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

To evaluate the antihypertensive and hormonal effects of oral magnesium supplementation, 17 inpatients with untreated, uncomplicated mild-to-moderate essential hypertension (EH) and 8 age-matched normotensive controls (controls) were given MgO orally 3 times a day at a daily dose of 1.0 g (0.6 g per day as Mg) for a period of 2 weeks. Supplementation of MgO elicited a significant fall in averaged mean blood pressure calculated with a 24-h ambulatory blood pressure monitoring system (MBP) in EH from a baseline value of 104.3 +/- 12.2 to 99.5 +/- 11.6 mmHg (p < 0.05), while controls remained unaltered from a baseline value of 85.1 +/- 11.5 to 84.5 +/- 13.3 mmHg. The percentage reductions in systolic and diastolic blood pressures were similar during daytime and nighttime in EH. According to the extent of reduction in MBP with magnesium supplementation, EH patients were divided into 2 groups, responder and nonresponder. The level of plasma renin activity (PRA) in the responder group was significantly higher than that of the nonresponder group (p < 0.05). After 2 weeks of magnesium supplementation, the plasma level of Na+, K(+)-ATPase inhibitory activity (PATPI), defined as equivalency to ouabain, was reduced significantly from 0.75 +/- 0.54 to 0.40 +/- 0.30 mumol ouabain/ml (p < 0.05) in the responder group, while it remained unaltered in controls and the nonresponder group. PRA, plasma aldosterone concentration, urinary epinephrine and norepinephrine excretion, and urinary sodium excretion did not change significantly in either control subjects or EH (responder and nonresponder groups). A significant negative correlation existed between the pretreatment PRA and changes in MBP after magnesium supplementation in EH (r = -0.65, p < 0.01), and there was a significant positive correlation between changes in PATPI and changes in MBP as a whole (r = 0.41, p < 0.05). These results support the view that oral magnesium supplementation is a useful approach to treatment of patients with uncomplicated essential hypertension, especially those with high plasmas renin activity. It appears that magnesium suppresses circulating Na+,K(+)-ATPase inhibitory activity to attenuate vascular tone, and thereby reduces blood pressure in EH.
 ...
PMID:Effects of dietary magnesium supplementation on diurnal variations of blood pressure and plasma Na+, K(+)-ATPase activity in essential hypertension. 133 97

The antihypertensive effect of a non-sulfhydryl, long acting ACE (angiotensin converting enzyme) inhibitor, MK-421, was evaluated by administering a single dose of 10 mg to 13 patients with mild to moderate essential hypertension. The pharmacokinetic profile of MK-421 and its potent active metabolite, MK-422, was also assessed, together with the effect on the various components of the renin-angiotensin system. A single dose of MK-421 produced a significant fall in MBP from 2 to 24 hours post-drug. As could be expected, plasma ACE activity was suppressed up to 24 hours after MK-421. The half-life of MK-422, Cmax and [AUC]24(0) of MK-421 and MK-422 were measured. No significant change in plasma bradykinin or urinary excretion rate of kallikrein was observed, whereas a slight increase was observed in the urinary excretion rate of kinins after MK-421 in 8 patients. Significant correlations were observed between pretreatment PRA levels and the maximum fall in MBP.
 ...
PMID:Serum concentration and effects of a single dose of enalapril maleate in patients with essential hypertension. 298 51

The role of thromboxane on norepinephrine release mediated by the presynaptic alphareceptor is studied in conscious rabbits. Intravenous administration of yohimbine, a preferential alpha-2 receptor antagonist increases mean arterial pressure (MBP) by 10 to 15%; the plasma norepinephrine concentration by 71 to 125%. OKY-046, a specific thromboxane synthetase inhibitor, fail to affect the baseline levels as well as yohimbine-induced increases in the MBP and plasma norepinephrine. Yohimbine administration increased plasma renin activity by 27 to 41% which are not affected by OKY administration. These results indicate that the thromboxane system does not affect the norepinephrine release from the nerve terminals by the presynaptic receptor-mediated mechanism. The effect of thromboxane on the renin release is minor and the thromboxane system per se may not play an important role for the renal renin regulation.
 ...
PMID:Effect of thromboxane synthetase inhibitors on yohimbine-induced norepinephrine release in the circulation. 343 50

