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Biomedical subjects

H Thurston

Publications and source records attributed to H Thurston.

At least 109 records · Page 6Linked to original sources
PubMed1982

Plasma renin in long-term diuretic treatment of hypertension: effect of discontinuation and restarting therapy.

1. Plasma renin activity, body weight and blood pressure were measured before and after 7 days' treatment with bendrofluazide in ten hypertensive subjects. They were then treated with bendrofluazide alone (5 mg daily) for a minimum of 3 years. The diuretic was then discontinued and the measurements were repeated before and again after 7 days with bendrofluazide. The results were compared with those obtained before chronic treatment with the diuretic. 2. Chronic diuretic treatment was associated with a persistent and progressive rise in plasma renin activity, that fell promptly to pretreatment levels when diuretics were discontinued. This was associated with significant weight gain but no immediate significant rise in blood pressure. 3. When acutely challenged with bendrofluazide the patients showed a greater increase in plasma renin activity on the second occasion than on the first. Three out of five patients with an initially subnormal diuretic treatment. 4. Chronic diuretic treatment increased the responsiveness of the juxtaglomerular apparatus in some hypertensive patients. 5. Classification of hypertensive patients into renin subgroups may be influenced by previous therapy, even when that therapy has been discontinued for 4 weeks. In particular 'low renin hypertension' may be masked by recent use of diuretics, as shown by three of the five patients in this subgroup in the present study.

Bendroflumethiazide↗
PubMed1982

The addition of prazosin to standard triple therapy in the treatment of severe hypertension.

1 A small dose of prazosin was added to the treatment regime of sixteen hypertensive patients poorly controlled on a combination of bendrofluazide, hydralazine and propranolol. 2 There was a significant improvement in blood pressure control in all patients at 1 month (P less than 0.01) and this was maintained at 9 months (P less than 0.02). Tolerance to prazosin was not a problem. 3 The addition of prazosin to conventional triple drug therapy produces a further useful fall in blood pressure.

Adult↗
PubMed1982

Effect of sodium, deoxycorticosterone and duration of hypertension on pressor responses in rats.

1. Enhanced pressor responsiveness to angiotensin II and noradrenaline has been demonstrated in the hypertension that follows deoxycorticosterone (DOC) and salt administration in the rat. The present studies were carried out to assess the importance of factors common to both pressor agents and those specific to individual agents such as receptor availability.2. Accordingly pressor reponses to angiotensin II and noradrenaline have been studied in normotensive salt-loaded and sodium depleted rats with and without DOC, and in rats with DOC-salt hypertension of short and long duration. These responses have been related to the plasma renin levels in the animals studied.3. Pressor reponses to angiotensin II were increased, dose-response curve (d.r.c.) shifted to the left, in salt-loaded rats and the administration of DOC produced a further increase. DOC-salt hypertension of short duration was associated with an even greater responsiveness. Sodium depletion, however, reduced responsiveness (d.r.c. shifted to the right) and concurrent DOC administration did not alter this. Angiotensin II responses were closely correlated with plasma renin concentration over a wide range of values (p.r.c, r = -0.77, P < 0.001). The differences between the groups could be explained therefore by the number of unoccupied angiotensin II receptors available.4. On the other hand only sodium loaded rats that were also receiving DOC showed any change in noradrenaline responsiveness, when the dose-response curve was shifted to the left. Noradrenaline responses showed no linear relationship to plasma renin concentration.5. The presence of hypertension did not significantly alter noradrenaline responses and the increase observed in angiotensin II responsiveness could be explained by the greater suppression of plasma renin in this group. Duration of hypertension had no effect on responsiveness to either agent.6. These results point to important differences in the pressor responsiveness to angiotensin II and noradrenaline with variation of salt intake and DOC administration.

Angiotensin II↗
PubMed1982

Vascular renin as a determinant of the circulatory response to renin.

The effect of an injection of partially purified rat renin on the blood pressure, plasma and aortic renin was studied in rats 18 hours after bilateral nephrectomy. Blood pressure rose and remained elevated 6 hours after renin injection, returning to normal at 9 hours. Aortic renin concentration was increased and showed a similar response pattern to blood pressure whereas plasma renin concentration fell to subnormal levels within 3 hours. The blood pressure response was prevented by converting enzyme inhibition and at 3 and 6 hours was reversed by saralasin infusion. These results demonstrate that circulating renin is taken up by vascular tissue and the pressor response to exogenous renin is related to aortic but not plasma renin.

Animals↗
PubMed1981

Haemodynamic changes after surgical reversal of chronic two-kidney, one-clip hypertension in the rat.

