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)

In recent years many investigators have reported the role of the sympathetic nervous system and the catecholamines in the regulation of renin secretion. It has been recently reported that plasma dopamine-beta-hydroxylase (DBH) excreted through the mechanism of the exocytosis with noradrenaline from the sympathetic postganglionic nervous endings is a mirror of the function of the sympathetic nervous system. In this investigation, blood pressure, urinary catecholamine excretion, plasma DBH activity and plasmsa renin activity (RPA) have been determined in normal individuals during the mecholyl test and insulin-induced hypoglycaemia. In the mecholyl test, plasma DBH activity and PRA markedly increased in five males who showed prominent responses of systolic blood pressure to mecholyl (S type) and changed slightly in eight males who showed minimal responses of systolic blood pressure to mecholyl (N type). It showed that there was a significant relationship between the maximal percent increases from their respective control values of plasma DBH activity and those of PRA following mecholyl. In insulin-induced hypoglycaemia, plasma DBH activity, blood pressure and PRA remarkably increased following a large dose of insulin administration (0.15 u/kg). In a dose of 0.1 u/kg, there was no significant increase of plasma DBH activity and blood pressure. PRA singificantly increased but was lower than a large dose of insulin. Also, it showed that their was a significant relationship between maximal percent increases from their respective control values of plasma DBH activity and those of PRA following insulin administration. These data indicate a close correlation between changes in plasma DBH activity and those of PRA during mecholyl and insulin-induced hypoglycaemia and lend additional support to the concept of sympathetic nervous system mechanism of renin secretion.
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PMID:[Studies of the relationship between renin secretion and the sympathetic nervous system responsiveness in man (author's transl)]. 123 20

Renin response to nifedipine, verapamil, propranolol and hypothiazide was studied in 133 patients with Stage II hypertensive disease. The common mechanism of action in all these drugs was an increase in baseline plasma renin activity (PRA). In patients with a baseline high RPA, propranolol and nifedipine lowered it, whereas verapamil and hypothiazide unchanged it. Group analysis indicated that enhanced PRA during therapy was unassociated with diminished antihypertensive effects of an agent as compared with patients in whom RPA showed no increase. Propranolol was more effective in patients with high PRA than the other agents. The best nifedipine tolerance was recorded in patients with lower PRA.
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PMID:[Changes in the renin-angiotensin system and the effectiveness of the treatment of hypertension with calcium antagonists, beta-adrenoblockers and diuretics]. 136 27

A prospective study was carried out on 12 patients with chronic hepatitis who were taking 546 mg/day of glycyrrhizin for 4 weeks in order to identify the factors responsible for the development of hypertension and hypokalemia. In 5 patients, blood pressure increased and serum potassium decreased after the treatment (responders). In the remaining 7 patients, these values were unchanged (nonresponders). There were no significant differences in age, plasma aldosterone, the catecholamine concentrations or serum transaminases. The basal plasma renin activity (PRA) in the responders was more than 1.5 ng/m/h (2.5 +/- 0.3 ng/m/h), while that in the non-responders was less than 1.5 ng/m/h (0.7 +/- 0.1 ng/ml/h). Furthermore, a positive correlation between the basal RPA and the changes in blood pressure, and a negative correlation between the basal PRA and the changes in potassium were found. These results suggest that patients with higher PRA levels are more likely to develop hypertension and hypokalemia when treated with glycrrhizin.
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PMID:Renin-dependency of glycyrrhizin-induced pseudoaldosteronism. 191 7

Analysis of examination and treatment of 104 patients who were periodically exposed to hemodialysis and 60 persons who sustained the allotransplantation of a cadaveric kidney enabled the authors to reveal the incidence of arterial hypertension before and after the transplantation. Pronounced arterial hypertension (AH) was documented in patients who were treated with hemodialysis sessions for the proper renal diseases developed in angionephrosclerosis (chronic glomerulo- and pyelonephritis). In those who sustained the transplantation, AH was pronounced in case of acute of chronic rejection, transplanted artery stenosis of renal renin hyperproduction. Higher incidence of AH (2.3-fold higher) was observed in posttransplantation patients with the native kidney left. It correlated with higher peripheral plasma renin activity (RRA). The authors suggested that the scheme should be used for the diagnosis of AH manifestation both before and after the transplantation which included the account for the cause of the disease terminal stage, the character of the AH variance in hemodialysis captopril testing, radiocardiographic examination, indirect renal angiography (99-Tc pertechnetate) or selective blood testing for RPA in case bilateral nephrectomy should be made in two stages. For the patients who had sustained the transplantation of the kidney, the diagnostic scheme should include a double pulse Doppler sonography, arteriographic investigation of the transplant and pharmacorenography with a captopril load test. Advisability of captopril stimulation of renin secretion during the selective sampling of the blood was demonstrated. The authors verified the time-course of renin activity, the concentration of aldosterone, cortisol and adrenocorticotrophic hormone in patients with a history of bilateral nephrectomy, defined the indications for bilateral nephrectomy associated with AH and discussed its possible outcomes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The diagnosis and treatment of arterial hypertension in patients on hemodialysis treatment and after a kidney allograft]. 220 67

