Central and peripheral mechanisms of arterial pressure lability following baroreceptor denervation

1987 ◽  
Vol 65 (8) ◽  
pp. 1615-1618 ◽  
Author(s):  
R. H. Alper ◽  
H. J. Jacob ◽  
M. J. Brody
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Humoral Factors ◽  
Neural Transmission ◽  
Sympathetic Transmission ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine ◽  
Alpha Adrenergic Agonist ◽  
Arterial Pressure Lability

Deafferentation of sinoaortic baroreceptors produces a marked increase in the lability of arterial pressure that is sustained chronically. Studies reviewed in this paper were designed to determine the mechanisms responsible for generating arterial pressure lability. Pharmacological interruption of the humoral vasopressin and angiotensin systems failed to alter arterial pressure lability. In contrast, blockade of sympathetic nervous system transmission at both ganglionic and alpha-adrenergic receptor levels significantly attenuated lability. A similar effect was observed with the peripheral neurotoxin, 6-hydroxydopamine. After blockade of sympathetic transmission, a further reduction in lability was produced by blocking the renin–angiotensin or vasopressin systems. The dissociation of the level of arterial pressure from lability was achieved with parachloroamphetamine which raised arterial pressure but reduced lability. A substantial peripheral contribution to lability was obtained in experiments in which the alpha-adrenergic agonist, phenylephrine, produced a marked increase in lability in both normal and baroreceptor-denervated animals in which humoral and neural transmission were blocked. These data demonstrate that following baroreceptor deafferentation, arterial pressure lability is produced primarily by the sympathetic nervous system and secondarily by circulating humoral factors that appear to act on vascular smooth muscle to induce fluctuations in the level of arterial pressure.

Role of vasopressin and sympathetic nervous system during hypertonic NaCl infusion in conscious dog

1985 ◽  
Vol 248 (5) ◽  
pp. H652-H657 ◽  
Author(s):  
E. M. Hasser ◽  
J. R. Haywood ◽  
V. S. Bishop
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Plasma Osmolality ◽  
Ganglionic Blockade ◽  
Osmotic Stimulus ◽  
Sympathetic Nervous ◽  
Subsequent Administration

The contribution of arginine vasopressin (AVP) and the sympathetic nervous system to the pressor response elicited by hypertonic NaCl infusion was investigated in conscious dogs with intact carotid sinus baroreceptors or in dogs subjected to chronic sinoaortic baroreceptor denervation (SAD). Infusion of 6% NaCl at 0.05 ml X kg-1 X min-1 for 60 min increased plasma osmolality an average of 12 +/- 2 mosmol/kg in both intact and SAD dogs. Arterial pressure increased 6 +/- 2 mmHg in intact animals and was normalized by subsequent administration of a specific vascular AVP antagonist. Pretreatment with the AVP antagonist did not alter resting arterial pressure but prevented the increase due to the osmotic stimulus. Pretreatment with ganglionic blockade reduced resting arterial pressure (-17 +/- 2 mmHg). Subsequent infusion of hypertonic NaCl elevated arterial pressure (21 +/- 7 mmHg) to a significantly greater level than that observed with the autonomic nervous system intact. In SAD dogs, the osmotic stimulus increased arterial pressure (16 +/- 1 mmHg) to a significantly greater extent than in intact animals. Subsequent administration of AVP antagonist normalized arterial pressure, and pretreatment with the antagonist prevented any pressor response. Pretreatment with ganglionic blockade did not alter the pressor response (15 +/- 2 mmHg) to hypertonic NaCl. Data suggest that the increase in arterial pressure due to an osmotic stimulus is due to AVP release and does not require a functional sympathetic nervous system. The response is normally buffered by arterial baroreflexes, presumably due to sympathetic withdrawal.

