Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Propranolol administration in the hypoxic model of acute renal failure (ARF) in rats has reduced plasma renin activity (PRA) and uraemia as compared to untreated controls. P113 has no effect on uraemia but increased PRA in ARF. A combination of both drugs is no more effective in reducing uraemia than propranolol alone. These results support the view that beta-adrenergic blockade by propranolol reduces the severity of ARF by preventing the post-hypoxic release of renin.
Proc Eur Dial Transplant Assoc 1976
PMID:beta-Adrenergic blockade reduces the severity of acute renal failure in rats. 0 58

The effects of two new beta blockers on renal function have been studied. There were significant decreases in urine flow, urea clearance, sodium and chloride excretion rates after acute administration. Fractional excretion of sodium (FeNa) fell significantly but did not continue to fall during chronic administration. Blood pressure and plasma renin activity decreased significantly after two months' therapy. These findings suggest that beta blockers in patients with unstable cardiovascular function increase the need for concomitant diuretic therapy.
Proc Eur Dial Transplant Assoc 1976
PMID:Acute renal effects of new beta-adrenergic receptor site blocking agents on renal function. 0 59

In normal supine man, a marked circadian rhythm was found in plasma renin activity (PRA) and in plasma aldosterone concentration, with highest levels in the morning and lowest in the evening. Short-term suppression of ACTH by dexamethasone did not eliminate the circadian variation of plasma aldosterone. In patients with a transplanted and thus denervated kidney, no such rhythm of PRA could be observed. From our data it is suggested that the normal circadian rhythm of PRA depends on intact renal innervation and is controlled by the central nervous system.
Proc Eur Dial Transplant Assoc 1975
PMID:Circadian rhythm of plasma renin activity and plasma aldosterone in normal man and in renal allograft recipients. 17 84

Seventeen hypertensive patients were treated with captopril, an orally active inhibitor of converting-enzyme. All patients showed a fall in blood pressure (BP), although in some patients only after the addition of diuretics. In 2 patients a skin rash developed. One patient developed proteinuria. A renal biopsy revealed membranous glomerulopathy. Correlations were found between pretreatment plasma renin activity (PRA) and the decrease in BP, and between pretreatment PRA and the decrease in plasma aldosterone concentration (PAC). Filtration fraction (FF) fell, indicating a decrease in renal vascular resistance. Captopril decreased the sensitivity to exogenous angiotensin I (AI), dependent on the captopril dose used. The sensitivity to exogenous bradykinin increased impressively even on the lowest dose of the drug. These observations suggest extrapulmonary conversion of AI to angiotensin II (AII).
Proc Eur Dial Transplant Assoc 1979
PMID:Treatment of moderate to severe hypertensive patients with an orally active converting-enzyme inhibitor. 23 14

Eight patients on chronic haemodialysis for six months to 7 years with hypertension resistant to ultrafiltration and antihypertensive therapy, received Captopril (SQ 14, 225) an orally active inhibitor of converting enzyme. With this therapy, blood pressure was controlled in the 4 patients with the highest plasma renin activity. In the other 4, this treatment had to be supplemented with "isovolumetric salt subtraction", i.e. following conventional dialysis, 1-2 litres of ultrafiltrate were replaced by an equal volume of 5% glucose. The slight hyponatraemia induced by this procedure (plasma sodium 128mmol/L) was well tolerated. This procedure allows the removal of an excess of body sodium and seems to be effective even when conventional ultrafiltration during dialysis has failed. Administration of Captopril either alone or combined with "isovolumetric salt subtraction" induced good control of blood pressure in all 8 patients.
Proc Eur Dial Transplant Assoc 1979
PMID:Captopril and salt subtraction to treat "uncontrollable" hypertension in haemodialysis patients. 23 15

