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)

Vasoactive intestinal peptide (VIP) is released both by neural endings and lymphocytes. Aim of our investigation was to study the effects of immunosuppressive therapy on VIP plasma concentrations. The research has been performed on 10 heart transplanted patients assuming cyclosporine (CYCL) and prednisone (PRED). The circulating T lymphocyte subsets, atrial natriuretic peptide (ANP), plasma renin activity (PRA), plasma aldosterone (PA) and plasma cortisol (PC) have been also assayed. Blood pressure (BP) and heart rate (HR) have been monitored over a 24-hour period to detect whether circulating VIP in heart transplanted patients is influenced by pharmacologically-induced interactions. Seriate samplings along the 24-hour span have been performed. Mean values of ANP, PRA and PA were increased, while VIP, PC and T lymphocyte subsets were decreased in heart transplanted patients as compared to clinically healthy subjects. ANOVA and Cosinor analysis showed, respectively, a statistically significant 24-hour variability and circadian rhythm for all the investigated variables only in normal subjects. BP and HR circadian rhythm in heart transplanted patients suggest that the adrenergic activity regulating the cardiovascular system is restored. This finding argues that the reduction in VIP plasma concentrations is likely due to the decreased lymphocyte production secondary to immunosuppressive therapy, or can also be ascribed to the inhibiting action of high circulating levels of ANP.
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PMID:[The circadian rhythm of plasma vasoactive intestinal peptide, atrial natriuretic peptide, renin activity, aldosterone and cortisol in heart transplantation. The effects of immunosuppressive therapy]. 129 75

We assessed blood pressure and neurohumoral factors at rest and during exercise in 10 patients with essential hypertension before and after treatment with the new angiotensin converting enzyme inhibitor, alacepril (25-50 mg day-1). Alacepril significantly lowered mean blood pressure at rest and at the same exercise load as before treatment without affecting heart rate response. The response of plasma renin activity, plasma aldosterone, and plasma adrenaline were not changed by alacepril, but increase of plasma angiotensin II and plasma noradrenaline during exercise were significantly attenuated after alacepril treatment (ANOVA, P = 0.04, both). The change in mean blood pressure during exercise was positively correlated with the decrease in plasma angiotensin II (r = 0.65, P < 0.05). These results demonstrated that alacepril was effective in essential hypertension both at rest and during exercise, suggesting that the antihypertensive effect during exercise might be related to the decrease in pressor hormones, especially in plasma angiotensin II.
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PMID:Effect of alacepril on blood pressure and neurohumoral factors at rest and during dynamic exercise in patients with essential hypertension. 145 72

The cardiovascular and renin-angiotensin-aldosterone effects of cilazapril, a new angiotensin-converting enzyme (ACE) inhibitor was evaluated in healthy Caucasians in a double-blind, placebo-controlled, cross-over study. Cilazapril significantly inhibited plasma ACE activity, with a peak inhibition of 82% at 2 h and a residual inhibition of 41% persisting at 24 h. There was a biphasic and significant hypotensive effect, corresponding temporally to plasma ACE inhibition (P less than 0.02, ANOVA). The hypotensive action was not accompanied by reflex tachycardia. Plasma renin activity rose significantly as a consequence of ACE inhibition (P less than 0.05, ANOVA) but plasma aldosterone was unaltered. Cilazapril is a potent ACE inhibitor with a rapid onset and prolonged duration of antihypertensive and endocrine effects. Studies of the effects on ACE inhibition on the renin-angiotensin system in Africans are required.
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PMID:The cardiovascular and endocrine effects of cilazapril, a new angiotensin-converting enzyme inhibitor, in man. 213 3

Concentrations of sodium-transport inhibitors (STI) which block the sodium-potassium-ATPase pump are increased in the plasma and urine of volume-expanded and low-renin hypertensive humans and animals. To evaluate the physiologic relevance of STI to blood-pressure-raising mechanisms, we have examined the in vitro properties of STI extracted from the urine of human subjects. STI produced a significant (by ANOVA: P less than .01) dose-contraction response in the isolated rabbit femoral artery. Moreover, small noncontractile doses of STI in this in vitro preparation produced a fivefold leftward shift in the contraction dose-response curve of norepinephrine (P less than .01) and a threefold shift for angiotensin II (P less than .01); at lower, physiologic, concentrations of these vasoconstrictor hormones the amplifications in contraction caused by STI ranged from 100% to 500%. In studies in calcium-free tissue bath solutions, the direct contractile action of STI was abolished; however, its amplification of responses to norepinephrine remained, suggesting that this latter effect of STI is not entirely dependent upon calcium influx into vascular smooth muscle cells. The glycoside ouabain produced effects identical to those of STI in arteries, but its actions on a rabbit atrium preparation were different: ouabain stimulated powerful inotropic effects, whereas human STI failed to cause myocardial contractions even though the amounts of STI administered had the same sodium-transport inhibitory capacity as the ouabain. Thus, the actions of human STI are primarily in the peripheral circulation, where they directly produce arterial contractions and also enhance contractile responses to other pressor hormones, suggesting that they may have a role in regulating systemic blood pressure.
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PMID:Effects of a human-derived sodium transport inhibitor on in vitro vascular reactivity. 280 70