Some Observations on the Sympathetic Nervous System

1939 ◽  
Vol 85 (358) ◽  
pp. 902-902
Author(s):  
E. Arnold Carmichael
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Cerebral Blood Flow ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Blood Vessels ◽  
Fluid Pressure ◽  
Spinal Fluid ◽  
Cerebral Blood Vessels ◽  
Sympathetic Nervous

Outline of physiology of sympathetic nervous system and its effect on the cerebral blood-vessels. Other factors controlling cerebral blood-vessels, such as local intra-arterial pressure and gas tension. The action of adrenalin-like and cholin-like substances on the cerebral blood-vessels. Alteration in cerebral blood flow during a convulsion, and the accompanying changes in cerebro-spinal fluid pressure. Evidence for systemic sympathetic disturbance during a convulsion. Discussion of “vaso-vagal” attacks and “diencephalitic” epilepsy.

Arterial pressure lability and renal sympathetic nerve activity are dissociated in SAD rats

1992 ◽  
Vol 263 (3) ◽  
pp. R639-R646 ◽  
Author(s):  
C. Barres ◽  
S. J. Lewis ◽  
H. J. Jacob ◽  
M. J. Brody
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
High Variability ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

The purpose of this study was to determine whether the sympathetic nervous system drives the high variability of arterial pressure (AP) observed after sinoaortic denervation (SAD) in rats. One or fourteen days after SAD, rats were instrumented chronically to record mean AP (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) in the conscious unrestrained state. Acute SAD increased MAP, HR, RSNA, and variability of MAP and decreased variability of both HR and RSNA. In rats with chronic SAD, variability of MAP remained high, whereas MAP, HR, RSNA, and variability of HR and RSNA returned to normal levels. Correlation analysis showed that, in sham-operated rats, AP and RSNA were negatively correlated in 90% of cases. In contrast, rats with both acute and chronic SAD exhibited only 30% negative and 25% positive correlations. These results indicate that 1) low AP variability in intact rats results from baroreflex-mediated inversely related fluctuations in RSNA and HR and 2) high variability of AP after acute and chronic SAD is correlated infrequently with RSNA. Because lability is reduced by interventions that block the sympathetic nervous system, we conclude that lability of AP associated with SAD appears to be mediated largely by a permissive role of sympathetic activity.

Relation of arterial pressure to spontaneous variations in digital volume

1960 ◽  
Vol 15 (1) ◽  
pp. 23-24 ◽  
Author(s):  
G. E. Burch ◽  
N. DePasquale
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Blood Vessels ◽  
Arterial Blood Pressure ◽  
Peripheral Blood ◽  
Normal Subjects ◽  
Arterial Blood ◽  
Sympathetic Nervous

Simultaneous digital plethysmographic and brachial arterial pressure recordings in 11 normal subjects at rest in bed in a comfortable atmosphere showed that the spontaneous variations in digital volume (alpha and beta deflections) were independent of variations in arterial blood pressure. This indicates that the regulation of the caliber of the peripheral blood vessels as well as the spontaneous variations in the volume of the digital vessels is not passively produced by fluctuations in arterial blood pressure, including the Traube-Hering waves, but must be controlled by different centers and pathways of the sympathetic nervous system. Submitted on July 27, 1959

Circulatory and humoral responses of sympathectomized fetal sheep to hypoxemia

1983 ◽  
Vol 245 (5) ◽  
pp. H767-H772 ◽  
Author(s):  
H. S. Iwamoto ◽  
A. M. Rudolph ◽  
B. L. Mirkin ◽  
L. C. Keil
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Fetal Sheep ◽  
Vascular Responses ◽  
Fetal Survival ◽  
Placental Blood ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine ◽  
Humoral Responses

In fetal sheep, hypoxemia causes arterial hypertension, bradycardia, a redistribution of blood flow, and an increase in plasma vasopressin and catecholamine concentrations. To assess the role of the sympathetic nervous system in mediating these responses, we administered 6-hydroxydopamine to 11 chronically catheterized fetal sheep. Some of the responses to acute hypoxemia, achieved by administration of a low-O2 gas mixture to the ewe, were similar to those in intact fetal sheep. Fetal arterial O2 tension decreased from 22 +/- 3 to 12 +/- 3 (SD) Torr; fetal heart rate decreased transiently; combined ventricular output and umbilical-placental blood flow, as measured by the radionuclide-labeled microsphere technique, were maintained; cerebral, myocardial, and adrenal blood flow increased, and pulmonary blood flow decreased. However, there was no significant change in arterial pressure or blood flow to the peripheral, renal, and splanchnic circulations in the chemically sympathectomized fetuses in response to hypoxemia. The sympathetic nervous system is important in certain fetal vascular responses to hypoxemia but is not necessary for vascular responses in certain critical organs and thus is not crucial for fetal survival during hypoxia.