Pathophysiology of malignant hypertension, of which underlying disease was essential hypertension (EHT) in 33 cases and chronic glomerulonephritis (CGN) in 26 cases, was studied with reference to the renin-angiotensin system. Plasma renin activity (PRA) was significantly higher in the EHT than in the CGN group, and angiotensin II antagonist [Sar1, Ile8]angiotensin II (AIIA) induced a significant lowering of blood pressure only in the former group. PRA was linearly correlated with both pretreatment mean blood pressure (MBP, r = 0.474, n = 29, p less than 0.01) and serum creatinine (r = 0.540, n = 29, p less than 0.01) in the EHT group but not in CGN patients, although there was an inverse correlation between PRA and serum sodium in both groups. Multiple regression analysis revealed that PRA was independently related to MBP, serum creatinine, and serum sodium in the EHT group, but not in the CGN group. These results suggest that the renin-angiotensin system plays a significant role in elevating blood pressure and deteriorating renal function in malignant hypertension derived from EHT, but it is less important in CGN related hypertension.
 ...
PMID:Pathophysiology in malignant hypertension: with special reference to the renin-angiotensin system. 362

By using aprotinin, a potent kallikrein inhibitor, the role of kinin formation in the cardiovascular and renal effects of captopril was assessed in pentobarbital-anesthetized dogs previously undergoing hydrochlorothiazide treatment (2.5 mg/kg, p.o., b.i.d.) for 5 days. A fall in mean arterial pressure (MBP) from 117 +/- 8 to 94 +/- 6 mmHg followed i.v. administration of captopril, 1 mg/kg. A concomitant rise in renal blood flow (RBF) from 168 +/- 18 to 205 +/- 20 ml/min occurred without changes in glomerular filtration rate (GFR) and with cardiac output tending to decrease. Urine flow (V) tended to rise while Na+ and K+ excretion were variable. With i.v. infusion of aprotinin (900 KIU/min) the hypotensive response to captopril was unaffected (from 103 +/- 5 to 75 +/- 8 mmHg) suggesting that captopril decreases BP independent of kinin accumulation. However, aprotinin completely abolished the renal vasodilator response to captopril (from 163 +/- 25 to 143 +/- 22 ml/min). In addition, there was a concomitant fall in GFR, V and electrolyte excretion. In comparison, the cardiovascular and renal effects of saralasin (3 micrograms/kg/min, i.v.) were not altered by aprotinin. It is, therefore, concluded that, in dogs with stimulated renin-angiotensin system, the plasma kinins do not contribute to the hypotensive action of captopril but play an important role in inducing renal vasodilatation and supporting kidney function.
 ...
PMID:Effect of aprotinin-induced kallikrein inhibition on the cardiovascular and renal action of captopril in diuretic-treated dogs. 619 27

The changes in haemoglobin concentration, haematocrit, plasma renin activity (PRA) and atrial natriuretic peptide (ANP) were studied in 10 haemodialysis patients with erythropoietin-associated hypertension. All patients received intravenously 1500 IU of recombinant human erythropoietin (rHuEPO) thrice weekly for 24 weeks. Treatment with rHuEPO induced significant rises in haemoglobin concentration (p < 0.001) and haematocrit (p < 0.01). However, the difference between post- and pretreatment levels of haemoglobin (delta Hb) was not correlated with that between post- and pre-treatment mean blood pressure (delta MBP). No correlation was found between delta Ht (difference between post- and pre-treatment values of haematocrit) and delta MBP. These results indicate that elevation of the haematocrit and haemoglobin concentration of haemodialysis patients does not necessarily lead to an increase in blood pressure. In these patients, no significant differences were observed in PRA and ANP, comparing pre-treatment values with those measured 4, 8, 12 or 24 weeks after commencing rHuEPO. This suggests that neither PRA nor ANP play a central role in the pathogenesis of rHuEPO-induced hypertension.
 ...
PMID:Change in haemoglobin concentration, haematocrit and vasoactive hormones in haemodialysis patients with erythropoietin-associated hypertension. 803 37

Diurnal changes in plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA) and plasma aldosterone as related to those in blood pressure (BP) were studied under hospital conditions in 18 diabetic subjects without proteinuria and 8 age-matched control subjects. Of 18 diabetic subjects, 10 had a normal diurnal BP rhythm with the peak value in the afternoon (group 1) and 8 had a reversed BP rhythm with the peak value during the night (group 2). Autonomic dysfunction estimated by measuring orthostatic BP and heart-rate changes and beat-to-beat heart-rate variations was more pronounced in group 2 than in group 1. Fasting plasma glucose and HbA1c were similarly high in both diabetic groups. Group 1 showed modestly elevated mean 24-h MBP and plasma ANP levels, modestly low mean 24-h PRA and plasma aldosterone levels, and a lack of diurnal ANP changes similar to that in controls. Group 2 showed markedly elevated mean 24-h BP and plasma ANP levels, markedly low mean 24-h PRA and plasma aldosterone levels, and nocturnal rises in plasma ANP and BP. PRA and plasma aldosterone exhibited circadian rhythms with their peak values found in the early morning in all three groups. The daytime/overnight excretion ratios of sodium and water were normal in group 1 and low in group 2. These results indicate that diurnal changes in plasma ANP, PRA and plasma aldosterone are altered in diabetic subjects with normal and reversed diurnal BP rhythms, predominantly in the latter.
 ...
PMID:Association of a nocturnal rise in plasma alpha-atrial natriuretic peptide and reversed diurnal blood pressure rhythm in hospitalized normotensive subjects with non-insulin dependent diabetes mellitus. 807 89

