Effect of Hypoglycemia on Auditory Cortex and Cochlear Receptor in the Cat

1957 ◽  
Vol 188 (2) ◽  
pp. 249-254 ◽  
Author(s):  
César Fernández ◽  
Arnold Brenman
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Auditory Cortex ◽  
Blood Sugar ◽  
Cochlear Function ◽  
The Central Nervous System ◽  
Sugar Levels

Effect of hypoglycemia induced by insulin and/or functional evisceration on auditory cortex and cochlear responses to sound stimuli was studied in cats. Both responses remained unchanged at blood sugar levels as low as 5 mg %. They diminished in size whenever blood pressure was allowed to fall to low values, and returned to nearly normal when it was restored. The observations suggest that carbohydrates are not essential for cochlear function or that the structure contains a large store of them. The presence of responses from auditory cortex during medullary stage of coma suggests that this area does not conform well to the concept of phyletic organization of the central nervous system.

RAS in the Central Nervous System: Potential Role in Neuropsychiatric Disorders

2018 ◽  
Vol 25 (28) ◽  
pp. 3333-3352 ◽  
Author(s):  
Natalia Pessoa Rocha ◽  
Ana Cristina Simoes e Silva ◽  
Thiago Ruiz Rodrigues Prestes ◽  
Victor Feracin ◽  
Caroline Amaral Machado ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Therapeutic Potential ◽  
Neuropsychiatric Disorders ◽  
Extensive Literature ◽  
Ang Ii ◽  
Mas Receptor ◽  
The Central Nervous System ◽  
The Brain

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

Blood Pressure and Pulse Rate in the Foetal Sheep

1945 ◽  
Vol 22 (1-2) ◽  
pp. 63-74
Author(s):  
JOSEPH BARCROFT ◽  
D. H. BARRON
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Pulse Rate ◽  
Umbilical Artery ◽  
The Central Nervous System ◽  
The Right ◽  
First Moment ◽  
Left Vagus ◽  
Stimulation Of

1. A method (the needle method) is described for the measurement of the pressure in the stream going through a vessel. 2. In the foetal sheep the needle method applied to the umbilical artery gives substantially the same results as the mercurial manometer applied to the carotid, until about half-way through the gestation period. 3. As gestation proceeds the needle method applied at the first moment at which it can be applied to the umbilical artery (or a branch) gives readings substantially lower, and increasingly lower as gestation proceeds, than does the mercurial manometer read at the first moment at which it can be read. 4. The discrepancy is due to the sum of a number of causes which are discussed, but of these the most important is an actual rise of pressure between the time of delivery and the completion of the dissections contingent on the use of the mercurial manometer. 5. The cause of this is not at present demonstrated, but either or both of two factors may be concerned: (a) a dulling of the central nervous system which weakens the depressor reflex; (b) the establishment of a greater degree of vasomotor tone consequent on the bombardment of the central nervous system with sensory stimuli. 6. The pulse rates in utero and just after delivery of the foetus into a saline bath at 39-40°C. (the umbilical circulation being unimpaired) are not significantly different. 7. The pulse rate quickens up to the 70th-80th day, after which it becomes slower as gestation proceeds. 8. If both vagi be severed, the pulse rate te to quicken throughout gestation. The pulse, therefore, comes increasingly under vagus inhibition from the 80th-90th day onwards. 9. Even after the vagi have been cut after the 120th day (it has not been tried before) adrenalin in sufficient quantity will cause a further quickening of the pulse. 10. The earliest date at which stimulation of the peripheral end of the right vagus was observed to slow the heart was the 77th day. On the 85th day peripheral stimulation of the left vagus also failed, but succeeded on the 101st day. 11. Central stimulation of the left vagus, with the right vagus intact, produced slowing on the 77th day. 12. Slowing of the heart synchronous with rise of arterial pressure has been observed on the 111th day. 13. Slowing of the heart which bears evidence of being reflex has been obtained by raising the blood pressure (clamping the cord) on the 121st day and by injection of adrenalin on the 118th day. 14. Approaching term both the carotid sinus and cardiac depressor mechanisms are functional. 15. Lowering of the blood pressure as the result of stimulation of the central end of the vagus and with both vagi severed can be demonstrated late in gestation.

Intracerebroventricular infusion of RU28318 blocks aldosterone-salt hypertension

1990 ◽  
Vol 258 (3) ◽  
pp. E482-E484 ◽  
Author(s):  
E. P. Gomez-Sanchez ◽  
C. M. Fort ◽  
C. E. Gomez-Sanchez
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Systolic Blood Pressure ◽  
Urine Volume ◽  
Intracerebroventricular Infusion ◽  
Mineralocorticoid Antagonist ◽  
Salt Hypertension ◽  
The Central Nervous System ◽  
Dose Dependent

