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Results for “Sympathetic Nervous System”

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At least 235 records · Page 13Linked to original sources

PubMed2000

Hemodynamic and sympathetic nervous system responses to stress during the menstrual cycle.

In this study, the impact of menstrual cycle phase on hemodynamic and sympathetic nervous system responses was examined during exposure to a battery of laboratory stressors. Participants were 40 healthy premenopausal women, aged 26 to 51. Impedance cardiography was used to measure stroke volume, heart rate, and cardiac output. Systemic vascular resistance was derived on the basis of concurrently recorded blood pressure and cardiac output. The menstrual cycle's effect on the sympathetic nervous system response was explored by evaluating plasma catecholamine responses during stress. In luteal compared with follicular subjects, systemic vascular resistance was significantly lower during all stress tasks (P < 0.03). Catecholamine responses were also significantly lower in luteal subjects (P < 0.004). The results suggest that the sympathetic nervous system may respond to stress differently during different phases of the menstrual cycle. This finding has implications for understanding "whitecoat hypertension" in women, and highlights the need to measure blood pressure during several office visits. Perhaps high blood pressure readings recorded during the follicular phase should be reexamined during the luteal phase before considering pharmacologic intervention.

Adult↗

PubMed1985

Increased body fat due to elevated energetic efficiency following chronic administration of inhibitors of sympathetic nervous system activity.

The effects on energy balance of drugs known to inhibit the sympathetic nervous system at different sites and with various modes of action were studied in lean mice of the CFLP strain. Metabolizable energy intake was monitored continuously over seven-week experimental periods and energy expenditure was determined by the comparative carcass method as well as by measurements of 24-hour oxygen consumption. Administration of either propranolol, phenoxybenzamine, clonidine, or mecamylamine had no influence on energy balance nor on body composition. On the other hand, administration of alpha-methyl para tyrosine, reserpine, and bethanidine, ie, drugs capable of reducing the levels of noradrenaline at sympathetic terminals, resulted in significant increases in body fat by 38%, 24%, and 46% respectively: this effect was brought about by a reduction in the metabolic rate of these drug-treated groups and the efficiency of energy utilization (both gross and net) was increased by three to nine times. These studies indicate that chronic administration of drugs that act at the receptor level to inhibit sympathetic activity fail to influence metabolic rate, thereby suggesting that thermogenesis under noradrenaline control may involve mechanisms other than the alpha and beta classification of adrenergic receptors. Nonetheless, the ability of some drugs which both reduce noradrenaline levels and decrease metabolic rate would support the concept of an important role of the sympathetic nervous system in the overall control of thermogenesis and in energy balance regulation.

Adipose Tissue↗

PubMed1990

Interactions between the sympathetic nervous system and atrial natriuretic factor in the control of renal functions.

We studied neural influences on the renal actions of atrial peptides in anaesthetized cats by comparing the response to atrial natriuretic factor (ANF) infusion in the innervated kidney and in the contralateral surgically denervated kidney. During ANF infusion arterial pressure decreased, the heart rate did not change and blood flow to both kidneys increased slightly. Vascular conductances became slightly but significantly higher in the denervated kidneys than in the controls. In both kidneys, the glomerular filtration rate increased transiently and significantly. Inhibition of renin release was more prompt and larger in the innervated than in the denervated kidneys. ANF infusion caused a significant increase in sodium and water excretion from both the innervated and denervated kidneys. However, the diuretic and natriuretic effect in the innervated kidneys, although proportionally greater than that in the denervated kidneys, was of shorter duration and subsided after 20 min of ANF infusion. Efferent renal nerve activity did not change during the initial 10 min of ANF infusion but thereafter increased progressively and significantly. We conclude that the effects of atrial peptides on renin release and excretory functions are influenced by renal nerve activity.

Animals↗

PubMed1998

Comparison of effects of enalapril and nitrendipine on cardiac sympathetic nervous system in essential hypertension.