1. Within 24 h of surgical reversal of chronic Goldblatt two-kidney, one-clip hypertension in the rat, of greater than 4 months duration, blood pressure had fallen to normal levels. At this time there was no difference between the effects of removal of the clip or the ischaemic kidney but, at 60 days after reversal, the blood pressure of rats which had been nephrectomized was significantly higher than that of normal controls. 2. The fall in blood pressure was associated with a fall in total peripheral resistance to normal by 24 h despite the previous established fact that structural vascular changes take much longer to reverse. There was a corresponding rise in cardiac output, mainly due to an increase in stroke volume. Nephrectomized rats had a significantly higher stroke volume compared with those unclipped 24 h after operation. 3. As blood pressure can become normal in the presence of structural cardiovascular change by a fall in total peripheral resistance it would seem unlikely that resistance vessel hypertrophy is responsible for the maintenance of blood pressure in this model. Another peripherally acting mechanism therefore has to be postulated.

Animals↗
PubMed1981

Chemical renal medullectomy; effect upon reversal of two-kidney, one-clip hypertension in the rat.

1. Chemical renal medullectomy was produced in rats by injection of 2-bromoethylamine hydrobromide. Plasma creatinine and blood pressure were unchanged although urine volume was increased fourfold. 2. Left renal artery constriction resulted in similar degrees of hypertension in both intact and medullectomized rats. This was associated with a significantly smaller rise in plasma renin concentration in the latter. 3. Blood pressure in conscious intact hypertensive rats became normal within 24 h of unclipping whereas blood pressure of medullectomized rats remained significantly elevated. 4. The presence of an intact renal medulla is essential to the complete reversal of two-kidney, one-clip hypertension in the rat. This may reflect the loss of a medullary vasodepressor system.

Animals↗
PubMed1981

Indapamide and bendrofluazide: a comparison in the management of essential hypertension.

1 To compare the efficacy of indapamide with that of bendrofluazide a randomised trial was carried out in twenty patients with essential hypertension. 2 Indapamide (2.5 mg a day) and bendrofluazide (5 mg a day) produced a significant but equivalent fall in blood pressure. 3 Both drugs caused a reduction in body weight and serum potassium with a rise in plasma renin activity but there were no other major side effects. 4 In twelve patients treated with a combination of indapamide and bendrofluazide there was no additional fall in mean blood pressure or serum potassium compared to treatment with bendrofluazide or indapamide alone.

Adult↗
PubMed1981

Effect of 12-hour infusions of saralasin or captopril on blood pressure in hypertensive conscious rats. Relationship to plasma renin, duration of hypertension, and effect of unclipping.

Saralasin (Sar1, Ala8 angiotensin II), a competitive antagonist of angiotensin II, or captopril, an angiotensin-converting enzyme inhibitor, were infused for 12 hr into conscious rats with Goldblatt two-kidney one-clip hypertension at an early stage (mean interval from clipping 36 days) and a chronic stage (151 days). In the early phase infusions of either saralasin or captopril produced a significant fall in blood pressure, which was maximal at 30 min, although the majority of animals remained hypertensive. In the chronic phase, saralasin produced a small and nonsignificant fall in blood pressure, whereas captopril produced a fall similar to that observed in the early group. No further fall in blood pressure was seen over the 12 hr period. PRC was markedly elevated in the early phase but did not differ significantly from normal in the chronic phase. The blood pressure fall produced by saralasin was significantly correlated with preinfusion PRC (r = 0.72 for the early group and 0.81 for the chronic group; p less than 0.01), whereas the fall in blood pressure produced by captopril was poorly correlated with PRC (r = 0.04 and 0.14, respectively). Captopril produced a minor fall and saralasin a minor elevation of blood 3 pressure in normal animals. Infusions of dextrose without inhibitor caused no change in blood pressure. Removal of the renal artery clip normalized blood pressure in the majority (88%) of animals in either the early or chronic phases. It is concluded that 12 hr infusions of these inhibitors are no more effective than 30 min infusions and do not fully correct hypertension in this model. Furthermore, the greater vasodepressor effect of captopril compared to saralasin in chronic hypertensive animals and the lack of correlation between PRC and change in blood pressure with captopril suggest that this agent has an action independent from blockade of the renin-angiotensin system. Removal of the renal artery clip is more effective than renin-angiotensin blockade in correcting Goldblatt two-kidney one-clip hypertension.

Angiotensin II↗
PubMed1980

Vasodepressor property of the converting enzyme inhibitor captopril (SQ 14 225): the role of factors other than renin-angiotensin blockade in the rat.

