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Biomedical subjects

R F Bing

Publications and source records attributed to R F Bing.

At least 109 records · Page 6Linked to original sources

Adenosine 3':5'-cyclic monophosphate production and steroidogenesis by isolated rat adrenal glomerulosa cells. Effects of angiotensin II and [Sar 1,Ala 8]angiotensin II.

Angiotensin II effects on cyclic AMP production and steroid output were studied in a sensitive preparation of isolated rat adrenal glomerulosa cells. With increasing concentrations of angiotensin II logarithmic dose-response curves for aldosterone and cyclic AMP production were similar. The minimum effective dose (0.2nm) for stimulation of aldosterone production also significantly (P<0.001) increased cyclic AMP output. For both aldosterone and cyclic AMP production, the peptide hormone concentration eliciting maximal response (0.2mum) and the ED(50) (median effective dose) values (1nm) were the same; this is consistent with cyclic AMP acting as an intracellular mediator for angiotensin II-stimulated aldosterone production by glomerulosa cells. The angiotensin II antagonist [Sar(1),Ala(8)]angiotensin II inhibited angiotensin II-stimulated corticosterone and aldosterone production in these cells. An equimolar concentration of antagonist halved the response to 20nm-angiotensin II, and complete inhibition was observed with 0.2mum-antagonist. In contrast, [Sar(1),Ala(8)]angiotensin II had no effect on maximally stimulated steroidogenesis induced by serotonin and a raised extracellular K(+) concentration. Increasing concentrations of [Sar(1),Ala(8)]angiotensin II alone decreased corticosterone and aldosterone outputs significantly (P<0.05) at concentrations of 20nm and 2nm of antagonist respectively. A significant (P<0.001) decrease in cyclic AMP production occurred with 2mum antagonist and this was comparable with the decrease in aldosterone production. It is concluded that [Sar(1),Ala(8)]angiotensin II can independently affect glomerulosa-cell steroidogenesis, possibly by modulating adenylate cyclase activity.

Adrenal Glands↗

Role of persistent vascular renin after bilateral nephrectomy in Goldblatt-two kidney hypertension.

1. Aorta homogenate contains renin-like activity which on incubation generates angiotensin I over a wide pH range. 2. Rat aortic renin measured at an incubation pH of 6.5 rose and fell in parallel to plasma renin with salt depletion and salt-loading respectively. Renin little relationship with plasma renin. 3. Aortic renin (pH 6.5) was elevated in Goldblatt-two kidney hypertension and slowly fell for 24h after bilateral nephrectomy whereas the fall in plasma renin was complete by the first hour. Aortic renin (pH 5.3) was also high, but did not fall after bilateral nephrectomy. 4. Aortic renin (pH 6.5) is probably derived from plasma renin whereas renin measured at pH 5.3 is probably a tissue renin. 5. The prolonged half-life of aortic renin (pH 6.5) explains the observation that the renin-angiotensin system appears to be active in maintaining blood pressure for several hours after bilateral nephrectomy whereas the decline in plasma renin is rapid and does not continue significantly beyond 1 h.

Angiotensin I↗

Renin subgroups in essential hypertension: an analysis and critique.

It has been claimed that measurement of renin levels in patients with essential hypertension enables identifiable subgroups of patients to be demarcated and that these subgroups exhibit important differences in prognosis and response to therapy. Accordingly, plasma renin activity (PRA) was measured in 181 patients referred to hospital outpatients for treatment of hypertension. Fifteen of these were excluded from study because of abnormality of renal function, an abnormal pyelogram or incidental disease. PRA of the remainder showed a smooth unimodal distribution with a 'tail' of high values (17%) which lay above the range of values observed in normotensive subjects. Following seven days treatment with bendrofluazide the percentage rise in PRA was much less than that of age-matched controls. A group of 55 patients (33%) fell below the range encountered in normotensive matched subjects treated similarly, although the distribution of PRA was still smooth and unimodal. Patients were divided into 'high', 'normal' and 'low' renin subgroups. Whilst there were significant differences in age between the high, normal and low renin groups, there were no significant differences in basal blood pressure, response to diuretics or beta blockers. It is concluded that renin levels in hypertension are influenced by several factors and that any attempt to subdivide patients into renin subgroups is therefore arbitrary. Measurement of renin does not significantly assist predicting the blood pressure response to either diuretics or beta-blockers combined with diuretics.

Angiotensin II↗

Thyroid carcinoma and concurrent hyperthyroidism: a study of ten patients.

Ten patients with thyroid carcinoma and co-existing thyrotoxicosis have been studied. In six patients thyroid carcinoma was suspected before thyroidectomy. In three of the four patients in whom neoplasia was not suspected before operation, the lesion was a small papillary carcinoma. In only one of the eight patients in whom serum long acting thyroid stimulator (LATS) and long acting thyroid stimulator protector (LATSP) were assayed was detectable activity found, a low incidence. The possible role of hyperthyroidism in initiating thyroid malignancy is discussed.

Adult↗

The urinary excretion of catecholamines and their derivatives in primary hypertension in man.

