Role of the Autonomic Nervous System in Mild Human Hypertension

1974 ◽  
Vol 48 (s2) ◽  
pp. 243s-252s ◽  
Author(s):  
S. Julius ◽  
M. D. Esler ◽  
O. S. Randall

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.

1981 ◽  
Vol 1 (s1) ◽  
pp. 71-75 ◽  
Author(s):  
Helmer Ring-Larsen ◽  
Jens H. Henriksen ◽  
Birger Hesse ◽  
Niels Juel Christensen

1982 ◽  
Vol 52 (6) ◽  
pp. 1438-1443 ◽  
Author(s):  
P. Escourrou ◽  
P. R. Freund ◽  
L. B. Rowell ◽  
D. G. Johnson

We conducted a two-part study to determine whether the renin-angiotensin system contributes to the rise in splanchnic vascular resistance (SVR) during heat stress (rectal temperature was raised 1 degree C). In experiment 1 (control) seven men on a normal salt diet were directly heated (water-perfused suits) for 40–50 min. Arterial pressure (85 Torr) was unchanged; plasma renin activity (PRA) rose from 102 to 239 ng angiotensin I.100 ml-1.3 h-1; and SVR increased 73% (from 63 to 109 units). Experiment 2 was a repetition of experiment 1 on the same subjects, except that propranolol (10 mg iv) was given at the onset of heating to block renin release. Propranolol attenuated the rise in heart rate and reduced mean arterial pressure from 82 to 72 Torr; it blocked the rise in PRA with heating in two subjects, reduced it in three, but increased it in two. Although changes in SVR paralleled those in PRA in three subjects, SVR still rose 60% (from 58 to 99 units) after PRA rise was blocked. In both experiments, plasma norepinephrine concentration rose indicating increased sympathetic nervous activity. During mild heat stress, increased PRA is not a major factor in the increase of SVR.


2010 ◽  
Vol 33 (6) ◽  
pp. 521-528 ◽  
Author(s):  
Kazuko Masuo ◽  
Gavin W Lambert ◽  
Murray D Esler ◽  
Hiromi Rakugi ◽  
Toshio Ogihara ◽  
...  

Folia Medica ◽  
2011 ◽  
Vol 53 (4) ◽  
Author(s):  
Mihail V. Cheshmedzhiev ◽  
Victor V. Knyazhev ◽  
Radoslav S. Radev ◽  
Emil D. Yordanov

1991 ◽  
Vol 261 (5) ◽  
pp. H1659-H1664 ◽  
Author(s):  
U. Leuenberger ◽  
K. Gleeson ◽  
K. Wroblewski ◽  
S. Prophet ◽  
R. Zelis ◽  
...  

Acute hypoxemia leads to activation of the sympathetic nervous system (SNS), yet adrenergic vasoconstriction does not occur and venous plasma norepinephrine (NE) fails to rise as expected. To examine whether this dissociation between SNS tone and plasma NE is due to altered metabolism of NE, we measured arterial NE kinetics ([3H]NE infusion technique) and sympathetic nervous outflow to muscle (peroneal microneurography) during 25-30 min of hypoxemia (spontaneous breathing, mean O2 saturation 74%) in six healthy young men. During hypoxemia, muscle sympathetic nervous activity (MSNA) rose significantly from 12.2 +/- 3.3 to 18.6 +/- 3.5 bursts/min, and the total amplitude increased from 123 +/- 36 to 255 +/- 50 mm/min. NE spillover, an index of NE release at the sympathetic nerve terminals, rose from 1.66 +/- 0.30 to 2.33 +/- 0.40 nmol.min-1.m-2 (P = 0.014). However, NE clearance increased also from 0.99 +/- 0.05 to 1.19 +/- 0.11 l.min-1.m-2 (P = 0.014), and arterial NE rose from 281 +/- 50 to 339 +/- 64 pg/ml (P = 0.023). Hypoxemia resulted in a significant rise in forearm blood flow and a decrease in forearm vascular resistance. The fact that skin blood flow and vascular resistance did not change implies that forearm vasodilation was localized to skeletal muscle. Our results suggest that during acute hypoxemia in humans the SNS is activated but the rise in plasma NE is attenuated because NE clearance is increased.


2009 ◽  
Vol 216 (S686) ◽  
pp. 41-48
Author(s):  
J. Rokkedal Nielsen ◽  
K.E. Pedersen ◽  
N.A. Klitgaard ◽  
T. Johansen ◽  
P.K. Pedersen ◽  
...  

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