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Biomedical subjects

H Thurston

Publications and source records attributed to H Thurston.

At least 127 records · Page 7Linked to original sources
PubMed1979

Salt intake and diuretic treatment of hypertension.

24 h urinary sodium excretion was used to monitor salt intake in 36 patients with essential hypertension to determine whether limitation of the antihypertensive action of thiazide diuretics could be explained by increased salt appetitie stimulated by salt depletion. Sodium excretion in these patients was similar before treatment to that observed in normotensive controls, and no change was observed during 2 years' treatment with bendrofluazide. However, plasma-renin rose progressively over the 2 years even in 5 of 8 patients whose renin was not stimulated initially by diuretics. Thus, there is no evidence that a voluntary increase in salt intake limits the efficacy of diuretic treatment; on the other hand, progressive stimulation of the renin-angiotensin system may be an important limiting factor to the antihypertensive action of diuretics. If so, the antihypertensive effect of dietary salt restriction may be similarly limited.

Adult↗
PubMed1979

Plasma renin activity in diabetes mellitus.

1. The plasma renin activity (PRA) was measured in 76 diabetic patients who were attending an outpatients clinic. Of these patients 16 had untreated hypertension and 28 had diabetic complications, which ranged from microaneurysms to renal failure and blindness. 2. Compared with age- and sex-matched normotensive control subjects, both normotensive and hypertensive diabetic patients had significantly higher PRA (P less than 0.001). 3. Hypertensive diabetic patients also showed a higher PRA than matched hypertensive control subjects (P less than 0.005). There were no significant differences between diabetic patients with hypertension or complications compared with those without these features. 4. Although this elevation of PRA could be due to a change in another component of the renin-angiotensin system, hypersecretion of renin is the most likely explanation.

Adult↗
PubMed1979

Pressor responsiveness to angiotensin in renovascular and steroid hypertension.

1. The pressor response to angiotensin II was reduced in rats with early (less than 6 weeks) and chronic (greater than 4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA-salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.

Angiotensin II↗
PubMed1978

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↗
PubMed1978

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↗
PubMed1977

Blood pressure response of nephrectomized hypertensive rats to converting enzyme inhibition: evidence for persistent vascular renin activity.

1. Blood pressure and plasma renin activity were studied after bilateral nephrectomy in groups of rats with hypertension caused by unilateral renal ischaemia with the opposite kidney left intact. 2. Although blood pressure showed only a small fall in the first hour after bilateral nephrectomy, plasma renin activity fell rapidly with a half-life of 10 min. 3. Infusion of converting enzyme inhibitor (SQ20881) produced a 26-1% fall in blood pressure 1 h after nephrectomy, 24-% at 2 h and 4-6% at 6 h. 4. An angiotensin antagonist (Sar1-Ala8-angiotensin II) was infused into hypertensive rats 1 h after nephrectomy; this blocked the vasodepressor action of the converting enzyme inhibitor, indicating that the fall in blood pressure produced by the inhibitor was due to its action upon the renin-angiotensin system. 5. The renin-angiotensin system maintains blood pressure in this model even after plasma renin has fallen to insignificant levels. This supports the view that vascular renin activity has a longer half-life than circulating renin and is important in the control of blood pressure.

Angiotensin II↗
PubMed1977

Sodium restriction and inhibition of the renin-angiotensin system in renovascular hypertension in the rat.

1. In the early phase of hypertension produced by renal artery constriction with the opposite kidney intact, infusion of the angiotensin antagonist Sar1-Ala8-angiotensin II or bilateral nephrectomy lowered blood pressure. However, the extent of the fall was variable and some animals remained hypertensive after each procedure. 2. To assess whether sodium retention was the additional factor which maintained blood pressure when the renin-angiotensin system was suppressed, rats were maintained on a low-salt diet before and during the development of hypertension. The blood pressure-lowering effect of bilateral nephrectomy or antagonist infusion was not enhanced. 3. Infusion of antagonist or converting-enzyme inhibitor 6 h after bilateral nephrectomy had only a minor blood pressure-lowering action, indicating that, at this late stage after nephrectomy, the renin-angiotensin system makes only a very small contribution to blood pressure maintenance.

Angiotensin II↗
PubMed1977

Plasma renin and angiotensin II measurement in hypertensive and normal subjects: correlation of basal and stimulated states.