1. The 24 h urinary excretion of adrenaline, noradrenaline, normetadrenaline, metadrenaline and vanilloylmandelic acid has been compared in 17 male normotensive subjects and 25 age-matched male hypertensive patients studied under similar in-patient conditions. 2. 24 h urinary metadrenaline was significantly lower in the hypertensive patients. With this exception, no significant differences were found between the two groups when the total 24 h excretion of free catecholamines and their metabolites was analysed. 3. Diurnal variation in free catecholamine excretion was found in both normotensive and hypertensive subjects. There was no corresponding variation in metabolite excretion. 4. No correlation could be established between systolic or diastolic blood pressure and the amounts of the catecholamines or their metabolites in the urine of either group. 5. The results are considered in the light of recent work demonstrating high plasma catecholamine concentrations in hypertension. They lend no support to the concept that excessive circulating catecholamines are responsible for the elevated blood pressure in essential hypertension.

Adult↗

Reversal of renovascular hypertension.

The fall in blood pressure observed in both early and chronic phase Goldblatt 2-kidney 1-clip hypertension produced by removing or unclipping the ischaemic kidney is due to a profound fall in peripheral resistance. The two procedures have an equal effect upon peripheral resistance and the lesser efficacy of nephrectomy in lowering blood pressure is due to a greater rise in stroke volume perhaps associated with a greater degree of sodium retention. Neither changes in sodium balance, in the renin-angiotensin system nor in vascular reactivity explain the fall in blood pressure. A reduction in renal sympathetic afferent activity and a medullary based vasoactive humoral system may play a role although the nature and extent of that role remain to be defined.

Animals↗

Reversal of two-kidney one clip renovascular hypertension in the rat.

Attempted correction of two-kidney, one clip Goldblatt hypertension in the rat was carried out by three techniques; removal of the constricting clip, removal of the ischemic kidney, and converting enzyme blockade by oral captopril. Since duration of hypertension is said to be a critical factor, groups of rats were studied after short term (less than 6 weeks from clipping) and chronic (greater than 4 months) hypertension. Blood pressure, sodium balance, and plasma renin concentration (PRC) were followed before and after these correcting procedures. In a control group of animals, removal of a loose renal artery clip did not influence blood pressure and only caused trivial postoperative retention of sodium. Unclipping, however, normalized blood pressure in both short-term and chronic hypertension. After a major postoperative fall, blood pressure returned to somewhat elevated levels after nephrectomy in animals with chronic (but not short-term) hypertension. Sodium balance became markedly positive with the fall in blood pressure of operated hypertensive animals and was significantly correlated with the fall in blood pressure of operated hypertensive animals and was significantly correlated with the fall in blood pressure in these four groups at 7 days (r = 0.43). Captopril also produced a fall in blood pressure at 24 hours, with a positive sodium balance, although the relationship between blood pressure fall and sodium balance did not reach statistical significance (r = 0.30). The PRC was elevated in all hypertensive groups, although individual values overlapped with values from normal rats and nonhypertensive rats with a loose renal artery clip. The PRC fell to normal or subnormal values after either operative procedure and stabilized for at least 2 months independently of whether blood pressure fell or not. It is concluded that neither sodium retention nor renin hypersecretion maintains blood pressure in this model. Also, the rapidity of the blood pressure fall is not consistent with a role for vascular hypertrophy. The greater efficacy of unclipping suggests that the revascularized kidney after this procedure exerts a vasodepressor function independent of sodium excretion or the renin-angiotensin system.

Animals↗

Surgical reversal of two-kidney one clip hypertension during inhibition of the renin-angiotensin system.

Conscious rats with two-kidney one clip Goldblatt hypertension had the constricting clip removed during continuous infusion of either dextrose, saralasin, or captopril. Other dextrose-infused animals underwent removal of the ischemic kidney or a sham procedure. Direct arterial blood pressure (BP) was recorded throughout the 15-hour preoperative and subsequent 24-hour postoperative period. Rats were studied in the "early" phase (1-3 weeks duration) or "chronic" phase (greater than 4 months) of hypertension. Animals subjected to a sham procedure returned to preoperative BP values. The BP of animals unclipped or nephrectomized did not return to previous hypertensive levels. Instead, a biphasic response was seen where BP partially recovered from an operative fall and then slowly declined to normal at 24 hours; this effect occurred in both stages of hypertension. At 24 hours, removal of the ischemic kidney was as effective as removal of the constricting clip in the correction of both early and chronic phase hypertension. Rats infused with saralasin or captopril demonstrated an acute (within 2 hours) and sustained fall in BP, but not to normotensive levels. This fall was significant in all animals (p less than 0.01) apart from chronic phase rats infused with saralasin where no significant fall was seen. Although animals infused with saralasin or captopril commenced at a lower preoperative BP, the biphasic pattern of response to unclipping was identical to that of dextrose-infused unclipped rats. Thus, sustained inhibition of the renin-angiotensin system did not modify the correction of hypertension produced by removal of the constricting clip, and the response to surgical correction did not appear to be entirely mediated by changes in the activity of the renin-angiotensin system, particularly in the chronic stage. Equally, the rapidity of correction is not consistent with a role of vascular hypertrophy.

Animals↗