Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Several extrarenal tissues contain enzymes which are similar to kidney renin: they hydrolyse angiotensinogen to form angiotensin I; they have characteristic substrate specificity; the physicochemical properties of kidney renin and of extrarenal tissue iso-renin are similar. 2. Results indicate that tissue iso-renins are part of a complex enzyme system with mainly local function. A possible biological role has been demonstrated in brain, adrenal gland and tissue culture.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Tissue iso-renins. 79 50

1. The anti-hypertensive effect of atenolol was greater than that of bendrofluazide. 2. The change in systolic blood pressure caused by bendrofluazide showed a significant inverse correlation iwth the plasma renin concentration (r=-0-47; P less than 0-01). 3. The correlation between the change in systolic blood pressure caused by atenolol and the plasma renin concentration was not significant (r =0-28; 0-1 greater than P greater than 0-05). 4. Plasma renin concentration was unaffected by atenolol.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Plasma renin concentration and the hypotensive effect of bendrofluazide and of atenolol. 79 51

1. Patients with cadaveric renal transplants and plasma creatinine less than 177 micronmol/l who had their own kidneys removed were studied. 2. The renin-angiotensin system appeared to behave in a normal fashion in response to alterations in sodium intake and posture. 3. The renin-angiotensin system had no major role in the establishment or maintenance of hypertension. 4. Mean arterial pressure was directly related to expansion of the extracellular fluid volume.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Plasma renin activity, plasma angiotensin II and extracellular fluid volume in patients after renal transplantation. 79 52

1. The anti-hypertensive actions of timolol and hydrochlorothiazide were analysed in a double-blind 2 x 2 factorial trial in twenty patients with essential hypertension. Each patient went through four phases of 8 weeks in randomized order, receiving timolol alone, hydrochlorothiazide alone, timolol plus hydrochlorothiazide, and placebo. 2. Supine mean arterial pressure fell from 119 mmHg in the placebo phase, to 110 mmHg during the thiazide phase, 106 mmHg during the timolol phase, and to 101 mmHg during the combined timolol plus hydrochlorothiazide phase. 3. Factorial analysis revealed that the hypotensive actions of the beta-receptor-blocking drug and the diuretic were additive, without any synergism or antagonism. 4. Plasma renin activity measured in ng 3 h-1 ml-1 rose from 5-02 in the placebo phase to 9-54 in the diuretic phase, but fell to 1-79 in the beta-receptor blockade. It was unchanged in the combined therapy phase, despite the greater drop in blood pressure. These results suggest that the fall in plasma renin activity during beta-receptor blockade is of little importance in the hypotensive action of beta-receptor-blocking drugs.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Quantitative effects of timolol and hydrochlorothiazide on blood pressure, heart rate and plasma renin activity: results of a double-blind factorial trial in patients with essential hypertension. 79 60

1. Serial measurements of plasma renin activity (PRA), plasma aldosterone concentration (PA) and blood pressure were performed overnight in patients with borderline (group 1) and sustained essential hypertension (group 2) before and after acute and chronic administration of either propranolol or pindolol. 2. Group 1 patients exhibited a typical rhythm of recumbent PRA with low values before midnight and large increases early in the morning. 3. In contrast, no rhythm and very low PRA values were observed in patients of group 2. Blood pressure was higher in group 2 than in group 1. There was a significant correlation between the hyporeninaemic and hypotensive effect of either acute (r = 0-79) or chronic (r = 0.4) beta-receptor blockade. 4. In group 1, after beta-receptor blockade the day-night profile of renin was similar to that observed in group 2 before treatment. Thus, in this latter subgroup, low-renin profiles might reflect reduced beta-adrenoreceptor activity. 5. Plasma aldosterone was lower in group 2 but appeared to be inappropriately high relative to renin. 6. The data suggest that in hypertensive patients classified according to their blood pressure and recumbent PRA profiles a significant relationship exists between changes in PRA and arterial pressure. Thus patients with high PRA respond better to treatment than patients with low renin. We conclude that in the patients studied sympathetic nervous system activity mainly determined renin values as well as anti-hypertensive effectiveness of the beta-blocking drugs.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Differential effects of acute and chronic beta-adrenoreceptor blockade on blood pressure and the renin-angiotensin-aldosterone system in essential hypertension. 79 64

