scholarly journals Somato–Autonomic Reflexes of Acupuncture

2020 ◽  
Vol 32 (6) ◽  
pp. 362-366
Author(s):  
Qiufu Ma
Keyword(s):  
Autonomic Reflexes

Effect of Curare on Autonomic Reflexes.

1949 ◽  
Vol 70 (4) ◽  
pp. 718-719 ◽  
Author(s):  
C. L. Burstein ◽  
A. Jackson ◽  
E. A. Rovenstine
Keyword(s):  
Autonomic Reflexes

Comparison of the Renin Response to Dopamine and Noradrenaline in Normal Subjects and Patients with Autonomic Insufficiency

1974 ◽  
Vol 46 (4) ◽  
pp. 481-488 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
A. B. Kurtz ◽  
J. D. H. Slater
Keyword(s):  
Autonomic Failure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Control Groups ◽  
Autonomic Reflexes ◽  
Fractional Increase ◽  
The Mean ◽  
Autonomic Insufficiency ◽  
Stimulation Of

1. The effect on plasma renin activity (PRA) of dopamine and noradrenaline infusions was studied in three patients with Shy—Drager syndrome, three patients with Parkinson's disease and normal autonomic reflexes, and three healthy volunteers. The patients with the Shy—Drager syndrome had functional evidence of a peripheral lesion of the sympathetic nervous system and subnormal PRA on a controlled sodium intake. 2. In all subjects catecholamines were infused step-wise for 4 min until a 30% rise in systolic blood pressure occurred. 3. In each subject, PRA fell after noradrenaline but rose after dopamine. The mean fractional increase in PRA after dopamine was no less in the Shy—Drager patients than in the control groups. 4. The results suggest, first, that stimulation of dopamine receptors can release renin, and secondly, that inadequate renin stores cannot explain the low PRA found in our patients with autonomic failure.

Plasma Renin in Idiopathic Orthostatic Hypotension: Differential Response in Subjects with Probable Afferent and Efferent Autonomic Failure

1971 ◽  
Vol 41 (4) ◽  
pp. 289-299 ◽  
Author(s):  
D. R. Love ◽  
J. J. Brown ◽  
R. H. Chinn ◽  
R. H. Johnson ◽  
A. F. Lever ◽  
...  
Keyword(s):  
Orthostatic Hypotension ◽  
Autonomic Function ◽  
Autonomic Failure ◽  
Plasma Renin ◽  
Sympathetic Block ◽  
Baroreceptor Reflexes ◽  
Idiopathic Orthostatic Hypotension ◽  
Autonomic Reflexes ◽  
Efferent Pathways ◽  
Venous Plasma

1. The changes of peripheral venous plasma renin concentration (PRC) induced by head-up tilting were studied in four patients with orthostatic hypotension. 2. Two of the patients had the Holmes—Adie syndrome and tests of autonomic function suggested that they had an afferent block from baroreceptors with intact efferent pathways; the others had no evidence of the Holmes—Adie syndrome and investigations suggested that they had interruption of efferent sympathetic pathways. 3. In the two patients in whom lesions of the afferent side of baroreceptor reflexes were suspected, a marked increase in PRC occurred with upright tilting, whereas no change in PRC occurred in the two patients thought to have an efferent sympathetic block. 4. During repeated tilting, supine blood pressure and PRC increased progressively in the two patients with suspected afferent block, but not in the two patients with suspected efferent block. 5. It is suggested that an increase in plasma renin may contribute to the supine hypertension sometimes observed in patients with orthostatic hypotension. 6. It is also suggested that renin release does not require intact autonomic reflexes although certain components of efferent sympathetic pathways, not dependent on baroreceptor reflexes, may be important.

Modulation of Neurocardiac Function by Oesophageal Stimulation in Humans

1997 ◽  
Vol 92 (2) ◽  
pp. 167-174 ◽  
Author(s):  
Gervais Tougas ◽  
Markad Kamath ◽  
Geena Watteel ◽  
Debbie Fitzpatrick ◽  
Ernest L. Fallen ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Power Spectrum ◽  
High Frequency ◽  
Low Frequency ◽  
Sensory Stimulation ◽  
Sensory Stimuli ◽  
Autonomic Reflexes ◽  
Low Frequency Power ◽  
Beat Heart

1. The heart and the oesophagus have similar sensory pathways, and sensations originating from the oesophagus are often difficult to differentiate from those of cardiac origin. We hypothesized that oesophageal sensory stimuli could alter neurocardiac function through autonomic reflexes elicited by these oesophageal stimuli. In the present study, we examined the neurocardiac response to oesophageal stimulation and the effects of electrical and mechanical oesophageal stimulation on the power spectrum of beat-to-beat heart rate variability in male volunteers. 2. In 14 healthy volunteers, beat-to-beat heart rate variability was compared at rest and during oesophageal stimulation, using either electrical (200 μs, 16 mA, 0.2 Hz) or mechanical (0.5 s, 14 ml, 0.2 Hz) stimuli. The power spectrum of beat-to-beat heart rate variability was obtained and its low- and high-frequency components were determined. 3. Distal oesophageal stimulation decreased heart rate slightly (both electrical and mechanical) (P < 0.005), and markedly altered heart rate variability (P < 0.001). Both electrical and mechanical oesophageal stimulation increased the absolute and normalized area of the high-frequency band within the power spectrum (P < 0.001), while simultaneously decreasing the low-frequency power (P < 0.005). 4. In humans, oesophageal stimulation, whether electrical or mechanical, appears to amplify respiratory-driven cardiac vagoafferent modulation while decreasing sympathetic modulation. The technique provides access to vagoafferent fibres and thus may yield useful information on the autonomic effects of visceral or oesophageal sensory stimulation.