Among 9 hypertensive recipients with kidney transplant artery stenosis (KTAS) evidence of increased activity of the renin system was present in 3. Surgical repair of KTAS in 4 recipients resulted in an increase in renal plasma flow and glomerular filtration rate associated with a decrease in exchangeable sodium and blood pressure. Peripheral plasma renin and aldosterone values were normal before and after operation in all. It is suggested that sodium retention may counterbalance increased activity of the renin system in KTAS. Preoperative determinations of plasma renin do not predict the effect of surgical repair of KTAS on hypertension.
Proc Eur Dial Transplant Assoc 1977
PMID:Kidney transplant artery stenosis. Interrelationship between blood pressure, kidney function, renin-aldosterone system and body sodium content. 34 Nov 39

The hormonal response to volume depletion by isolated ultrafiltration has been studied in seven non-nephrectomised haemodialysis patients. The mean reduction in blood volume was 14%, and pulmonary artery wedge pressure reduction averaged 77%. No increments in heart rate were observed in any of the patients. Cardiac output decreased while systemic vascular resistance increased. Mean arterial blood pressure remained stable in all but two patients. Significant increments in plasma vasopressin concentration were only found during hypotensive episodes, while in the whole group no significant increase was found. Both plasma renin activity, plasma aldosterone and plasma cortisol increased significantly during isolated ultrafiltration. The moderate increase in systemic vascular resistance indicates that the peripheral sympathetic nervous system - at least partly - was functioning. It was, however, not correlated with changes in any of the measured hormones. Furthermore the adrenal and cardiac response appeared to be absent.
Proc Eur Dial Transplant Assoc 1979
PMID:Hormonal response to volume depletion in non-nephrectomised patients on regular haemodialysis. 39 94

Thirteen patients with chronic renal insufficiency who had been transferred from haemodialysis to haemofiltration treatment because of dialysis and drug resistant hypertension (10 with high plasma renin activity) showed normalisation of blood pressure during a treatment period of 8 months, after which only one patient required antihypertensive drug therapy. During the first period blood pressure drop paralleled body weight loss and after 3--4 weeks blood pressure remained normal in spite of an increase in body weight. In the course of the second phase the effect of fluid withdrawal on blood pressure was directly proportional to the blood pressure at the beginning of the procedure. Adaptation of baroreceptor function must be assumed. In contrast to haemodialysis, haemofiltration did not influence the inulin space. Because of the reduced removal of small molecular substances compared with haemodialysis, extracellular osmolarity was kept stable during haemofiltration. Withdrawal of even large amounts of fluid was sustained without collapse reactions or signs of orthostatic dysregulation.
Proc Eur Dial Transplant Assoc 1977
PMID:Treatment of severe hypertension in chronic renal failure by haemofiltration. 60 Sep 48

This study was carried out to assess the influence of saralasin (SAR), an angiotensin II-analogue, on peripheral and central angiotensin II-receptors by measurements of plasma renin activity (PRA) and arginine-vasopressin (AVP) release. Before and during i.v. infusion of 10 microgram/kg/min of SAR over a 30 minute period, blood samples were obtained from 15 recumbent hypertensive patients (7 renovascular, 8 essential) to determine hormone activities by radioimmunoassay. In 10 patients with a decrease of blood pressure following SAR, PRA increased significantly whereas AVP levels increased significantly in only 7 of these patients. In the remaining 5 patients without a fall of blood pressure, PRA and AVP remained virtually unchanged. The results indicate that an enhanced AVP release may be due to a hypotensive stimulus induced by SAR in angiotensinogenic hypertension. A direct influence of SAR on central receptors is unlikely under the conditions studied.
Proc Eur Dial Transplant Assoc 1978
PMID:Effect of saralasin on plasma renin activity and arginine-vasopressin in hypertensive man. 74 Jun 74

Basal and stimulated plasma renin activity (PRA) and plasma aldosterone (PA) were measured in 13 hypertensive and 16 normotensive patients with kidney allografts one to nine years after transplantation. In both groups no significant differences were observed between mean basal and stimulated PRA and PA values. Therefore, we conclude that abnormal renin secretion might not be the main factor causing hypertension in renal allograft recipients. Other mechanisms seem to be involved in the pathogenesis of hypertension in these patients.
Proc Eur Dial Transplant Assoc 1976
PMID:Plasma renin activity (PRA) and plasma aldosterone (PA) in hypertensive kidney allograft recipients. 77 39


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