The chronic intracerebroventricular (icv) infusion of aldosterone in rats and dogs elevates the blood pressure within 10-14 days at doses far below those that produce hypertension systemically. The effect in rats is dose dependent and blocked by the concomitant icv infusion of the antimineralocorticoid, prorenone. The effect of the icv infusion of RU28318, another specific spironolactone mineralocorticoid antagonist, on the hypertension produced by chronic subcutaneous (sc) administration of aldosterone in sensitized rats was reported. Miniosmotic pumps were used to deliver 1 micrograms/h aldosterone sc and 1.1 micrograms/h RU8318 icv. Over a 24-day period the indirect systolic blood pressure of the control, RU28318 icv, and aldosterone sc plus RU28318 icv groups increased from 105 to 123 mmHg and were not significantly different from each other, whereas the aldosterone sc group increased to 156 mmHg. RU28318, icv or sc, did not alter the increase in urine volume produced by aldosterone sc, and there was no significant differences in weight between the groups. This study provides evidence of the importance of the central nervous system in the pathogenesis of hypertension produced by systemic mineralocorticoid excess.

The Pathogenesis of Somatic Disease in Mental Defectives

1951 ◽  
Vol 97 (409) ◽  
pp. 792-800 ◽  
Author(s):  
L. Crome
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Scientific Basis ◽  
The Body ◽  
Normal Person ◽  
Somatic Disease ◽  
The Central Nervous System ◽  
Mental Defectives ◽  
The Brain

The problems of the interdependence and unity of the brain and body have been put on a scientific basis by Pavlov and his successors. Bykov (1947) has, for example, been able to demonstrate that the cortex plays a leading part in the regulation of somatic processes, such as secretion of urine, blood pressure, peristalsis and metabolism. It is therefore reasonable to argue that lesions of the central nervous system will be reflected in the pathogenesis and course of morbid processes in the body. It does not follow, however, that this influence will necessarily be in the direction of greater lability, more rapid pathogenesis or more extensive destruction. The outstanding feature of the central nervous system is its plasticity and power of compensation. It is therefore possible and probable that those parts of the nervous system which remain intact will take over and compensate for the function of the lost ones. Emotion may, for example, lead to polyuria, but it does not follow that urinary secretion will be impaired in a leucotomized patient. The brain may well play an important part in the infective processes of a normal person, but the defence against infection in a microcephalic idiot may remain perfectly adequate, and may even be more effective than in a normal person, provided that the mechanism of the immunity and phagocytosis had been more fully mobilized in the course of his previous life.

Reserpine-induced central effects: pharmacological evidence for the lack of central effects of reserpine methiodide

2005 ◽  
Vol 83 (6) ◽  
pp. 509-515 ◽  
Author(s):  
Srinivas Nammi ◽  
Krishna Murthy Boini ◽  
Sushruta Koppula ◽  
Satyanarayana Sreemantula
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Target Tissue ◽  
Central Effects ◽  
Anaesthetized Rats ◽  
The Central Nervous System ◽  
Rats And Mice ◽  
Dose Dependent ◽  
Higher Doses

Reserpine, an alkaloid from Rauwolfia serpentina, was widely used for its antihypertensive action. However, its use has been reduced because of its sedative and extra pyramidal symptoms. In the present investigation, reserpine methiodide (RMI), a quaternary analogue of reserpine, was synthesized and pharmacologically evaluated in rats and mice for its central (barbiturate hypnosis, spontaneous motor activity, body temperature, and avoidance of conditioned response) and peripheral actions (blood pressure) in comparison with reserpine. The results indicate that reserpine produced a dose-dependent depression of the central nervous system. RMI at doses equal to and double the equimolar doses of reserpine did not produce any behavioural changes compared with control animals. Nevertheless, both reserpine and RMI were found to produce dose-dependent reduction in the blood pressure of anaesthetized rats, although only at higher doses of RMI, indicating that quaternization of reserpine not only attenuated the entry of RMI into the central nervous system, but also reduced its access to the target tissue in the periphery. It is speculated that the hypotensive actions of RMI may also be due to peripheral depletion of catecholamines. Key words: resperine methiodide (RMI), reserpine, behaviour, blood pressure, mice, rats.

Central Nervous System Pressor Responses in Rats Susceptible and Resistant to Sodium Chloride Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 225s-227s ◽  
Author(s):  
T. Ikeda ◽  
L. Tobian ◽  
J. Iwai ◽  
Patricia Goossens
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Hypertonic Saline ◽  
Pressor Effect ◽  
Left Lateral Ventricle ◽  
Pressor Responses ◽  
The Central Nervous System

1. The pressor responses to hypertonic saline and angiotensin II introduced into the left lateral ventricle were both significantly greater in salt-sensitive (S) rats compared with salt-resistant (R) rats, with all rats on a low Na diet. 2. When S rats were given thiazide to nullify the pressor effect of dietary NaCl, their blood pressure averaged only 5 mmHg higher than that of the R rats; nevertheless, these S rats had significantly higher central nervous system pressor responses to angiotensin II and hypertonic saline. 3. Thus, if excessive dietary Na increases blood pressure by way of action on the central nervous system, these heightened pressor responses could partially account for the NaCl hypertension in S rats. Alternatively, depressed central nervous system pressor responses in R rats could partially explain the resistance of R rats to NaCl hypertension.

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