Plasma renin activity (PRA) and angiotensin II (AII) were measured in peripheral venous samples obtained from the following subgroups: normal ambulant subjects (n = 61): normal subjects after 7 days treatment with a thiazide diuretic (n = 27): hypertensive subjects before and after a thiazide diruretic (n = 35); severely hypertensive subjects after diazoxide treatment (n = 14) and untreated severely hypertensive subjects (n = 27). In addition aortic (n = 27) and renal vein (n =48) samples were taken from the latter group during investigation of possible renovascular hypertension. Values for PRA and AII were clearly correlated in all groups. Further, calculated regression lines of PRA upon AII did not differ significantly from that calculated for normal subjects, with the exception of the intercept of the diazoxide treated group. However, when the regression line for renal venous samples was compared with that calculated for peripheral venous samples of all other subjects (199), there was a relative increase in the ratio of PRA to AII at all values. Thus, except in the renal vein, measurement of AII and PRA appear to reflect changes in activity of the renin-angiotensin system equally well and there is no support for the view that there is a discrepancy between measured AII and PRA in peripheral venous blood in the clinical situations examined here.

Adult↗
PubMed1976

Low renin hypertension. A distinct entity.

In an attempt to resolve conflicting reports about the identity of a low-renin subgroup in essential hypertension, the distribution of plasma-renin activity (P.R.A.) has been examined in 82 hypertensive subjects before and after stimulation with bendrofluazide. The unstimulated basal P.R.A. showed no evidence of a separate subgroup of patients with low P.R.A. values although the distribution was slightly skewed with a tail to the right when compared with 83 normotensive subjects. In 38 of the patients post-stimulation P.R.A. observed in age and sex matched normotensive controls exposed to the same stimulus. However the percentage rise in P.R.A. in all 83 patients was less than half that of the controls. Thus the identification of a low-renin subgroup of hypertensive patients is critically determined by the standard of comparison employed: if the percentage rise is considered subnormal responsiveness is a feature of essential hypertension. If absolute post-stimulation values are used, there is a substantial group of patients with "low renin hypertension". The demarcation of such a group is, however, essentially arbitrary.

Adolescent↗
PubMed1976

Vascular angiotensin receptors and their role in blood pressure control.

The renin angiotensin system has an important role in regulating arterial blood pressure in homeostasis and disease. A reciprocal relationship exists between sodium balance and the circulating levels of renin and angiotensin II. The vascular responsiveness to angiotensin II, the major vasconstrictor component of the renal pressor system, can be impaired by numerous factors including sodium depletion or a reduction in effective plasma volume. In situations in which the renin-angiotensin system is activated, a negative relationship between the angiotensin II pressor response and the circulating angiotensin II level is observed. This effect seems to involve a change of the angiotensin II receptor interaction in the vascular smooth muscle. The prevention of angiotensin II generation by the inhibition of converting enzyme causes an immediate increase in the pressor response to angiotensin; after bilateral nephrectomy, it takes much longer to develop. In addition, the depressor response to angiotensin antagnoists and converting enzyme inhibitor is preserved after bilateral nephrectomy for much longer periods than can be accounted for by the disappearance of circulating renin. These observations support the view that the decrease in vascular response to angiotensin II during sodium deprivation or when body fluid volumes are reduced is the result of prior occupancy of the receptor sites by endogenous hormone generated both in the plasma and locally within blood vessel walls. Therefore, a change in the number or affinity of receptors consequent to a change in sodium balance or as a modulating function of the renin-angiotensin system need not be postulated to explain changes in angiotensin vascular responsiveness.

Angiotensin II↗
PubMed1976

Influence of sodium restriction upon two models of renal hypertension.

1. Restriction of dietary salt intake does not affect the development or maintenance of hypertension in rats with unilateral renal ischaemia whether the contralateral kidney is present (Goldblatt 2 model) or not (Goldblatt 1 model). 2. Acute dietary salt depletion induces a similar loss of sodium and fall in body weight with little change in blood pressure in both normal and hypertensive rats. 3. Excision of the ischaemic kidney in rats with short-term (less than 50 days) Goldblatt 2 hypertension restores the mean blood pressure to normal, whereas Goldblatt 1 hypertensive rats show only a partial response. Previous salt depletion of this model enhances the blood pressure response to nephrectomy. 4. Sodium retention plays no part in the development or maintenance of Goldblatt 2 kidney hypertension. However, although sodium retention is normally involved in the Goldblatt 1 model, hypertension can develop in the absence of dietary sodium.

