Prazosin in normal subjects: plasma levels, blood pressure and heart rate [letter].

Abstract:This paper proposes a method for decomposing heart rate fluctuations into background, respiratory and blood pressure oriented fluctuations. A signal cancellation scheme using the adaptive RLS algorithm has been introduced for canceling respiration and blood pressure oriented changes in the heart rate fluctuations. The computer simulation confirmed the validity of the proposed method. Then, heart rate fluctuations, instantaneous lung volume and blood pressure changes are simultaneously recorded from eight normal subjects aged 20-24 years. It was shown that after signal decomposition, the power spectrum of the heart rate showed a consistent monotonic 1/fa type pattern. The proposed method enables a clear interpretation of heart rate spectrum removing uncertain large individual variations due to the respiration and blood pressure change.

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The Involvement of Platelets and the Coronary Vasculature in Collagen-Induced Sudden Death in Rabbits

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661239 ◽

1985 ◽

Vol 53 (01) ◽

pp. 070-074 ◽

Cited By ~ 4

Author(s):

G Mallarkey ◽

G M Smith

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Platelet Count ◽

Sudden Death ◽

Myocardial Ischaemia ◽

Plasma Levels ◽

Sodium Citrate ◽

Plasma Samples ◽

Calcium Entry Blockers

SummaryThe mechanism of collagen-induced sudden death in rabbits was studied by measuring blood pressure (BP), heart rate, ECG, the continuous platelet count and the plasma levels of thromboxane B2 (TxB2) and 6-keto prostaglandin Fia (6-keto PGF1α). Death was preceded by myocardial ischaemia and a sharp fall in BP which occurred before any fall in platelet count was observed. The calcium entry blockers (CEBs), verapamil, nifedipine and PY 108-068 protected the rabbits from sudden death without any significant effect on the decrease in the platelet count or increase in plasma TxB2 levels. 6-keto PGF1α could not be detected in any plasma samples. Indomethacin and tri-sodium citrate also protected the rabbits but significantly reduced the fall in platelet count and plasma TxB2. In vitro studies on isolated aortae indicated that verapamil non-specifically inhibited vasoconstriction induced by KC1, adrenaline and U46619 (a thromboxane agonist). It is concluded that CEBs physiologically antagonize the vasoconstricting actions of platelet-derived substances and that it is coronary vasoconstriction that is primarily the cause of death.

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Postprandial changes in supine and erect heart rate, systemic blood pressure and plasma noradrenaline and renin activity in normal subjects

European Journal of Clinical Pharmacology ◽

10.1007/bf00637672 ◽

1987 ◽

Vol 32 (5) ◽

pp. 471-476 ◽

Cited By ~ 15

Author(s):

C. de Mey ◽

D. Enterling ◽

E. Brendel ◽

I. Meineke

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Normal Subjects ◽

Systemic Blood Pressure ◽

Renin Activity ◽

Plasma Noradrenaline ◽

Systemic Blood

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Effects of the cold pressor test on short-term fluctuations of finger arterial blood pressure and heart rate in normal subjects

Clinical Autonomic Research ◽

10.1007/bf01827331 ◽

1993 ◽

Vol 3 (5) ◽

pp. 303-310 ◽

Cited By ~ 39

Author(s):

Frank Weise ◽

Dominique Laude ◽

Arlette Girard ◽

Philippe Zitoun ◽

Jean-Philippe Siché ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Cold Pressor Test ◽

Cold Pressor ◽

Normal Subjects ◽

Short Term ◽

Pressor Test ◽

Arterial Blood

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γ-l-Glutamyl-l-Dopa is a Dopamine Pro-Drug, Relatively Specific for the Kidney in Normal Subjects

Clinical Science ◽

10.1042/cs0690207 ◽

1985 ◽

Vol 69 (2) ◽

pp. 207-214 ◽

Cited By ~ 44

Author(s):

D. P. Worth ◽

J. N. Harvey ◽

J. Brown ◽

M. R. Lee

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Glomerular Filtration Rate ◽