OBJECTIVES: The purpose of this study was to assess the effects of enalapril and nitrendipine on the cardiac sympathetic nervous system. BACKGROUND: Angiotensin-converting enzyme inhibitors and long-acting calcium channel blockers have been widely used in the treatment of cardiovascular diseases, in some of which sympathetic overactivity plays a major role in the pathophysiology and prognosis. However, little information is available on the effects of these drugs on the cardiac sympathetic nervous system. METHODS: 123I-metaiodobenzylguanidine (MIBG) cardiac imaging was performed before and 3 months after drug administration in 46 patients with mild essential hypertension. Twenty-two patients were treated with 5 to 10 mg of enalapril once a day, and the other 24 with 5 to 10 mg of nitrendipine once a day. For comparison, 20 normotensive subjects were also studied. RESULTS: There were no significant differences between the basal characteristics in the 2 hypertensive groups. In both hypertensive groups, both systolic and diastolic blood pressures were significantly reduced to similar levels after the 3-month drug treatment. Before the drug treatment, the 2 hypertensive groups had a significantly higher washout rate and lower MIBG uptake than the normotensive subjects. The heart-to-mediastinum ratio significantly increased (p < 0.0001), with decreased (p < 0.002) washout rate after drug treatment in the enalapril group, but with no significant changes in the nitrendipine group. CONCLUSION: Enalapril could suppress cardiac sympathetic activity and nitrendipine had no effect on it. The knowledge of antihypertensive drugs on the cardiac sympathetic nervous system appears to be helpful in selecting appropriate treatment in cardiovascular diseases.

3-Iodobenzylguanidine↗

PubMed1991

The effects of low dose insulin infusions on the renin angiotensin and sympathetic nervous systems in normal man.

To examine the effects of physiological insulin concentrations on the renin-angiotensin and sympathetic nervous systems, healthy volunteers were studied by the euglycaemic glucose clamp technique with sequential 60 min 0.5 and 1.0 mU kg-1 min-1 insulin infusions and, subsequently, by a control infusion simulating clamp conditions. Plasma renin activity increased from 0.8 +/- 0.1 ng ml-1 h-1 basally to 1.0 +/- 0.2 ng ml-1 h-1 during the 0.5 mU infusion to 1.4 +/- 0.1 ng ml-1 h-1 during the 1 mU infusion but did not change during control infusion (0.9 +/- 0.3 ng ml-1h-1 to 0.9 +/- 0.2 ng ml-1h-1 to 1.0 +/- 0.1 ng ml-1h-1) (P less than 0.001 insulin vs. control by ANOVAR). Plasma angiotensin II increased during insulin (21.2 +/- 1.8 to 25.2 +/- 2.3 to 29.3 +/- 2.4 pg ml-1) but not during control infusion (24.0 +/- 2.8 to 23.6 +/- 2.6 to 23.5 +/- 2.5 pg ml-1) (P less than 0.001 insulin vs. control). Serum aldosterone did not change significantly during either infusion (insulin: 239 +/- 89 pmol l-1 to 237 +/- 50 pmol l-1 to 231 +/- 97 pmol l-1, control: 222 +/- 79 to 237 +/- 50 to 213 +/- 97 pmol l-1). Plasma noradrenaline increased to a greater extent during insulin (1.03 +/- 0.2 to 1.14 +/- 0.8 to 1.27 +/- 0.17 nmol l-1) than control infusion (0.86 +/- 0.09 to 0.97 +/- 0.09 to 0.99 +/- 0.09 nmol 1-1 (P less than 0.01 insulin vs. control). Changes in mean systolic blood pressure during insulin infusion were significantly different from control (+ 3 vs. -4 mmHg, P less than 0.001). In conclusion acute hyperinsulinaemia within the physiological range increases circulating hormones of the renin-angiotensin and sympathetic nervous systems and also increases systolic blood pressure.

Adult↗

PubMedDate not supplied

Role of renin-angiotensin and sympathetic nervous systems in the chronic phase of two-kidney, one-clip hypertension in rats.

