EFFECTS OF CHEMORECEPTOR AND BARORECEPTOR STIMULATION ON THE DISCHARGE OF HYPOTHALAMIC SUPRAOPTIC NEURONES IN RATS

1979 ◽  
Vol 82 (1) ◽  
pp. 115-125 ◽  
Author(s):  
M. C. HARRIS
Keyword(s):  
Supraoptic Nucleus ◽  
Carotid Sinus ◽  
Carotid Bifurcation ◽  
Cardiovascular Reflexes ◽  
Nacl Solution ◽  
Baroreceptor Stimulation ◽  
Vasopressin Secretion ◽  
Carotid Body Chemoreceptors ◽  
Hypothalamic Supraoptic Nucleus ◽  
Slight Inhibition

SUMMARY Experiments have been performed to examine the effects of activating the carotid body chemoreceptors and the arterial baroreceptors on the discharge of neurones within the hypothalamic supraoptic nucleus of the rat. Chemoreceptors were activated by intracarotid injection of 0·9% NaCl solution equilibrated with 100% CO2. The baroreceptors of the carotid sinus and aortic arch were activated by raising the blood pressure with an intravenous injection of phenylephrine. Chemoreceptor stimulation activated and baroreceptor stimulation inhibited the discharge of all the phasically discharging neurones tested. Neither stimulus had any consistent effect on non-phasically discharging neurones, although slight inhibition occasionally occurred. Anaesthesia of the carotid bifurcation abolished the effects of cardiovascular stimulation on the supraoptic neurones. Responses resumed when the anaesthesia wore off. However, the anaesthesia also seemed to alter the phasic pattern of discharge. The results are discussed with reference to the influence of the cardiovascular receptors upon the neurones in the supraoptic nucleus, and with reference to possible roles for the cardiovascular reflexes in control of vasopressin secretion.

Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons

1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm
Keyword(s):  
Blood Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

Carotid bifurcation sympathectomy and deafferentation: respiration during hypercapnia

1988 ◽  
Vol 255 (2) ◽  
pp. R252-R258
Author(s):  
D. B. Jennings ◽  
P. C. Szlyk
Keyword(s):  
Carotid Sinus ◽  
Carotid Bifurcation ◽  
The Other ◽  
Afferent Activity ◽  
Nerve Section ◽  
Absolute Level ◽  
Respiratory Effects ◽  
Percent Change ◽  
Fractional Concentration ◽  
Awake Cats

The respiratory effects of hypercapnia were studied in six awake cats 1) after bilateral sympathectomy of the carotid bifurcations and 2) after bilateral section of the carotid sinus nerves. When cats breathed either 2 or 4% CO2 in air, neither denervation affected the absolute level of ventilation, the percent change in ventilation, or the range of breath-to-breath variability in ventilation (V). However, in all six cats tidal volume (VT) increased for some levels of breath V after sympathectomy of the carotid bifurcations during inhalation of 4% CO2 in air. Moreover, after the subsequent carotid deafferentation, increased VT during fractional concentration of inspired CO2 (FICO2) of 4% persisted in four of six cats. Thus increased VT after sympathectomy could not be attributed to increased carotid chemoreceptor afferent activity but may have been due to reduced baroreceptor activity. On the other hand, sympathectomy-induced differences in breath timing, present during inhalation of 2% CO2, were reversed to intact values after sinus nerve section. In contrast to 2% CO2, changes in respiratory timing in intact cats associated with 4% CO2 were not altered significantly by sympathectomy or deafferentation of the carotid bifurcations. The latter indicates that above a critical FICO2 central mechanisms, unrelated to the carotid bifurcation, dominated respiratory timing in the hypercapnic awake cats.

Regulation of plasma vasopressin by plasma osmolality and carotid sinus pressure in anesthetized rabbits

1994 ◽  
Vol 266 (3) ◽  
pp. R796-R801
Author(s):  
C. S. Scott ◽  
J. Sharp-Kehl ◽  
C. A. Redekopp ◽  
J. R. Ledsome
Keyword(s):  
Linear Regression ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Lower Plasma ◽  
Plasma Vasopressin ◽  
Baroreceptor Stimulation ◽  
The Relationship ◽  
Sinus Pressure

The purpose of the experiments was to investigate the effect of changes in carotid sinus baroreceptor stimulation on plasma vasopressin (AVP) at different plasma osmolalities in the anesthetized artificially ventilated rabbit. Both carotid sinuses were isolated and perfused with blood at servo-controlled pressures. The vagus and aortic depressor nerves were sectioned bilaterally to eliminate input from atrial and aortic arch baroreceptors. Saline (0.3%, wt/vol) was infused to lower plasma osmolality, and 5% saline was infused to raise plasma osmolality. At three plasma osmolalities, the carotid sinus pressure (CSP) was changed from 100 mmHg to 40 and 140 mmHg and returned to 100 mmHg. There were no changes in plasma AVP in response to changes in CSP at low plasma osmolality (289 mosmol/kgH2O), but at medium (309 mosmol/kgH2O) and high (323 mosmol/kgH2O) osmolality, plasma AVP was higher at 40 than at 140 mmHg CSP. The relationship between plasma AVP and plasma osmolality was expressed as a linear regression at each CSP. Changes in CSP changed the sensitivity but not the threshold of the osmotic control of AVP release.

Water ingestion provides an early signal inhibiting osmotically stimulated vasopressin secretion in rats

2000 ◽  
Vol 279 (3) ◽  
pp. R756-R760 ◽  
Author(s):  
Wan Huang ◽  
Alan F. Sved ◽  
Edward M. Stricker
Keyword(s):  
Hormone Secretion ◽  
Plasma Osmolality ◽  
Nacl Solution ◽  
Adult Rats ◽  
Water Ingestion ◽  
Water Drinking ◽  
Early Signal ◽  
Neurohypophyseal Hormone ◽  
Vasopressin Secretion ◽  
Per Se

Dehydrated dogs are known to inhibit secretion of vasopressin (VP) within minutes after drinking water, before plasma osmolality (Posmol) diminishes. The present studies determined whether water ingestion causes a similar rapid inhibition of neurohypophyseal hormone secretion in rats. Adult rats were infused with 1 M NaCl (2 ml/h iv) for 240 min to stimulate VP and oxytocin (OT) secretion. After 220 min of infusion, rats were given water to drink for 5 min, and blood samples were taken 5 and 15 min later for RIA. Plasma VP (pVP) was much lower when rats ingested water than when they drank nothing even though Posmol was not significantly altered. Plasma OT (pOT) was affected similarly. In contrast, no effects on pVP or pOT occurred when rats drank isotonic NaCl solution for 5 min in amounts comparable to the water intakes (∼5.5 ml). These results suggest that neurohypophyseal secretion of VP and OT in rats is inhibited rapidly by water drinking, and that this inhibition is mediated by a visceral signal of osmotic dilution rather than by the act of drinking per se.

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