The hypotensive and hormonal effects of the angiotensin converting enzyme (ACE) inhibitor enalapril (10 mg twice daily) were compared with those of hydrochlorothiazide (25 mg twice daily), with the two drugs in combination and with placebo in 21 patients with essential hypertension. For each patient there were four randomised double-blind treatment phases, each of four weeks' duration, which comprised a 2 X 2 factorial experiment. All blood pressure parameters were reduced in the three active treatment phases compared to placebo (p less than 0.001). Supine mean blood pressures were 119 mmHg (placebo), 113 mmHg (hydrochlorothiazide), 108 mmHg (enalapril), and 98 mmHg (hydrochlorothiazide plus enalapril) (SEM 3 mmHg, ANOVA). Enalapril and hydrochlorothiazide were equally effective and well tolerated and their hypotensive effects were additive. Enalapril increased plasma renin activity (PRA), reduced plasma angiotensin II (AII) and aldosterone concentrations, and reduced ACE activity, whereas hydrochlorothiazide increased PRA, plasma AII, and aldosterone concentrations without altering ACE activity. With combination treatment the effects of enalapril on PRA and plasma AII concentrations were potentiated whereas those on plasma aldosterone concentration and ACE activity were additive. Atrial natriuretic factor plasma concentration in the placebo phase was 92 pg/ml and increased to 145 pg/ml in the hydrochlorothiazide phase (p less than 0.001, SEM 13 pg/ml), but there was no significant change in either the enalapril or combination phases.
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PMID:Effects of enalapril and hydrochlorothiazide on blood pressure, renin-angiotensin system, and atrial natriuretic factor in essential hypertension: a double blind factorial cross-over study. 302 94

Clinical and experimental studies suggest an association between low-level lead exposure and hypertension. This association was investigated in six 3-month-old dogs who were randomly paired with their littermates. The daily oral dose of lead acetate was 1.0 mg Pb/kg body wt for 5 months; the controls received equimolar sodium acetate. Blood pressure was measured indirectly without anesthesia and was similar in the two groups at the start of the study. The mean blood pressure was higher in the lead-exposed group at every follow-up, from 10 days to 20 weeks. This treatment group difference in profiles was statistically significant (repeated-measures ANOVA, p = 0.0048). The final mean blood pressures were 120 +/- 6.4 (x +/- SE) vs 108 +/- 1.5 mm Hg. At 4 weeks the plasma renin activity was higher in the lead-exposed group: 3.4 +/- 0.25 vs 1.2 +/- 0.15 ng/ml/hr. The difference decreased during the study but the elevated trend persisted (repeated-measures ANOVA, p = 0.014). Lead exposure did not alter renal functions or extracellular fluid volume. This study shows that low-level lead intake in young dogs can cause an early increase in blood pressure which persists during ongoing exposure and which is associated with a small increase in the activity of the renin-angiotensin system.
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PMID:Blood pressure elevation in young dogs during low-level lead poisoning. 328 20

In order to evaluate the effect of the angiotensin I-converting enzyme inhibitor, captopril, on lipid metabolism, we measured serum lipoperoxides concentration ( LPX ) as well as plasma levels of renin activity (PRA), aldosterone (PAC) and bradykinin ( PBK ) before and after captopril administration in 15 hypertensive patients. Captopril significantly lowered the LPX (p less than 0.05 by repeated measures ANOVA) from the control value of 3.25 +/- 1.16 (mean +/- S.D.) to 2.92 +/- 0.94, 2.83 +/- 1.10, and 2.89 +/- 1.31 nmol/ml 30, 60, and 120 min after the administration, respectively. A significant reduction of blood pressure (p less than 0.0001) and PAC (p less than 0.01) was observed following captopril administration, while PBK increased significantly (p less than 0.001) from a baseline level of 10.85 +/- 4.07 to 13.95 +/- 5.29, 16.25 +/- 6.85, and 15.71 +/- 7.65 pg/ml 30, 60, and 120 min after captopril administration, respectively. There was no significant correlation between changes in serum LPX and in mean blood pressure, PRA and PAC, though a significant inverse relationship was found between changes in serum LPX and in PBK 120 min after the administration (r = -0.576, p less than 0.05, n = 13). Although the mechanisms by which serum LPX is decreased by captopril are not clear, it is suggested from the results that captopril is a beneficial antihypertensive agent for preventing LPX -induced atherosclerosis in hypertensive patients.
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PMID:[The effects of the angiotensin I-converting enzyme inhibitor, captopril, on serum lipoperoxides level and the renin-angiotensin-aldosterone and kallikrein-kinin systems in hypertensive patients]. 637 99