Plasma Renin Activity ◽

Filtration Rate ◽

Renal Plasma Flow ◽

Plasma Renin ◽

Normal Subjects ◽

Urinary Sodium Excretion ◽

Systemic Effects

1. γ-l-Glutamyl-l-dopa was given by intravenous infusion to eight normal subjects at doses of 12.5 and 100 μg min−1 kg−1. 2. Both doses of the dipeptide resulted in an increase in mean urinary sodium excretion. 3. Mean effective renal plasma flow rose at both doses, but mean glomerular filtration rate increased only at the lower dose. 4. There was a fall in mean plasma renin activity after the infusion of both 12.5 and 100 μg min−1kg−1. 5. Mean urine free dopamine excretion increased by 280- and 2500-fold at infusion rates of 12.5 and 100 μg min−1 kg−1 respectively. 6. Mean plasma free dopamine rose at both doses but the increase at 12.5 μg min−1 kg−1 was not to a level previously associated with systemic effects of the catecholamine. 7. On administration of the dipeptide at 12.5 μg min−1 kg−1 there were no changes in blood pressure or heart rate, but at the higher dose there was a fall in diastolic blood pressure. 8. At a dose of 12.5 μg min−1 kg−1 in man, there is kidney specific conversion of gludopa to dopamine.

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Spectral analysis of blood pressure and heart rate, catecholamine and neuropeptide Y plasma levels in a new model of neurogenic orthostatic hypotension in dog

Clinical Autonomic Research ◽

10.1007/bf02291227 ◽

1996 ◽

Vol 6 (2) ◽

pp. 75-82 ◽

Cited By ~ 10

Author(s):

P. Verwaerde ◽

J. -M. Senard ◽

M. Mazerolles ◽

M. -A. Tran ◽

C. Damase-Michel ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Spectral Analysis ◽

Orthostatic Hypotension ◽

Neuropeptide Y ◽

Plasma Levels ◽

Neurogenic Orthostatic Hypotension ◽

New Model

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Fractal Component of Variability of Heart Rate and Systolic Blood Pressure in Congestive Heart Failure

Clinical Science ◽

10.1042/cs0920543 ◽

1997 ◽

Vol 92 (6) ◽

pp. 543-550 ◽

Cited By ~ 32

Author(s):

Gary C. Butler ◽

Shin-Ichi Ando ◽

John S. Floras

Keyword(s):

Heart Failure ◽

Blood Pressure ◽

Heart Rate ◽

Heart Rate Variability ◽

Systolic Blood Pressure ◽

Spectral Power ◽

Normal Subjects ◽

Total Spectral Power ◽

Systolic Blood Pressure Variability ◽

Harmonic Components

1. There is a substantial non-harmonic or fractal component to the variability of both heart rate and blood pressure in normal subjects. Heart rate is the more complex of these two signals, with respect to the slope, β, of the 1/fβ relationship. In congestive heart failure, heart rate spectral power is attenuated, but the fractal and harmonic components of heart rate and systolic blood pressure variability have not been characterized. 2. Two groups, each comprising 20 men, were studied during 15 min of supine rest and spontaneous respiration: one with functional class II—IV heart failure (age 52 ± 2 years; mean ± SEM) and a second group of healthy men (age 46 ± 2 years). 3. Total spectral power for heart rate was significantly reduced in heart failure (P < 0.02), whereas total spectral power for systolic blood pressure was similar in the two groups. In both heart failure and normal subjects, 65–80% of total spectral power in these two signals displayed fractal characteristics. 4. In heart failure, the slope of the 1/fβ relationship for heart rate was significantly steeper than in normal subjects (1.40 ± 0.08 compared with 1.14 ± 0.05; P < 0.05), indicating reduced complexity of the fractal component of heart rate variability. There was no significant difference in the 1/fβ slope for systolic blood pressure variability between these two groups, but the blood pressure signals were less complex than heart rate variations in both heart failure (2.31 ± 0.15; P < 0.006) and normal subjects (2.47 ± 0.15; P < 0.0001). 5. Parasympathetic nervous system activity, as estimated from heart rate variability was reduced (P < 0.01) in patients with heart failure, whereas trends towards increased sympathetic nervous system activity and decreased non-harmonic power were not significant. 6. The non-harmonic components of cardiac frequency are reduced in heart failure. Non-harmonic power is not attenuated, but the complexity of the heart rate signal is less than in subjects with normal ventricular function. A reduction in parasympathetic modulation appears to contribute to this loss of complexity of heart rate. Consequently, the heart rate signal comes to resemble that of blood pressure. In contrast, the variability and complexity of the systolic blood pressure signal is similar in heart failure and normal subjects. This reduced complexity of heart rate variability may have adverse implications for patients with heart failure.

