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Query: UNIPROT:P06889 (Mol)
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1. Intra-arterial pressure, cardiac output, renal blood flow and glomerular filtration rate were measured in 19 patients with low-renin hypertension and in 30 patients with normal-renin hypertension. 2. Cardiac output and renal blood flow were significantly lower in low-renin hypertension. Total peripheral and renal vascular resistance were markedly higher in this group. 3. Plasma renin concentration correlated inversely with both total peripheral and renal vascular resistance as well as with age. Multiple regression analysis indicated that part of the relationship between renin and haemodynamic variables did not depend on age. Furthermore, plasma renin concentration did not decrease with age in a group of 40 normotensive control subjects of similar age to the hypertensive patients. 4. The results provide further confirmation that renin decreases as hypertension progresses.
Clin Sci Mol Med 1977 Apr
PMID:Haemodynamic characteristics of low-renin hypertension. 86 36

1. The intrarenal distribution of plasma flow was determined with a technique based on the analysis of the transit time of sodium o-[131I]- iodohippurate through the kidney in 43 patients with cirrhosis with near-normal total renal perfusion. 2. Twenty-five of the patients had an abnormal pattern of transit times, suggesting a redistribution of plasma flow from outer cortical to juxtamedullary nephrons. 3. Plasma renin activity ranged from below normal to six times normal and high values were found only in patients showing an abnormal pattern of transit times. The latter was also found to be related to sodium retention and a reduced renal capacity to excrete free water.
Clin Sci Mol Med 1977 May
PMID:Intrarenal distribution of plasma flow in cirrhosis as measured by transit renography: relationship with plasma renin activity, and sodium and water excretion. 86 40

1. The intrarenal role of angiotensin II in controlling sodium excretion was examined in anaesthetized, dehydrated dogs by infusing the angiotensin II antagonist Sar1-Ile8-angiotensin II directly into the renal artery. Comparisons were made with dehydrated dogs receiving only sodium chloride solution intrarenally. 2. Intrarenal angiotensin II blockade resulted in significant increases in urinary sodium excretion and urine flow rate. 3. The results indicate that during the high-renin state of dehydration endogenous angiotensin II has intrarenal effects which lead to salt and water retention.
Clin Sci Mol Med 1977 May
PMID:Intrarenal role of angiotensin II in controlling sodium excretion during dehydration in dogs. 86 48

1. A single oral dose of clonidine hydrochloride (300 microgram) lowered systolic blood pressure by 20+/-2 mmHg and diastolic blood pressure by 15+/-2 mmHg in seven healthy normotensive subjects. 2. Resting supine plasma noradrenaline concentration fell from 2-42+/-0-47 nmol/l before dosing to a minimum of 0-59+/-0-18 nmol/l at 6 h. The value subsequently rose and was not significantly different from that before the dose at 12 h. There was a significant reduction in urinary free catecholamine excretion in the first 12 h after dosing. 3. Resting supine plasma renin activity before dosing was 0-95+/-0-16 pmol of angiotensin I h-1 ml-1 of plasma and rose significantly after clonidine to 3-50+/-0-39 pmol of angiotensin I h-1 ml-1 of plasma at 6 h. By 12 h plasma renin activity had returned to control values. 4. When the same subjects were studied on a control, drug-free, day under the same conditions, there was no significant change in blood pressure or plasma noradrenaline. Although plasma renin activity rose during this control day, it was significantly lower than after clonidine. 5. In normotensive subjects single doses of clonidine lower blood pressure and are associated with a reduction of sympathetic nervous activity. Delayed elevation of plasma renin activity may be secondary to the fall in blood pressure. There is no evidence for an overshoot of sympathetic activity after a single dose of clonidine.
Clin Sci Mol Med 1977 Jul
PMID:Effects of clonidine on biochemical indices of sympathetic function and plasma renin activity in normotensive man. 87 20

1. In 29 patients with acromegaly, plasma renin activity and growth hormone were measured during fasting and recumbency on free diet. Exchangeable sodium was measured in all cases and expressed as a percentage of the expected value on the basis of lean body mass. 2. Twenty-two control subjects without evidence of cardiovascular, renal or endocrine disease were studied in the same way. 3. There was a significant increase in exchangeable sodium and suppression of plasma renin activity in the acromegalic patients in comparison with control subjects. 4. There was a significant positive correlation between exchangeable sodium and plasma growth hormone. 5. Hypertensive acromegalic patients (diastolic blood pressure larger than or equal to 100 mmHg) tend to have a lower (although not significantly so) exchangeable sodium than normotensive subjects. 6. We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly.
Clin Sci Mol Med 1977 Jul
PMID:An investigation into the pathogenesis of hypertension in acromegaly. 87 24