Sequential changes in renin-aldosterone secretions and blood pressure (BP) response during acute sodium (Na) loading were studied in 50 patients with essential hypertension (EH) and nine normotensive volunteers. Following an infusion of 2 L of isotonic saline at a rate of 500 mL/h, plasma renin activity (PRA) and the plasma aldosterone concentration (PAC) were similarly suppressed, while sodium excretion appreciably increased in hypertensive as well as normotensive subjects. When patients were divided into two subgroups according to the extent of renin suppression, 26 were classified as adequate responders with the proportion of decrement of PRA at the end of the infusion exceeding 50% of the baseline values, while 24 were inadequate responders with a decrement of less than 50%. The extent of renin suppression was consistently greater in adequate responders than in inadequate responders throughout the course of infusion. Adequate responders also had a higher pre-saline PRA and attained a smaller post-saline natriuretic response than inadequate responders. Although the mean BP in both subgroups remained stable at all periods, inadequate responders had a minor but significantly higher percent of increment of MBP at the end of the infusion than adequate responders (3.6 +/- 2.0 vs -1.7 +/- 1.4%, p < 0.05). These results suggest that renin suppressibility during acute Na loading may be either linked with maintenance of BP homeostasis or may merely reflect the sodium-volume status of essential hypertension, with patients with greater suppression of renin being more Na-volume resistant than those with less inhibition.
 ...
PMID:Renin suppressibility and blood pressure response during acute sodium loading in patients with essential hypertension. 810 77

In this study the efficacy and safety of short-term amlodipine administration on renal haemodynamics were evaluated in mild to moderate hypertensive subjects. Our final goal was to evaluate whether the reduced blood pressure induced by treatment was associated with maintenance of renal function. After a run-in period with placebo, 30 hypertensive patients without cardiac or renal diseases were randomly allocated to a double-blind 4 weeks controlled study with amlodipine 10 mg once a day (15 patients) or placebo (15 patients). Renal haemodynamic measurements included effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) by radionuclide study using 131I-hippuran and 99mTc, with methods described by Schlegel and Gates, respectively. In addition, effective renal blood flow [ERBF = ERPF/(1-Ht)], filtration fraction (FF = GFR/ERPF) and renal vascular resistance (RVR = MBP x 80/ERBF) were calculated. Plasma renin activity (PRA), serum aldosterone (ALD) and urinary excretion of sodium (NaU) were evaluated. At the end of amlodipine administration a significant decrease (P < 0.001) in SBP, DBP and MBP from baseline values was observed. A significant decrease (P < 0.01) in RVR and significant increases (P < 0.05) in ERPF, ERBF and in NaU were also found, without relevant changes in GFR, FF, PRA and ALD. No significant variation in clinical and renal measurements was observed in the placebo group. No relevant side effects were observed in either group. In conclusion, amlodipine was effective in lowering blood pressure in mild to moderate hypertension and exerted favourable effects on renal haemodynamics and function.
 ...
PMID:Effects of amlodipine on renal haemodynamics in mild to moderate hypertensive patients. A randomized controlled study versus placebo. 829 61

The aim of this work was an evaluation of the effect of the acute hypervolemia induced by 90 min intravenous infusion of 1500 ml 0.9% NaCl (16.7 ml/min) on blood pressure, plasma concentration of the atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP), aldosterone (ALDO), plasma renin activity (PRA) in patients with essential hypertension on the normal, low and high sodium intake. Twelve patients with noncomplicated essential sodium-sensitive arterial hypertension participated in the study. Sodium chloride infusions were performed three times: first--on the fifth day of normal daily sodium u intake (110-120 mmol/day), second--on the fifth day of low sodium intake (10-20 mmol/day), third--on the fifth day of high sodium intake (200-220 mmol/day). Acute intravenous sodium chloride load induced a significant increase of the mean arterial pressure (MBP) only when the patients were on the high sodium diet. This increase of the MBP was associated with a significantly lower increment of plasma ANP, cGMP, lower decrement of ALDO and PRA when compared to normal- or low- sodium intake. The results suggest an impairment of the adaptive homeostatic mechanisms induced by an acute intravenous sodium load in patients with noncomplicated salt-sensitive essential hypertension ingesting high-sodium diet.
 ...
PMID:[Effect of intravenous sodium chloride load on levels of atrial natriuretic peptide (ANP) and 3'5' guanosine monophosphate (cGMP) in plasma of patients with uncomplicated sodium-sensitive arterial hypertension maintained on different dietary sodium intake]. 838 45


1 2 Next >>