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The Autonomic Nervous Tone Abnormalities in the Genesis of the Impaired Baroreflex Responsiveness in Borderline Hypertensive Subjects

Clinical Science ◽

10.1042/cs0620581 ◽

1982 ◽

Vol 62 (6) ◽

pp. 581-588 ◽

Cited By ~ 16

Author(s):

Massimo Volpe ◽

Bruno Trimarcoy ◽

Bruno Ricciardelli ◽

Carlo Vigorito ◽

Nicola De Luca ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Pressure ◽

Normal Subjects ◽

Tissue Pressure ◽

Combined Administration ◽

Propranolol Treatment ◽

The Mean ◽

Pressure Changes ◽

Neck Chamber

1. The effects of intravenous administration of neostigmine and propranolol, individually or in combination, on baroreflex responsiveness have been evaluated in 18 borderline hypertensive subjects and in 14 age-matched control subjects. 2. Baroreceptor sensitivity was tested by evaluating both heart rate response to phenylephrine-induced increase in arterial pressure, and heart rate and blood pressure changes induced by increasing neck-tissue pressure by means of a neck-chamber. 3. In borderline hypertensive subjects a reduced baroreflex responsiveness was demonstrated with both stimuli as compared with normal subjects. Neostigmine administration improved consistently both reflex responses. Similarly, after propranolol treatment, borderline hypertensive subjects showed a significant enhancement of the baroreflex sensitivity. Finally, the combined administration of neostigmine and propranolol restored the baroreflex responses. In fact, both the mean slopes of the regression lines between blood pressure and R-R interval after phenylephrine and the increase in mean arterial pressure and heart rate induced by the reduction in carotid transmural pressure in borderline hypertensive subjects were similar to those observed in normals. 4. These findings indicate that in borderline hypertensive subjects the impairment of baroreflex responsiveness is mainly due to abnormalities of autonomic regulation.

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Renin and Aldosterone Release during Sympathetic Stimulation in Tetraplegia

Clinical Science ◽

10.1042/cs0600399 ◽

1981 ◽

Vol 60 (4) ◽

pp. 399-404 ◽

Cited By ~ 17

Author(s):

C. J. Mathias ◽

H. L. Frankel ◽

I. B. Davies ◽

V. H. T. James ◽

W. S. Peart

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Plasma Renin Activity ◽

Diastolic Blood Pressure ◽

Pressor Response ◽

Plasma Renin ◽

Normal Subjects ◽

Plasma Aldosterone ◽

Renin Activity ◽

Sympathetic Stimulation

1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. Data from infusion studies were compared with data from six normal subjects studied in an identical manner. 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. 3. Noradrenaline infusion resulted in an enhanced pressor response in the tetraplegic patients when compared with the normal subjects. Heart rate fell in both groups. Plasma renin activity and plasma aldosterone did not change in either group. 4. Isoprenaline infusion caused a fall in both systolic and diastolic blood pressure in the tetraplegic patients, unlike the normal subjects in whom there was a rise in systolic and a fall in diastolic blood pressure. Heart rate and plasma renin activity rose in both groups. Plasma aldosterone did not change in either group. 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. Isoprenaline increases plasma renin activity to the same extent as in normal subjects. Renin release mechanisms in tetraplegic patients therefore do not appear to be hypersensitive to catecholamines. Plasma aldosterone is not influenced by any of the stimuli.

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