Pressure diuresis and autonomic function in conscious dogs

1991 ◽  
Vol 261 (4) ◽  
pp. R802-R810
Author(s):  
P. H. Brand ◽  
K. B. Coyne ◽  
K. A. Kostrzewski ◽  
D. Shier ◽  
P. J. Metting ◽  
...  
Keyword(s):  
Renal Function ◽  
Autonomic Function ◽  
Sound Intensity ◽  
Conscious Dogs ◽  
Normal Operation ◽  
Arterial Blood ◽  
Autonomic Blockade ◽  
Autonomic Reflexes ◽  
Experimental Interference

Pressure diuresis is thought to be a major long-term regulator of arterial blood pressure (AP). Previously, pressure diuresis has been characterized using pharmacological or surgical blockade of other mechanisms known to affect renal function. This study evaluated pressure diuresis in conscious dogs with minimal experimental interference. Dogs were chronically instrumented under pentobarbital anesthesia with aortic and urinary bladder catheters. AP was increased by 10% in resting dogs by exposure to increased light and sound intensity (arousal) for 90 min. During arousal, urine flow (UV) and Na+ excretion (UNa+ V) correlated with AP (UV vs. AP, r = 0.12, P less than 0.05; UNa+ V vs. AP, r = 0.19, P less than 0.005; 17 trials in 7 dogs). Arousal did not affect the plasma concentration of atrial natriuretic factor, suggesting that this hormone did not contribute to the correlations between UV or UNa+ V and AP. Because arousal may induce an autonomically mediated antidiuresis, studies were repeated during autonomic ganglionic blockade with hexamethonium. During autonomic blockade, the correlations between UV or UNa+ V and AP were increased (UV vs. AP, r = 0.72; UNa+ V vs. AP, r = 0.72, P less than 0.001; 6 trials in 4 dogs). We conclude that the effect of pressure diuresis on UV and UNa+ V can be detected in the intact animal, during normal operation of all the mechanisms that control renal function. Furthermore, when autonomic reflexes are blocked, the pressure-diuresis mechanism is a major determinant of UV and UNa+ V.

Comparison of responses to sarafotoxins 6a and 6c in pulmonary and systemic vascular beds

1992 ◽  
Vol 262 (3) ◽  
pp. H852-H861
Author(s):  
R. K. Minkes ◽  
J. A. Bellan ◽  
T. R. Higuera ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Venous Pressure ◽  
Constant Flow ◽  
Flow Conditions ◽  
Arterial Perfusion ◽  
Intravenous Injections ◽  
Autonomic Reflexes ◽  
Pressure Changes

Cardiovascular and pulmonary responses to sarafotoxin (S) 6a and S6c were investigated in the anesthetized cat. Intravenous injections of the peptides in doses of 0.1-1.0 nmol/kg caused decreases or biphasic changes in arterial pressure (AP) and increases in central venous pressure, pulmonary arterial pressure (PAP), and cardiac output (CO). Secondary decreases in CO were observed in response to higher doses, and biphasic changes in systemic (SVR) and pulmonary (PVR) vascular resistances were observed. Under constant-flow conditions, the peptides only increased pulmonary lobar arterial perfusion pressure and lobar vascular resistance. AP responses to S6a, S6c, endothelin (ET)-1, ET-2, vasoactive intestinal contractor (VIC), and Lys7-ET-1 were similar, whereas AP responses to S6b and ET-3 were similar. S6a, S6b, S6c, ET-1, ET-2, ET-3, VIC, Lys7-ET-1, and big ET-1 increased PAP. S6a and S6c increased distal aortic and superior mesenteric arterial (SMA) blood flow and caused biphasic changes at the highest doses. Under constant-flow conditions, S6a and S6c produced dose-dependent biphasic changes in hindquarters perfusion pressure. Changes in SVR and PVR in response to the peptide were not affected by hexamethonium, glyburide, or meclofenamate, indicating that responses are independent of autonomic reflexes, activation of ATP-regulated K+ channels, or release of cyclooxygenase products. In contrast, N-nitro-L-arginine methyl ester decreased hindquarters vasodilator response to S6a and S6c. The present data show that S6a and S6c produce both vasodilation and vasoconstriction in the systemic vascular bed and increase lobar vascular resistance and that hindquarters vasodilator responses are mediated, in part, by the release of endothelium-derived relaxing factor.

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