertension redevelops after cessation of long-term therapy.

Long-term therapy (1.5-27 years, average 7.5 years) was ceased in 11 patients with essential hypertension. The return of supine hypertension during the ensuing 10 weeks was slow and incomplete, contrasting with previous studies when blood pressure (BP) had been lowered for shorter periods. After prolonged therapy in these patients, non-autonomic total peripheral resistance index (TPRI) was near normal, but left ventricular mass index (LVMI) was still high in six of the 11 patients. The latter was directly related to duration of effective treatment of BP and to BP when therapy was stopped. These findings may indicate that with antihypertensive therapy, structural changes in the peripheral vasculature regress more quickly than cardiac hypertrophy.

Adult↗
PubMed1980

Relationship between maximum chronotropic response to isoproterenol in man and generation of cyclic adenosine monophosphate by lymphocytes.

The maximum change in heart period caused by bolus doses of isoproterenol was measured in 10 normal subjects. This was linearly related to the amount of cyclic adenosine monophosphate generated from lymphocytes in the same subjects in vitro after incubation with isoproterenol. This high correlation between cardiac and lymphocyte beta-adrenoceptor stimulation suggests that maximum response does not depend on innervation. Other factors, such as cell membrane properties or levels of circulating catecholamines, may be of greater importance.

Adult↗
PubMed1976

Relationship of age and blood pressure to baroreflex sensitivity and arterial compliance in man.

1. The relationship between baroreflex sensitivity (BRS) and arterial compliance index (ACI) has been investigated (a) in paired subjects matched in one instance for systolic blood pressure with differing ages, and (b) in another instance matched for age with differing systolic blood pressures. 2. There was a significant negative correlation between BRS and age and between ACI and age in the twelve systolic blood pressure-matched subjects. 3. A significant negative correlation of systolic blood pressure with both BRS and ACI was observed in the fourteen age-matched subjects. 4. Both BRS and ACI appear to decrease with increasing age and systolic blood pressure. This decrease in BRS is probably due at least in part to the observed reduction in arterial distensibility.

Adult↗
PubMed1975

Relation of renin status to neurogenic vascular resistance in borderline hypertension.

The relation of renin-angiotensin status to general hemodynamics and to neurogenic vascular resistance was studied in patients with border-line hypertension. Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Among 22 patients with borderline hypertension the renin level was high in 8, low in 4 and within normal limits in the remaining 10. In patients with borderline hypertension and high or normal levels of plasma renin activity, the blood pressure elevation was due to increased total peripheral vascular resistance. In contrast, in patients with low renin borderline hypertension, total peripheral resistance was not significantly elevated; the blood pressure elevation reflected a cardiac index 12 percent higher than that in normal subjects. The neurogenic contribution to total peripheral vascular resistance was assessed by studying the effects of alpha adrenergic blockade with phentolamine, after prior autonomic blockade of the heart with atropine (0.04 mg/kg body weight) and propranolol (0.2 mg/kg). Phentolamine (15 mg) produced an immediate reduction in total peripheral resistance of 12.0 +/- 6.7 percent in patients with high renin borderline hypertension (P less than 0.01) but no change in normal subjects or those with borderline hypertension and normal or low renin levels. Normalization of the blood pressure followed "total" autonomic blockade with atropine, propranolol or phentolamine only in patients with high renin borderline hypertension. It is concluded from these preliminary data that in high renin borderline hypertension the blood pressure elevation is sustained by neurogenic mechanisms. The elevated renin level in these patients is probably an expression of increased sympathetic nervous activity. Although the elevated plasma renin level may possibly be contributing to the generation of higher sympathetic tone, or data do not support a direct role of circulating angiotensin in the maintenance of the elevated vascular resistance.

Adolescent↗
PubMed1975

Role of the autonomic nervous system in mild human hypertension.

1. Some of the haemodynamic abnormalities in mild (borderline) human hypertension appear to be neurogenic, since they can be completely abolished by pharmacological autonomic blockade. 2. The cardiac output is elevated in 30% of patients through increased sympathetic drive and decreased parasympathetic inhibition. 3. In the remainder, the higher blood pressure is maintained by increased total peripheral vascular resistance. 4. In approximately 30% of this latter group, the higher vascular resistance is maintained solely by increased alpha-adrenergic tone. 5. Elevated plasma renin activities in a proportion of cases are probably due to generalized increase in sympathetic nervous activity. 6. Patients with mild hypertension thus show increased sympathetic drive to the heart and arterioles as well as decreased cardiac parasympathetic inhibition. It is presumed that the increased plasma renin is also neurogenic. 7. Such a widespread distribution of altered autonomic tone suggests aberration of the function of the integrative centres of cardiovascular control. 8. Evidence is presented of a possible psychosomatic origin of these changes in some cases.

Adolescent↗