1. Factors involved in the neural control of renin release have been reviewed. 2. Experimental evidence has been obtained that sympathetic stimulation releases renin from the kidney independently of local vasomotor changes. 3. The reflex control of renin release on postural change has been established. 4. The effect of diuretics on renin release has been studied and evidence of neural and non-neural mechanisms obtained. 5. The effect of suprarenal aortic stenosis has been studied; the findings suggest that renin release is in some way dependent on neural mechanisms. 6. The pathological significance of the neural control of renin release has been discussed.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Neural control of renin release. 80 38

1. Some of the haemodynamic abnormalities in mild (borderline) human hypertension appear to be neurogenic, since they can be completely abolished by pharmacological autonomic blockade. 2. The cardiac output is elevated in 30% of patients through increased sympathetic drive and decreased parasympathetic inhibition. 3. In the remainder, the higher blood pressure is maintained by increased total peripheral vascular resistance. 4. In approximately 30% of this latter group, the higher vascular resistance is maintained solely by increased alpha-adrenergic tone. 5. Elevated plasma renin activities in a proportion of cases are probably due to generalized increase in sympathetic nervous activity. 6. Patients with mild hypertension thus show increased sympathetic drive to the heart and arterioles as well as decreased cardiac parasympathetic inhibition. It is presumed that the increased plasma renin is also neurogenic. 7. Such a widespread distribution of altered autonomic tone suggests aberration of the function of the integrative centres of cardiovascular control. 8. Evidence is presented of a possible psychosomatic origin of these changes in some cases.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Role of the autonomic nervous system in mild human hypertension. 80 40

1. Postural changes of plasma renin activity (PRA) before and after the administration of a beta-blocking agent (oxprenolol) were studied in nine patients with renal homotransplantation and in ten normal subjects. 2. In normal subjects PRA always increased during upright posture without any correlation with postural changes in mean arterial pressure. Oxprenolol reduced the postural increase of PRA. 3. A postural increase of PRA could be detected as early as 20--25 days after renal transplantation, and appeared with increasing frequency as time elapsed. 4. There was a significant inverse correlation (r = -0.794, P less than 0.001) between the postural changes of PRA and those of mean arterial pressure. 5. These results suggest that in patients with renal homotransplantation the postural increase of PRA can only partly be due to circulating catecholamines or the sympathetic nervous system and may be explained by inverse changes in the mean arterial pressure.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Postural changes of plasma renin activity after renal transplantation. 80 41

1. The effects of propranolol and RO3-4787, a new beta-adrenoceptor antagonist with a partial agonist activity, have been studied in a blind, cross-over comparison with placebo. 2. In ten patients who completed the study, the two drugs produced a similar reduction in blood pressure; the reduction in heart rate with propranolol was significantly (P less than 0.001) greater than that produced by RO3-4787. 3. Plasma renin activity averaged 4.13 +/- 1.37 ng h-1 ml-1 on placebo, fell to 3.64 +/- 1.47 ng h-1 ml-1 on propranolol and to 2.50 +/- 1.39 ng h-1 ml-1 on RO3-4787. 4. No correlation was demonstrable between the log plasma concentration of either propranolol or RO3-4787 and change in blood pressure.
Clin Sci Mol Med Suppl 1975 Jun
PMID:A comparison of propranolol and compound RO3-4787 in the treatment of arterial hypertension in man. 80 44

1. Propranolol was given to eight haemodialysed patients with resistant arterial hypertension for periods ranging from 6 to 16 months. 2. The treatment brought about an excellent control of blood pressure in all cases. 3. After withdrawal of propranolol plasma renin activity rose on average 40% compared with the value obtained during treatment. However, no significant relationship was found between the change in plasma renin activity and the change in the diastolic blood pressure. 4. Stopping propranolol resulted in a prompt rebound of arterial pressure toward pretreatment values. However, hypertension was always controlled on resuming drug treatment. 5. The results show that this form of hypertension can be controlled on a long-term basis with propranolol. However, the effect on blood pressure seems not to be mediated by suppression of renin secretion.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Long-term propranolol treatment of resistant arterial hypertension in haemodialysed patients. 80 45


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