In 16 patients with chronic aortic regurgitation, we studied the acute hormonal and hemodynamic effects of 12.5 to 25 mg captopril; in 12 patients the changes after a 4 to 8 week treatment period (mean 6.3 +/- 2 weeks; doses: 3 times 12.5 to 3 times 25 mg/day) were investigated. The following baseline variables were evaluated: the radionuclide left ventricular ejection fraction (EF) at rest and during exercise, left ventricular end-diastolic volume (EDV), regurgitant blood volume (RBV); and plasma renin activity (PRA). Repeated determinations of EF, EDV and RPA were carried out 90 minutes after application of the drug. In patients with chronic therapy, EF at rest and during exercise, EDV, RBV and PRA were reinvestigated at the end of the study. Acute administration of captopril was followed by an increase of EF (from 49 +/- 12 to 55 +/- 12%, p less than 0.001) and a slight decrease of EDV (from 389 +/- 160 to 376 +/- 146 ml, p less than 0.05). PRA significantly increased (from 1.6 to 3.1 ng/ml/h, p less than 0.05). Chronic therapy resulted in a moderate decrease of systolic and diastolic blood pressure (from 156/70 +/- 31/15 to 140/63 +/- 23/15 mm Hg, p less than 0.01). However, no significant changes were observed in EF at rest and during exercise (51 +/- 9 vs. 53 +/- 10% and 45 +/- 14 vs. 47 +/- 14%), EDV (433 +/- 179 vs. 422 +/- 179 ml) and RBV (136 +/- 81 vs. 129 +/- 77 ml). PRA was significantly increased (6.3 ng/ml/h, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of captopril in chronic aortic insufficiency]. 352 33

Three children with a Bartter's syndrome have been investigated: all of them had growth retardation, hypokalemia (less than 3 mmol/l), raised plasma renin activity and urinary prostaglandins (PGE2 and PGF2 alpha) and a decreased sensibility for angiotensin. In the siblings two children had also growth retardation with mild biological signs of Bartter's syndrome, and two children had normal growth slight hypokalemia raised RPA and urinary PH, and normal sensibility for angiotensin. These data suggest mild forms of this syndrome which could be the Bartter's syndrome diagnosed in adults after laxatives or diuretics absorption. Besides these data stated a negative correlation (p less than 0,01) between plasma K+ and RPA, negative correlation (p less than 0,01) between plasma K+ and urinary PGE2 and a positive correlation (p less than 0,01) between RPA and urinary PGE2. From these observations physiopathology of Bartter's syndrome is discussed.
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PMID:[Bartter's syndrome: seven cases in siblings. Hypothesis of mild forms (author's transl)]. 699 Mar 83

To investigate the relation between renin content in each juxtaglomerular apparatus and reduction of plasma renin activity (PRA) with aging, the PRA and microdissected superficial or juxtamedullary single nephron renin content (SNRC) were determined in 5 young (3-6 months) and 5 aged (13-18 months) rats fed on a normal salt diet. The mean value of the PRA in the aged group was significantly lower than that of the young group. A highly significant correlation was found between the RPA and mean values of the superficial SNRC. The mean values of both the superficial and deep SNRC in the aged rats were significantly lower than those of the corresponding zones in the young rats. It is suggested that decreased synthesis of renin in each juxtaglomerular apparatus is an important factor in the decreased PRA observed with aging.
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PMID:Effect of aging on single nephron renin content in rats. 702 86

Insulin-induced hypoglycemia by unknown mechanism(s) increases plasma arginine vasopressin (AVP) levels in humans. Mechanisms for increased AVP levels during central nervous system glucoprivation were investigated by administering 20-min i.v. infusions of 2-deoxy-d-glucose (50 mg/kg), a competitive inhibitor of glucose utilization, or normal saline (sham), to 24 normal volunteers. Some of the infusions were administered in combination with neuropharmacological blocking agents (placebo). The behavioral, physiological, metabolic, and hormonal correlates of 2-deoxy-d-glucose (2DG)-induced gluco-privation and AVP secretion were studied in a group (n = 5) pretreated for 1 wk with either mazindol (1 mg per os three times per day), a potent norepinephrine and dopamine-reuptake blocker, or placebo. A second group (n = 5) received either propranolol (3 mg/3 min followed by 80 mug/min) or normal saline infusion before and during 2DG administration. With 2DG alone, plasma AVP levels increased from 1.3+/-0.3 pg/ml at base line to a peak of 4.5+/-1.4 pg/ml at 60 min and remained elevated for 150 min. From 30 to 180 min after 2DG administration, the 2DG-infused volunteers increased their water intake in comparison with sham-infused volunteers. Marked increases in epinephrine and slight increases in norepinephrine were associated with increases in plasma glucose and renin activity and decreases in plasma potassium. Plasma sodium and osmolality increased transiently and mean arterial pressure (MAP) fell. These changes, however, were small and inconstant and could not account for the observed increases in thirst and AVP levels. Pretreatment with mazindol prevented the decrease in MAP and the increase in plasma renin activity (PRA) following 2DG infusions without modifying increased thirst, water intake, or AVP responses to glucoprivation. Pretreatment with propranolol effectively blocked beta-adrenoreceptors as evidenced by increased MAP and plasma epinephrine, and abolition of the RPA increases during 2DG-induced glycoprivation, but did not suppress AVP and thirst responses. A cervical cord-sectioned patient lacking descending sympathetic out-flow had a potentiated thirst response to 2DG-induced glucoprivation in the absence of increases in sodium, catecholamines, and PRA. Thus 2DG administration activates mechanisms for increased thirst and AVP which are unrelated to changes in peripheral catecholamines, MAP, PRA, and osmolality.
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PMID:Increased thirst and plasma arginine vasopressin levels during 2-deoxy-D-glucose-induced glucoprivation in humans. 720 69