An Investigation of the Nature of the Neural and Local Mechanisms That Regulate Vascular Functioning

Barfaraz, Alireza (1994) An Investigation of the Nature of the Neural and Local Mechanisms That Regulate Vascular Functioning. PhD thesis, University of Glasgow.

Full text available as:
[img]
Preview
PDF
Download (24MB) | Preview

Abstract

1. In the pithed rat, stimulation of the autonomic outflow at different levels between C1 and L3 produced characteristic increases in blood pressure and heart rate. Stimulation between C6 and T1 and between T2 and T4 produced large increases in heart rate with only small increases in blood pressure. Stimulation at T8-9 produced the largest increase in blood pressure and a large increase in heart rate. 2. Spinal nerve stimulation at T8-9 characteristically produced pressor responses during stimulation and a secondary, pressor response that persisted after stimulation ceased. These responses were frequency- dependent so that the response at 20 Hz (supramaximal voltage, 0.4 ms pulse-width, 100 pulses) was larger than that at 2 Hz (supramaximal voltage, 0.4 ms pulse-width, 100 pulses). 3. The pressor response to stimulation at T8-9 to 2 Hz and 20 Hz probably resulted from stimulation of nerve fibres to blood vessels and also to the adrenal glands, which contributed both to the component of the pressor response that occurred during stimulation and to the secondary component that persisted after stimulation ceased. This was indicated by experiments in which adrenalectomy reduced the first component of the pressor response that occurred during stimulation at T8-9 and abolished the second component that persisted after stimulation. 4. The effect of propranolol (2 mg kg-1) on both components of the pressor response to spinal nerve stimulation at T8-9 was complex and dependent on the basal blood pressure of the pithed rat. In most pithed rats, propranolol enhanced both components of the pressor response to nerve stimulation. This was most marked at 2 Hz and most obvious in the secondary poststimulation component, which probably resulted from adrenaline released from the adrenals. 5. In some experiments where the blood pressure was low (<18-22 mm Hg) propranolol did not enhance the pressor response to spinal nerve stimulation. This may have been because in these few rats propranolol impaired cardiac output and as a result the ability of the heart to pump blood through the constricted blood vessels diminished, so that despite nerve stimulation-induced peripheral vasoconstriction, blood pressure did not increase. 6. alpha,beta-methylene ATP (alpha,beta-mATP,2x0.05 and 5x0.1 mg kg-1) produced pressor responses that showed tachyphylaxis. There was no evidence that alpha,beta-mATP desensitized the pressor response to spinal nerve stimulation at T8-9.7. Captopril inhibited pressor responses to nerve stimulation and to exogenous NA (9 mug kg-1). This result suggests that angiotensin contributes to the pressor response to spinal nerve stimulation. An alternative explanation of this effect is that bradykinin breakdown might be inhibited by captopril so that more nitric oxide (NO), released by bradykinin, might be available to act as a physiological antagonist of NA. 8. There was no evidence of a prazosin-resistant pressor response to spinal nerve stimulation at T8-9 in the pithed rat. 9. L-NAME (45 mg kg-1) increased the basal blood pressure in the anaesthetized rat and also, but to a lesser extent, in the pithed rat in the presence of propranolol (2 mg kg-1). There was little difference in the extent to which L-NAME increased the basal blood pressure in the anaesthetized and the pithed rats in the absence of propranolol. In pithed rats but not in anaesthetised rats, the increment in the basal blood pressure caused by L-NAME was proportional to the level of the basal blood pressure. It appears that endogenous NO was continuously produced in both anaesthetized and pithed rats and had a role in keeping the basal blood pressure low. The greater increase in the basal blood pressure produced by 1 L-NAME (45 mg kg-1) in anaesthetized rats was probably due to the withdrawal of the inhibitory effect of NO on the sympathetic tone, which was thereafter able to operate unopposed and raise the blood pressure. Such a mechanism would not occur in the pithed rat. (Abstract shortened by ProQuest.).

Item Type: Thesis (PhD)
Qualification Level: Doctoral
Additional Information: Adviser: T W Stone
Keywords: Pharmacology
Date of Award: 1994
Depositing User: Enlighten Team
Unique ID: glathesis:1994-74966
Copyright: Copyright of this thesis is held by the author.
Date Deposited: 27 Sep 2019 14:57
Last Modified: 27 Sep 2019 14:57
URI: http://theses.gla.ac.uk/id/eprint/74966

Actions (login required)

View Item View Item

Downloads

Downloads per month over past year