Animals↗
PubMed1976

The role of sodium retention in Goldblatt 2-kidney hypertension in the rat.

1. Infusion of angiotensin II antagonist failed to restore the blood pressure of short-term Goldblatt 2-kidney hypertensive rats to normal levels before and after sodium restriction. 2. The blood pressure of both normal and sodium-restricted Goldblatt 2 hypertensive rats remained elevated 6 h after bilateral nephrectomy. 3. The residual hypertension found during antagonist infusion and after bilateral nephrectomy is not maintained by the renin-angiotensin system or sodium retention.

Angiotensin II↗
PubMed1976

Impedance cardiography for determination of stroke index.

Stroke index obtained by impedance cardiography was compared with values obtained by dye-dilution technique in 17 subjects in 122 determinations made within 2 min of each other. Fifty of these determinations were done after drug administration, postural change, or saline infusion. All values obtained by both methods correlated significantly, but with wide scatter (r=0.49, n = 122, P less than 0.001). The series of determinations within each subject, however, correlated only in one subject significantly; thus any changes of stroke index measured by both techniques were not commensurate. In addition, the impedance stroke index values were significantly lower than the dye-dilution technique, impedance cardiography presently does not determine reliably absolute values of stroke index and is not suitable to evaluate changes of stroke index.

Adult↗
PubMed1976

Triamterene-induced changes in aldosterone and renin values in essential hypertension. Evidence of a role for aldosterone in preventing blood pressure reduction.

The effect of triamterene, a potassium-retaining natriuretic and diuretic agent, on arterial blood pressure was studied in 31 patients with essential hypertension; there were seven patients with low plasma renin activity and 24 patients with normal plasma renin activity. Triamterene exhibited mild antihypertensive action, somewhat more pronounced in the low-renin group. The patients were also analyzed by considering them in terms of their blood pressure response. Of the 21 patients in the nonresponder group, no blood pressure decrease occurred, despite induced volume depletion accompanied by an increased plasma renin activity and a concomitant rise in the aldosterone excretion. In contrast, the ten patients in the responder group exhibited a fall in blood pressure, but the aldosterone excretion rate did not change significantly, even though plasma renin activity increased significantly. Moreover, only in the nonresponder group did the stimulated aldosterone excretion rate correlate significantly with the stimulated plasma renin activity. Thus, the failure of triamterene to lower blood pressure in the nonresponder group can be closely related to a significant increase in aldosterone excretion rate. The data suggest the operation of a reactive pressor action mediated by aldosterone, independent of its sodium-retaining effect.

Aldosterone↗
PubMed1975

Reciprocation of renin dependency with sodium volume dependency in renal hypertension.

An angiotensin II inhibitor was administered to rats with two-kidney Goldblatt hypertension. The inhibitor produced a marked drop in blood pressure after 5 weeks but no significant change after 15 weeks of hypertension. However, even after 15 weeks of hypertension, following sodium depletion by either diuretics or a low sodium diet, the animals again became renin dependent as readministration of the inhibitor induced a significant fall in blood pressure. The data indicate that two-kidney Goldblatt hypertension is initially renin dependent but subsequently becomes sodium volume dependent in a way similar, although more protracted, to that already described for one-kidney Goldblatt hypertension.

Angiotensin II↗
PubMed1975

Prior receptor occupancy as a determinant of the pressor activity of infused angiotensin II in the rat.

The pressor responsiveness to angiotensin II and norepinephrine was examined in rats before and during blockade of coverting enzyme activity with the nonapeptide SQ 20881. Responses to angiotensin II were impaired by sodium deprivation but enhanced by sodium loading or bilateral nephrectomy. During the period of converting enzyme blockade, a twofold increase in the angiotensin II pressor response was observed in the salt-restricted rats, whereas only a small change occurred in the salt-loaded rats. Infusion of the inhibitor produced a profound fall in the blood pressure of the salt-depleted rats with a relatively minor fall in the sodium-loaded rats. Norepinephrine pressor responses were slightly potentiated in the salt-restricted rats after administration of SQ 20881, but no change occurred in the salt-loaded or the nephrectomized rats. These observations support the view that the decreased angiotensin II pressor activity during salt deprivation is the result of a prior occupancy of receptor sites by endogenous hormone. Therefore, a change in the number or the affinity of receptors consequent to changes in sodium balance need not be postulated to explain the phenomenon.

Angiotensin II↗