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Biomedical subjects

B Jarrott

Publications and source records attributed to B Jarrott.

At least 181 records · Page 10Linked to original sources
PubMed1979

The characteristics of [3H]-clonidine binding to an alpha-adrenoceptor in membranes from guinea-pig kidney.

1. [3H]-clonidine binds to membranes prepared from guinea-pig kidney. 2. At 25 degrees C the binding is rapid and saturable. 3. Scatchard analysis of the binding data showed that the Kd for [3H]-clonidine binding in kidney membranes is 8.54 nM and the density of binding sites 12.5 pmol/g wet wt. tissue. 4. Hill plots of the binding data showed that there were no cooperative site interactions associated with binding. 5. [3H]-clonidine binding could be displaced by drugs, the most potent being drugs with a high affinity for the alpha-adrenoceptor. The neuroleptic drugs (+)-butaclamol, cis-clopenthixol and cis-flupenthixol at high concentration also displaced [3H]-clonidine binding. 6. Drugs acting as agonists or antagonists of beta-adrenoceptors, histamine receptors, acetylcholine receptors as well as prostaglandins E1, E2, F1alpha and F2alpha, angiotensin II, arginine vasopressin, naloxone, nalorphine and pargyline had little effect on binding. 7. It is likely that the binding site labelled by [3H]-clonidine in guinea-pig kidney membranes is an alpha-adrenoceptor similar in some pharmacological aspects to an alpha2-adrenoceptor.

Animals↗
PubMed1978

Acute and chronic administration of alpha-methyldopa: regional levels of endogenous and alpha-methylated catecholamines in rat brain.

Acute administration of alpha-methyldopa (200 mg kg-1 s.c.) produced a short-lived decrease in dopamine levels in 5 regions of the rat brain. Maximal dopamine depletion was 55% in the corpus striatum and over 75% in other regions and occurred 4--6 h after alpha-methyldopa injection; dopamine levels recovered within 12 h. Maximal noradrenaline depletion of over 80% occurred in all regions 4--24 h after alpha-methyldopa and after 24 h noradrenaline levels were still significantly reduced from control values. In these acute studies alpha-methyldopamine accumulated rapidly in amounts equal to or greater than the depleted dopamine in all regions, reaching a peak at 4 h. By contrast, alpha-methylnoradrenaline accumulated more slowly reaching a peak at 6--24 h and was never present in amounts greater than the depleted noradrenaline. Following chronic administration of alpha-methyldopa (40 mg kg-1 s.c., twice daily 5 days) there was a similar depletion of noradrenaline and dopamine to that seen in the acute studies. The depletion was associated with a much smaller accumulation of alpha-methyldopamine. The striking feature of these results, however, was the large accumulation of alpha-methylnoradrenaline in all brain regions. This probably reflects the slow turnover and resistance to degradation by monoamine oxidase of alpha-methylnoradrenaline.

Animals↗
PubMed1978

The combined use of L-alpha-methyldopa hydrazine and methyldopa in the treatment of hypertension.

1. The combined use of alpha-methyldopa and L-alpha-methyldopa hydrazine (a peripheral decarboxylase inhibitor) has been studied, in a double-blind cross-over comparison, with alpha-methyldopa and L-alpha-methyldopa hydrazine placebo in the treatment of eight patients with essential hypertension. 2. L-alpha-methyldopa hydrazine did not enhance the antihypertensive effect of alpha-methyldopa. This suggests that because methyldopa can inhibit its own decarboxylation, peripheral decarboxylation is not an important metabolic pathway for methyldopa and elevated brain levels of methyldopa do not necessarily result in elevated brain levels of methyldopamine.

Adult↗
PubMed1978

Disposition of clonidine in rats as determined by radioimmunoassay.

The disposition of the potent antihypertensive drug clonidine has been poorly understood through the lack of a convenient and sensitive assay. A radioimmunoassay for clonidine has been developed and is capable of detecting as little as 10 pg of clonidine. 2,6-Dichlorophenyl-guanidine, a known metabolite of clonidine, did not cross-react with the antiserum whereas another metabolite, 4-hydroxyclonidine, was as potent as clonidine in displacing labeled clonidine from the antibody. However, a simple solvent extraction step before the radioimmunoassay selectively extracted clonidine from a mixture of clonidine and 4-hydroxyclonidine in alkaline plasma and this procedure permitted a specific assay for clonidine. The plasma levels of clonidine in rats after the administration of a hypotensive dose (100 microgram/kg i.v.) were determined by radioimmunoassay and these data indicated that the disposition of clonidine conforms to an open two-compartment, pharmacokinetic model. Clonidine rapidly accumulated in the brain as shown by the attainment of peak concentrations within 2 min of i.v. injection.

Animals↗
PubMed1977

Studies of neurotransmitter release in the pathogenesis of hypertension.

Studies using a sensitive radioenzymatic assay for plasma noradrenaline suggest there is a selective overactivity of the sympathetic nervous system in essential hypertension. Methodology which allows the study of local sympathetic turnover in CNS nuclei and peripheral blood vessels is described. This approach has been used to study the non-innervated sympathetic turnover phaeochromocytoma. It is suggested that studies of local regulatory mechanism in neurotransmitter release are required to give a greater understanding of the central and peripheral role of the sympathetic nervous system in the pathogenesis of hypertension.

Adrenal Gland Neoplasms↗
PubMed1976

Mitochondrial abnormalities in human phaeochromocytoma.

Mitochondrial abnormalities are reported in four cases of phaeochromocytoma. These abnormalities include swelling and scant cristae, intramitochondrial dense bodies, septate-like junctions, intercristal fusion plus spheroidal bodies, and intramitochondrial rodlets. These structural mitochondrial changes are associated with reduction in activity of the mitochondrial enzymes, monoamine oxidase and succinic dehydrogenase.

Adrenal Gland Neoplasms↗
PubMed1976

The role of noradrenaline and other transmitter hormones in the pathogenesis of hypertension.

1. Studies with a sensitive radioenzymatic assay for plasma noradrenaline suggest there is a selective overactivity of the sympathetic nerous system in essential hypertension. 2. Serotonin turnover in the mesenteric vessels is approximately twice that of noradrenaline and it is suggested that serotonin may interact with noradrenaline to maintain vascular resistance. 3. Methodology which allows the study of local sympathetic turnover in nuclei of the central nerous system and in peripheral blood vessels is decribed. This approach has been used to study non-innervated sympathetic turnover observed in phaceochromocytoma.

Adrenal Gland Neoplasms↗