1. The peptide converting enzyme inhibitor captopril was given (1.25 mg/kg intravenously) to normal and nephrectomized rats and rats with renovascular and deoxycorticosterone hypertension. 2. Captopril lowered blood pressure to a small extent in normal and nephrectomized rats. Bradykinin infusion in nephrectomized animals, however, potentiated the vasodepressor action of captopril. 3. Captopril produced a major blood pressure fall in the early stages of Goldblatt two-kidney one-clip hypertension: even when hypertension had been present for more than 4 months, a substantial vasodepressor action was seen. Rats with deoxycorticosterone-induced hypertension also showed a significant blood pressure fall. 4. Captopril was given to salt-loaded and salt-depleted rats in which the renin-angiotensin system had been blocked by infusion of the competitive angiotensin II antagonist saralasin. Captopril still lowered blood pressure in the salt-depleted group. 5. Captopril lowers blood pressure in situations where the renin-angiotensin system is not responsible for blood pressure maintenance. Further, the fall in blood pressure produced in Goldblatt two-kidney one-clip hypertension is greater than would be predicted on the basis of renin-angiotensin blockade. It is likely therefore that captopril lowers blood pressure by an action additional to angiotensin blockade. Bradykinin potentiation is one possible mechanism by which this may take place.

Angiotensin II↗
PubMed1980

Response of chronic renovascular hypertension to surgical correction or prolonged blockade of the renin-angiotensin system by two inhibitors in the rat.

1. Removal of the renal artery constriction but not of the clipped kidney restored the blood pressure to normal levels in Goldblatt two-kidney rats with hypertension of more than 4 months' duration. 2. Despite the differences in blood pressure response, both surgical procedures lowered plasma renin concentration to normal or below normal values. 3. Administration of the oral converting enzyme inhibitor SQ 14 225 produced a marked fall in blood pressure in Goldblatt kidney rats with chronic hypertension. However, a prolonged infusion of the angiotensin II antagonist saralasin was quite ineffective. The difference in response to the two inhibitors may have been due to bradykinin potentiation by the converting enzyme inhibitor. 4. Although plasma renin is often elevated in Goldblatt two-kidney rats with hypertension of more than 4 months' duration, the renin-angiotensin system plays no role in the maintenance of blood pressure at this stage.

Angiotensin II↗
PubMed1980

Reversible hypertension and hypothyroidism.

Six patients with hypothyroidism and hypertension whose blood pressure fell to normal when treated with thyroxine (172 +/- 7.2/112 +/- 2.1 to 140 +/- 3.2/84+/- 1.6 mmHg, P < 0.001) are described. Plasma renin activity (1.76 +/- 0.63 ng angiotensin I.ml-1.h-1) was low before treatment. Hypertension with low plasma renin is consistent with sodium retention. Hypertension in the hypothyroid patient only requires further evaluation if it persists after adequate treatment with thyroxine.

Adult↗
PubMed1980

Surgical correction of renovascular hypertension: dissociation between post-operative changes in plasma renin and blood pressure.

Conventionally used criteria for predicting the blood pressure response to surgery in renovascular hypertensive disease rely on the demonstration of renin dependency. To assess the validity of this, we have related post-operative changes in plasma renin to the efficacy of surgical treatment of renovascular hypertension. We report nine hypertensive patients with unilateral renal disease and raised peripheral plasma renin activity (PRA), who were studied before and after either nephrectomy or renal artery stenosis bypass. In four patients blood pressure fell to normal levels, and has remained normal without treatment for periods varing from one to four years. In only one of these patients did renal vein renin studies indicate hypersecretion of renin on the operated side with contralateral suppression. Of the remaining five patients, three showed partial reduction of diastolic blood pressure and in two blood pressure was unchanged, although it was more easily controlled with antihypertensive medication. In all patients studied, peripheral venous plasma renin activity fell significantly after surgery, becoming normal in seven patients: in one of these blood pressure was unchanged, and it remained significantly elevated in two. Thus, correction of renin hypersecretion is not necessarily associated with restoration of blood pressure to normal. Tests for surgical correctability of renal hypertension which attribute a central role to renin hypersecretion may therefore yield misleading results.

Adult↗
PubMed1980

Plasma renin in hypertensive patients: significance in relation to clinical and other biochemical features.

Presenting features of 221 hypertensive patients were examined in relation to plasma renin. One hundred and seventy-six patients had essential hypertension, of these 47 had high plasma renin activity (PRA), 80 had normal PRA and 49 low PRA. When the groups with high and low PRA were compared with age and sex matched patients with normal PRA there was no difference with respect to clinical, radiological, electrocardiographic and biochemical characteristics. Twenty-five patients had radiological evidence of unilateral renal or renovascular disease and twenty patients had accelerated hypertension with advanced fundal changes: both these groups had more severe hypertension, a higher plasma renin and evidence of greater cardiovascular morbidity than patients with essential hypertension. Morbidity was equally high in patients with accelerated hypertension whether PRA was high or normal. There is therefore no evidence to support the view that renin is an important factor in assessing risk in hypertension. If, on the other hand, specially referred patients with renovascular and accelerated hypertension are pooled with other hypertensive patients, a spurious association between renin and cardiovascular morbidity will be created.

Adult↗