Plasma Noradrenaline and the Pressor Action of Exogenous Noradrenaline in Normotensive Subjects and Patients with Essential Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 61s-63s ◽  
Author(s):  
T. Philipp ◽  
A. Distler ◽  
U. Cordes ◽  
H. P. Wolff

1. An inverse relationship was found between plasma noradrenaline and reactivity to exogenous noradrenaline in normotensive subjects. 2. The relationship between plasma noradrenaline and reactivity was disturbed in age-matched patients with essential hypertension. 3. A multiple-regression analysis showed a highly significant correlation between adrenergic activity and reactivity to noradrenaline and the mean arterial blood pressure level (r = 0·91). The results suggest that adrenergic activity and pressor response to noradrenaline combined are important determinants of arterial blood pressure. 4. An inverse relationship could also be demonstrated between plasma renin activity and reactivity to exogenous angiotensin II. No difference was observed between normotensive and hypertensive subjects.

1981 ◽  
Vol 60 (3) ◽  
pp. 7P-7P
Author(s):  
P. S. Parfrey ◽  
N. D. Markandu ◽  
J. E. Roulston ◽  
B. E. Jones ◽  
G. A. MacGregor

1979 ◽  
Vol 57 (s5) ◽  
pp. 387s-389s ◽  
Author(s):  
J. S. Floras ◽  
P. Fox ◽  
M. O. Hassan ◽  
J. V. Jones ◽  
P. Sleight ◽  
...  

1. Twenty-four hour intra-arterial blood pressure measurements and electrocardiograms were obtained from 12 subjects with untreated essential hypertension. 2. The patients kept records of their activity, paying particular attention to times of retiring to bed, and times of waking in the morning. 3. All subjects were treated with a single daily dose of atenolol (50 to 200 mg) for between 2 and 9 months, and then underwent a second 24 h blood pressure study. 4. Arterial blood pressure was lowered significantly throughout the 24 h period with a single daily dose of atenolol.


1979 ◽  
Vol 1 ◽  
pp. S1-7 ◽  
Author(s):  
Julia Mulvihill-Wilson ◽  
Robert M. Graham ◽  
William Pettinger ◽  
Carolyn Muckleroy ◽  
Shirley Anderson ◽  
...  

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.


1963 ◽  
Vol 205 (1) ◽  
pp. 57-59 ◽  
Author(s):  
Francois M. Abboud ◽  
Michael G. Wendling ◽  
John W. Eckstein

Some adrenergic blocking drugs reduce the mobilization of free fatty acids (FFA) in response to administration of catecholamines. The present experiments were done to see if potentiation of the pressor effect of norepinephrine by reserpine is accompanied by a greater increase in plasma FFA. Norepinephrine was infused intravenously into 16 anesthetized dogs. Eight of them had been treated with reserpine, 0.25 mg/kg daily, intraperitoneally for 2 days; the others were not treated. Arterial blood samples were drawn before, during, and after norepinephrine for determination of plasma FFA concentrations. Systemic arterial blood pressure was measured continuously. In the treated animals the maximal increase in arterial blood pressure as well as the progressive increments in FFA concentration were greater than in the untreated dogs. The experiments indicate that potentiation of the pressor response to norepinephrine after reserpine is accompanied by a greater FFA response.


1978 ◽  
Vol 55 (s4) ◽  
pp. 81s-83s ◽  
Author(s):  
H. M. Brecht ◽  
W. Schoeppe

1. Plasma noradrenaline was measured in 125 patients with stable essential hypertension (WHO I—II) and in 107 normotensive control subjects lying and standing. 2. In normotensive subjects and in patients with essential hypertension no sex-related differences of plasma noradrenaline were found between age-matched groups. 3. Plasma noradrenaline was not related to sodium balance indexed by urinary sodium/creatinine ratio. 4. In patients with essential hypertension plasma noradrenaline increases with age. 5. Mean plasma noradrenaline concentrations are significantly higher in patients with essential hypertension compared with age-matched normotensive subjects both lying and standing. 6. In patients with essential hypertension diastolic blood pressure and heart rate correlated significantly with supine plasma noradrenaline concentrations.


1981 ◽  
Vol 60 (5) ◽  
pp. 483-489 ◽  
Author(s):  
W. Kiowski ◽  
F. R. Bühler ◽  
P. Vanbrummelen ◽  
F. W. Amann

1. Plasma noradrenaline concentrations and blood pressure were measured in 45 patients with essential hypertension and 34 matched normotensive subjects. Plasma noradrenaline was similar in both groups, but in the hypertensive patients plasma noradrenaline correlated with blood pressure. 2. The increase in forearm flow in response to an intra-arterial infusion of phentolamine was determined in 12 of the hypertensive and 14 of the normotensive subjects to assess the α-adrenoceptor-mediated component of vascular resistance. Although the dilator response to phentolamine was similar in both groups, in the hypertensive patients it was correlated with the control plasma noradrenaline (r = 0.83, P<0.01) as well as the height of mean blood pressure (r = 0.73, P<0.01). 3. These results suggest that in hypertensive patients plasma noradrenaline can be a marker for both sympathetic activity and the α-adrenoceptor-mediated component of vascular resistance.


2004 ◽  
Vol 97 (6) ◽  
pp. 2077-2082 ◽  
Author(s):  
Makoto Takahashi ◽  
Akihiro Sakaguchi ◽  
Kanji Matsukawa ◽  
Hidehiko Komine ◽  
Kotaro Kawaguchi ◽  
...  

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C6-C7). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.


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