Central alpha-adrenoceptors and blood pressure regulation in the rat.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M J Morris.
Explore the source record for details and available documents.
The effect of bilateral sino-aortic denervation on cardiac and renal cortical alpha- and beta-adrenoceptor concentrations was studied in rats by radioligand binding experiments using [3H]-prazosin (alpha 1), [3H]-yohimbine (alpha 2) and [125I]-iodocyanopindolol (beta). Cardiac alpha 1- and beta-adrenoceptor concentrations were not altered by sino-aortic denervation. There was a significant increase in beta-adrenoceptor concentration in the renal cortex of sino-aortic denervated rats compared to sham-operated controls.
Changes in the activity of hypothalamic and brain-stem adrenergic neurons have been reported in young spontaneously hypertensive rats (SHR) prior to the development of hypertension. We have measured central alpha- and beta-adrenoceptor concentrations in 4-week-old SHR and Wistar-Kyoto (WKY) controls by direct radioligand binding studies using [3H]prazosin (alpha 1), [3H]clonidine (alpha 2), and [125I]iodohydroxybenzlpindolol (beta). The concentration of alpha 2-adrenoceptors was significantly elevated in the hypothalamus of the SHR, 156.9 +/- 10.4 compared with WKY, 119.4 +/- 10.0 fmole/mg protein (n = 7, mean +/- SEM, p less than 0.0125). Alpha 2-adrenoceptor concentrations in both the brain stem and cerebral cortex were similar in the two groups of animals. The increase in hypothalamic adrenoceptors was specific for alpha 2-adrenoceptors, since similar concentrations of alpha 2- and beta-adrenoceptors were found in this region.
Neuropeptide Y (NPY) and noradrenaline are co-localised in central neurones and both transmitters exert cardiovascular effects. Using microdialysis and push-pull techniques to measure transmitter release in vivo, and microinjection studies, we examined the role(s) of central noradrenaline and NPY in blood pressure regulation in the hypothalamus and nucleus tractus solitarius (NTS) of the rat. Hypothalamic noradrenaline release was increased following haemorrhage and reduced after phenylephrine infusion. Ageing is associated with markedly reduced NPY concentrations in the hypothalamus. 18-month old animals showed a reduced ability to release both NPY and noradrenaline to a potassium depolarisation stimulus. NTS administration of NPY induced dose-dependent decreases in blood pressure and heart rate. The depressor but not the bradycardic response was attenuated by prior administration of yohimbine. NTS microinjection of 23 pmol NPY induced similar cardiovascular effects in spontaneously hypertensive and Wistar Kyoto rats. NPY and noradrenaline appear to interact at several sites in the brain known to be important for blood pressure control.
The mechanisms responsible for recruitment of antibody-forming cells (AFC) into lung lobes exposed to antigen are not known. Because instillation of antigen induces inflammation, AFC may enter immunized lung lobes by changes in vascular permeability and/or in response to the release of mediators. The purposes of this study were to evaluate inflammatory responses produced by particulate antigens or interleukin-1 (IL-1) and to examine the recruitment of AFC and lymphocytes into the lung in response to these inflammatory stimuli. Two peaks of inflammation were observed in the lung lobes of dogs exposed to sheep red blood cells (SRBC), one at 1 day and the second around 9 days after instillation. Lymphocytes did not enter the lung during the first inflammatory response. However, lymphocytes and anti-SRBC AFC did enter immunized lung lobes during the second inflammatory response. AFC and lymphocytes also entered a lung lobe instilled with rabbit red blood cells (RRBC) at 6 days after immunization with SRBC. The observation that lymphocytes did not enter at 1 day after instillation of SRBC, but did enter the RRBC lung lobe at 1 day after instillation of RRBC, suggested that a population of lymphocytes, including AFC, were present in blood several days after immunization with SRBC that were capable of entering sites of inflammation in the lung. Instilled IL-1 was chemotactic in vivo for neutrophils and induced inflammation in the lung. However, IL-1 was not directly chemotactic for AFC or lymphocytes in vivo.