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J McQueen

Publications and source records attributed to J McQueen.

36 records · Page 2Linked to original sources
PubMed1987

Cation-dependent and cation-independent stages in regulation of the vascular angiotensin receptor after alteration of sodium balance in the rat.

The role of cations in vascular angiotensin receptor regulation has been investigated by radioligand receptor assay using a cell membrane fraction derived from mesenteric arterial muscle of the rat. In arterial membrane fractions from normal rats, the apparent receptor density varied with the ambient [Ca++] over the range, 0-10 mM. Receptor densities of 50 +/- 4, 102 +/- 4, and 156 +/- 5 fmol/mg membrane protein were obtained in low (0 mM), normal (4.8 mM), and high (25 mM) [Ca++], respectively. After 2 days of sodium loading, sodium depletion, and converting enzyme blockade altered receptor densities were detected in normal assay but not in high [Ca++] or low [Ca++], indicating changes in the relationship between [Ca++] and apparent receptor density. Similar results were obtained after 12 days of sodium loading or converting enzyme blockade. After 12 days of sodium depletion, there was no difference in receptor density between normal and high [Ca++] (44 +/- 5 fmol/mg protein) and the value obtained in low [Ca++] (27 +/- 2 fmol/mg protein) was significantly below that for all other groups. No change in receptor affinity was observed. These results suggest that there are two stages in vascular angiotensin receptor regulation; an initial masking-unmasking process which involves Ca++, and with prolonged agonist occupancy, an actual loss of receptors.

Angiotensin II↗
PubMed1984

Identification of the angiotensin II receptor in rat mesenteric artery.

Specific binding sites of high affinity and low capacity for 125I-angiotensin II have been identified in a membrane fraction derived from arterial arcades of the rat mesentery. Heterogeneity of binding sites and extensive tracer degradation necessitated the use of nonlinear regression methods for the analysis of radioligand binding data. Forward and reverse rate constants for the high affinity sites obtained by three experimental approaches were in good agreement and gave a dissociation equilibrium constant (Kd) of 19-74 pM (95% confidence interval). Affinities for a number of angiotensin-related peptides calculated from competitive binding curves were in the order 125I-angiotensin II = angiotensin II greater than angiotensin III greater than [Sar1,Ile8]angiotensin II greater than [Sar1,Gly8]angiotensin II. Angiotensin I and biochemically unrelated peptides had virtually no effect on binding of tracer angiotensin II. The divalent cations Mn2+, Mg2+ and Ca2+ stimulated 125I-angiotensin II binding at concentrations of 2-10 mM, as did Na+ at 50-100 mM. In the presence of Na+ or Li+, K+ had a biphasic effect. The chelating agents EDTA and EGTA were inhibitory, as were the thiol reagents dithiothreitol and cysteine. This study defined angiotensin II binding sites in a vascular target tissue of sufficiently high affinity to interact rapidly with plasma angiotensin II at physiological concentrations.

Angiotensin II↗
PubMed1983

Gynaecology.

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Climacteric↗
PubMed1983

Angiotensin II receptors in resistance vessels.

We have studied binding of 125I-angiotensin II (AII) to a membrane fraction prepared from mesenteric arterial arcades of the rat. Two problems were encountered: heterogeneity of binding sites and appreciable degradation of tracer that could not be inhibited without adversely affecting binding capacity. Analysis of binding results was carried out using a non-linear regression method allowing correction for tracer and receptor degradation and direct estimation of binding constants. From saturation and dissociation curves it was apparent that there were two classes of binding sites. KD of the high affinity site was within the physiological range of plasma AII concentration at between 0.05 and 0.5 nM. Calcium, magnesium and manganese increased binding capacity, whereas EDTA and EGTA had the opposite effect. Potassium increased binding capacity but had a biphasic effect in the presence of sodium.

Angiotensin II↗
PubMed1980

Uterine rupture as a complication of second trimester abortion using intraamniotic prostaglandin E2 and augmentation with other oxytocic agents.

Two cases of ruptured uterus are presented following attempted induction of midtrimester abortion using intraamniotic prostaglandin E2 and augmentation with other oxytocic agents. With continued uterine stimulation the diagnosis of rupture may not be obvious and the diagnostic features are discussed. Patients of high parity appear to be particularly susceptible to uterine rupture during induced midtrimester abortion.

Abortifacient Agents↗
PubMed1978

The modifying effect of progestogen on the response of the post-menopausal endometrium to exogenous oestrogens.

Cyclical regimes of unopposed oestrogens are associated with the development of both cystic glandular and atypical hyperplasia, and the incidence of hyperplasia is related to the dose of oestrogen prescribed. Atypical hyperplasia develops later than, and perhaps from, cystic glandular hyperplasia. With sequential oestrogen/progestogen therapy the incidence of this condition was greatly reduced, and therefore, progestogens appear to protect against the development of this condition. In all cases but one, sequential regimes also reversed both spontaneously-arising and oestrogen-induced hyperplasia to a normal endometrium. Cyclical high-dose unopposed oestrogen therapy may not be capable of reversing spontaneously-arising hyperplasia, and this condition may progress to endometrial adenocarcinoma. Spontaneously-arising hyperplasia can be present before therapy commences, but may be unsuspected, as it can occur in the absence of abnormal vaginal bleeding. Therefore, cyclical oestrogen therapy should not be prescribed unless pre-treatment curettage has been performed and spontaneously-arising hyperplasia has been excluded; and unless subsequent monitoring of the endometrial response is being performed by serial biopsy.

Endometrial Hyperplasia↗
PubMed1978

Clinical considerations in the management of the menopause: the endometrium.

Exogenous oestrogens prescribed for the relief of menopausal symptoms are being given in pharmacological doses and the term 'hormone replacement therapy' is inappropriate. The frequent development of endometrial hyperplasia during unopposed cyclical oestrogen therapy is therefore to be expected, but no single pattern of vaginal bleeding accurately reflected the histology of the endometrium. As such doses of oestrogens are required for effective relief of symptoms, progestogens must be given to protect against endometrial hyperstimulation. Patient acceptability of sequential oestrogen/progestogen therapy is high (90%) and with such therapy breakthrough bleeding may subsequently be shown to be a reliable indicator of underlying endometrial pathology.

Endometrial Hyperplasia↗