Contribution of sodium to the mechanism of one-kidney, renal-wrap hypertension

1984 ◽  
Vol 247 (5) ◽  
pp. H797-H803 ◽  
Author(s):  
J. R. Haywood ◽  
S. F. Williams ◽  
N. A. Ball
Keyword(s):  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Renal Hypertension ◽  
Dietary Sodium ◽  
Nervous System Function ◽  
Sympathetic Nervous ◽  
Angiotensin Receptor Blockade

The early and chronic stages of one-kidney, figure-8 renal-wrap hypertension were studied during low or normal dietary sodium intake in rats. The renal-wrap procedure caused a significant elevation in arterial pressure at 3 and 28 days postwrap with normal sodium diet. Sodium-depleted rats did not experience an increased arterial pressure following renal wrapping. Blockade of angiotensin II receptors with [Sar1-Ala8]angiotensin II caused a greater decrease in arterial pressure in the sodium-depleted, renal-wrapped animals compared with sham-operated rats. In sodium-replete rats, angiotensin receptor blockade did not lower arterial pressure. Total ganglionic blockade decreased arterial pressure significantly more in the wrapped animals than in the sodium-replete sham-operated rats and the wrapped or sham-wrapped, sodium-deplete animals. Thus the early and chronic phases of normal sodium, one-kidney, figure-8 renal hypertension are supported by an increased sympathetic nervous system function. These observations suggest that sodium is necessary for the development of one-kidney, figure-8 renal-wrap hypertension and that the presence of sodium in the diet permits a functional activation of the sympathetic nervous system in response to the renal-wrap procedure.

Sympathectomy and beta-adrenergic blockade during lung maturation stimulated by TRH and cortisol in fetal sheep

1993 ◽  
Vol 75 (1) ◽  
pp. 141-147 ◽  
Author(s):  
J. C. Schellenberg ◽  
G. C. Liggins ◽  
J. A. Kitterman ◽  
C. C. Lee
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Adrenergic Blockade ◽  
Lung Maturation ◽  
Fetal Sheep ◽  
Beta Adrenergic ◽  
Adrenergic Mechanisms ◽  
Adrenergic Blocker ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine

To test whether beta-adrenergic mechanisms and the sympathetic nervous system are involved in the synergistic action of thyrotropin-releasing hormone (TRH) and cortisol on lung maturation, fetal sheep (n = 32) were infused from 121 to 128 days of gestation with saline, TRH + cortisol, TRH + cortisol + beta-adrenergic blocker, or TRH + cortisol after chemical sympathectomy with 6-hydroxydopamine. TRH + cortisol increased lung distensibility and stability and alveolar concentrations of saturated phosphatidylcholine two- to threefold over control fetuses. beta-Adrenergic blockade prevented the increase in distensibility in response to TRH + cortisol. Sympathectomy did not impair the increase in distensibility and stability in response to TRH + cortisol but inhibited the increase in alveolar total phospholipids. Tissue concentrations of saturated phosphatidylcholine increased in TRH + cortisol-treated fetuses after either sympathectomy or beta-adrenergic blockade. We concluded that during lung maturation by TRH + cortisol 1) sympathetic mechanisms are requisite for surfactant release, 2) nonneurogenic beta-adrenergic mechanisms are requisite for the maturation of the mechanical properties of the lung and 3) stimulation of surfactant synthesis is independent of beta-adrenergic action and the sympathetic nervous system.

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