The purpose of the present study was to examine the role of the renin-angiotensin and the sympathetic nervous systems during the chronic phase (greater than 16 weeks) of two-kidney, one-clip hypertension in conscious unrestrained rats. During this phase, the mean arterial pressure (MAP) (p less than 0.001) and plasma angiotensin II (31.9 +/- 1.5 to 125.8 +/- 19.9 pg/ml, p less than 0.005) were significantly increased as compared to normotensive group. Converting enzyme inhibition by captopril produced a significant decrease of MAP (181.2 +/- 8.2 to 140.0 +/- 5.5 mmHg, p less than 0.001). This hypotensive response was similar when aprotinin (a Kallikrein inhibitor) and captopril were infused simultaneously. Alpha 1-adrenergic receptor blockade by phenoxybenzamine (POB) significantly decreased but did not normalize MAP (179.8 +/- 12.4 to 135.8 +/- 10.4 mmHg, p less than 0.001). However, when infused after POB, captopril induced a further decrease of MAP to 86.7 +/- 9.4 mmHg (p less than 0.001). This MAP level was not different from that found in normotensive rats after infusion of the two drugs (83.2 +/- 5.3 mmHg). These results suggest that both the renin-angiotensin system and the sympathetic nervous system, by activating peripheral alpha 1-adrenergic receptors, maintain the high blood pressure during the chronic phase (greater than 16 weeks) of two-kidney, one-clip hypertension in conscious rats.

Angiotensin II↗

PubMed1963

The action of guanethidine with particular reference to the sympathetic nervous system.

It has been suggested that guanethidine can release and then deplete postganglionic sympathetic nerve endings of noradrenaline. However, no release of noradrenaline from postganglionic nerve endings or from the adrenal medulla by guanethidine was found by direct experiment. Although release of noradrenaline from postganglionic sympathetic nerve endings in response to nerve stimulation was rapidly reduced and finally abolished by guanethidine, the drug did not appear to affect the release of catechol amines from the adrenal medulla in response to splanchnic nerve stimulation. The nature of the action of guanethidine is discussed, and it is concluded that it blocks the effect of postganglionic sympathetic nerve stimulation by interfering with the synthesis of transmitter and that it also has a direct sympathomimetic effect.

Adrenal Medulla↗

PubMed1995

The effect of the sympathetic nervous system upon susceptibility to acoustic trauma.

This study was designed to determine whether the sympathetic nervous system exerts a protective or enhancing effect in acoustic overstimulation. The compound action potential of the cochlea (CAP) was recorded in guinea pigs while the cervical sympathetic nervous system (SNS) was electrically stimulated or after it was surgically eliminated. The stimulation or the elimination of the cervical SNS has no effect on the threshold of CAP. The threshold shift in CAP after acoustic overstimulation (110, 115, or 130 dB SPL for 10 min) was measured in the cervical SNS stimulation group, in the cervical SNS elimination group, and in the control group. When the animal was under insufficient sedation, there was no difference among these three groups. However, the CAP threshold shift was significantly smaller in the cervical SNS stimulation group than in the other two groups when the animals were sufficiently sedated. The cervical SNS stimulation had some protective effect on the susceptibility to acoustic trauma when the systemic SNS activity was suppressed.

Acoustic Stimulation↗

PubMed1992

Evidence against the hypothesis that hyperinsulinemia increases sympathetic nervous system activity in man.

To test the hypothesis that physiologic hyperinsulinemia activates the sympathetic nervous system in humans, we measured changes in plasma norepinephrine as well as epinephrine concentrations during euglycemic hyperinsulinemic clamp experiments in which normal volunteers were infused with insulin for up to 12 hours, at rates chosen to simulate the basal and postprandial hyperinsulinemia seen in insulin-resistant states. Infusions of insulin increased plasma insulin threefold (to approximately 200 pmol/L) and 15-fold (to approximately 1,000 pmol/L) in simulations of fasting and postprandial hyperinsulinemia. In neither experiment did plasma norepinephrine or epinephrine change significantly. In control experiments in which saline was infused for 12 hours, plasma epinephrine increased twofold (P less than .05), but plasma norepinephrine did not change. Therefore, we conclude that hyperinsulinemia of the magnitude seen in the insulin-resistant humans does not increase sympathetic nervous system activity.

Adult↗

PubMed1953