FK506 can show efficacy in transplant rejection even after other immunosuppressive drugs have been ineffective. However, the lack of a suitable animal model has hindered the study of FK nephrotoxicity, which has been noted as a common adverse effect in human trials. In this paper, we report a model of chronic FK nephrotoxicity in which renal structure and function are worsened by sodium depletion. Pair-fed male Sprague-Dawley rats were given FK (6 mg/kg p.o.) or vehicle for 21 days on a low-salt or normal diet. There was no significant difference in body weight between FK and vehicle groups. The FK whole-blood trough levels (3-10 ng/ml) in rats are similar to those in FK treated transplant patients. In sodium-depleted rats, FK clearly decreased GFR (0.09 +/- 0.03 ml/min/100 g vs. 0.94 +/- 0.06 ml/min/100 g in the vehicle group, P < 0.01), urinary osmolarity (UOsm, P < 0.01) and plasma magnesium (P < 0.01) and increased plasma creatinine (Pcr, P < 0.01), fractional excretion of magnesium (P < 0.01), urine volume (P < 0.01), plasma renin activity (PRA, P < 0.05), and alanine aminopeptidase (AAP, P < 0.05) as compared with those in the vehicle group. Salt depletion significantly potentiated these functional changes as compared with those in the normal salt group (GFR, UOsm, Pcr, PRA, and AAP of the low salt group vs. those of the normal salt group, P < 0.05 by ANOVA). In the sodium-depleted rats, the main lesion in the rat kidneys was focal collapse and vacuolization in proximal tubules, but there was also significant interstitial fibrosis. In contrast, no injury was observed in the sodium-replete rat kidneys. In conclusion, an experimental model of FK nephrotoxicity in sodium-depleted rats has been developed that is characterized by reduced GFR and structural damage to the proximal tubule accompanied by interstitial fibrosis. Sodium depletion appears to potentiate these changes at blood levels similar to those achieved in patients receiving FK.
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PMID:Enhancement of FK506 nephrotoxicity by sodium depletion in an experimental rat model. 750 14

The present study examines the effects of dietary magnesium on the development of hypertension and hypertensive vascular lesions in deoxycorticosterone acetate and salt induced (DOCA-salt) and 2 kidney one clip (2K1C) hypertensive as well as normotensive control rats. Animals received a regular (0.12% Mg), high (0.4% Mg) or low (0.03% Mg) magnesium diet for 6 wks. Dietary magnesium did not alter the growth or blood pressure in control, DOCA-salt and 2K1C rats even though the plasma magnesium concentration was significantly altered by the diets (ANOVA, p < 0.05 in control, DOCA-salt and 2K1C, respectively). Dietary magnesium did not alter the urinary potassium excretion, plasma sodium, potassium, total calcium concentration and plasma renin activity in any group, while the high magnesium diet significantly increased the urinary sodium excretion in DOCA-salt (p < 0.05) but not in control and 2K1C rats when compared with the regular magnesium diet. In histological studies, dietary magnesium did not alter the percentage media area of intramyocardial arteries, or glomerular and renal arterial and arteriolar lesions in DOCA-salt and 2K1C rats. This study suggests that moderate alterations of dietary magnesium do not modify blood pressure in normotensive control, DOCA-salt and 2K1C hypertensive rats, nor do they modify vascular disease in these 2 hypertensive models.
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PMID:Effects of dietary magnesium on blood pressure and vascular lesions in hypertensive rats. 789 33

The purpose of this study was to assess the G-tolerance and G-induced changes in plasma renin activity (PRA), serum cortisol, testosterone, thyroid hormones and blood concentrations of serotonin and histamine. Experiments were performed on 26 student pilots aged 22.7 +/- 0.7 years using simulated aerial combat manoeuvres (SACM) in a centrifuge with radius 7.5 m. G-tolerance was assessed by loss of vision criteria, G-induced loss of consciousness and significant disturbances in heart rhythm. PRA, cortisol, testosterone and thyroid hormones were measured by radioimmunoassay, serotonin and histamine by spectrofluorimetric methods 24 hours before and 5 min after SACM. The statistical significance of hypergravitation and G-tolerance were determined by ANOVA. We found a significant increase in PRA (p = 0.001) and thyroxine concentration (p = 0.005) after hypergravitation loads. It is known that these changes are indicative for cardiovascular adaptation and enhancement of energy mobilization. Histamine levels differed significantly by G-tolerance (p = 0.031), while serotonin concentrations changed by hypergravitation (p = 0.004). Significant dependence on hypergravitation x G-tolerance was found for serotonin values (p = 0.024). Studying G-induced hormonal changes can reveal individual peculiarities in G-tolerance, a limiting factor for the exploitation of high performance aircraft.
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PMID:Changes in some biochemical and physiological indexes after hypergravitation. 802 24


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