1. Plasma renin concentration, intra-arterial pressure, cardiac output and total peripheral resistance have been studied in 50 patients with essential hypertension and normal renal function. 2. Total peripheral resistance and plasma renin were negatively correlated (r = -0-45), indicating that 'high-renin' essential hypertension is not necessarily associated with arteriolar vasoconstriction. 3. The inverse relation between mean arterial pressure and plasma renin (r = -0-46) suggests a role for the renal baroreceptor mechanism in the suppression of renin in 'low-renin' hypertension. 4. Cardiac output was positively related to plasma renin concentration (r = +0-42). 5. Multiple regression analysis indicates that the described relationships were independent of age.
Clin Sci Mol Med 1977 Jun
PMID:Plasma renin levels and systemic haemodynamics in essential hypertension. 88 30

1. Renin secretion rates in normal rats were determined with two different methods: (a) the product of renal plasma flow as measured by sodium p-aminohippurate and the difference between renal and peripheral vein renin activity; (b) the product of this latter difference and the renal plasma flow as calculated from the clearance and extraction of inulin. 2. The renin secretion rates, as calculated by these two methods, were not significantly different (P greater than 0-1) and were found to be highly correlated (r = 0-943; P less than 0-001).
Clin Sci Mol Med 1977 Sep
PMID:Two methods for determination of renin secretion rates in rats. 91 53

1. The initial blood pressure response to saralasin (Sar1-Ala8-angiotensin II) infusion was examined in 15 normal subjects, eight patients with untreated essential hypertension and 65 patients established on chronic haemogialysis (including six anephric patients), and related to measurements of plasma renin activity (PRA), angiotensin II, plasma catecholamines (noradrenaline and adrenaline), blood volume and extracellular fluid volume ([35S]sulphate space or exchangeable sodium). 2. A transient rise in arterial pressure, maximum after 5-6 min, occurred in all normal subjects, patient with essential hypertension and anephric patients, and in 41 of the 59 dialysis patients with kidneys. 3. In the normal subjects, saralasin infusion resulted in a significant rise in plasma noradrenaline (mean increase 360%, P less than 0-02) without change in plasma adrenaline concentration. The change in noradrenaline was significantly related to the change in mean blood pressure (P less than 0-05) and was similar to the response to 5 min of a 40 degree head-up tilt. 4. An increase in plasma noradrenaline also occurred in dialysis patients (P less than 0-005) but the change in mean blood pressure with saralasin in this group was inversely related to PRA (P less than 0-001) and angiotensin II (P less than 0-001), directly related to blood volume (P less than 0-001), but unrelated to the change in plasma noradrenaline. 5. The pressor response to saralasin may be mediated not only by angiotensin-like action on vascular receptors but also by an action on the central or peripheral autonomic nervous system.
Clin Sci Mol Med 1977 Oct
PMID:Plasma catecholamines and the pressor response to Sar1-Ala8-angiotensin II in man. 91 58

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.
Clin Sci Mol Med 1976 Jul
PMID:Effect of sotalol on haemodynamics and renin-angiotensin-aldosterone system in hypertensive patients. 93 70

1. The effect of low-frequency stimulation of the renal nerves on renal function and renin release has been investigated. The experiments were performed in unilaterally nephrectomized, anaesthetized cats in which the nerves to the remaining kidney were sectioned. 2. When stimulation frequency was adjusted to reduce renal blood flow by approximately 15% for 15 min, glomerular filtration rate was hardly affected. The ratio sodium clearance/glomerular filtration rate was significantly reduced and plasma renin activity was significantly increased. 3. When the renal nerves were similarly stimulated in the presence of the beta-adrenergic receptor blocking agent, propranolol, the glomerular filtration rate was significantly reduced and the rise in plasma renin activity was significantly inhibited. The reduction of sodium clearance/glomerular filtration rate was as great as in the control animals. 4. The results are consistent with the view that the maintenance of glomerular filtration rate, during renal nerve stimulation which reduced renal blood flow, may be mediated by the local generation of angiotensin. The results also suggest that angiotensin does not play an important role in the sodium retention associated with increased renal nerve activity.
Clin Sci Mol Med 1976 Jul
PMID:The sodium-retaining effect of renal nerve activity in the cat: role of angiotensin formation. 93 71


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