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)

Acute renal failure (ARF) was produced by the single intraperitoneal injection of 3 mg/kg mercuric chloride (HgCl2) in male Wistar rats. Immediately after, and in the 1st, 3rd, 6th, 24th and 48th hour after HgCl2 administration the following variables were monitored: plasma renin concentration (PRC), renal renin concentration (RRC) blood-urea nitrogen (BUN), plasma sodium (PNa), plasma creatinine (PCr) concentrations and haematocrit (Ht). Haematocrit and PNa increased during the first hour and returned to the control value in the 3rd hour. Thereafter, their level remained unchanged. Plasma renin concentration increased threefold during the first six hours after the HgCl2 injection, however, by the 48th hour it returned to the control value. In the first 24 hours of ARF, RRC remained unchanged. However, by the 48th hour its level increased four times the control value. After mercury injection BUN and PCr increased progressively. We were not able to establish any significant correlation between the changes of PRC and BUN. A gradual increase of RRC was observed in the course of ARF.
 ...
PMID:Changes of plasma renin and renal renin concentration in HgCl2 induced acute renal failure in rats. 39 61

In this study, rats recovering from glycerol-induced acute renal failure were found to be protected from mercury-induced nephropathy, and HgCl2 poisoning protected rats from developing myohemoglobinuric renal failure. In view of the widely disparate nature of the renal failure models used, refractoriness appears to relate to an altered sensitivity of the organism itself rather than reflecting resistance to a particular nephropathic challenge. Renal renin content of the rats at the time of rechallenge was normal or high, a finding which contrasts sharply with that of chronically saline-loaded animals which also are refractory to ARF but have a maximally suppressed renal renin content. Renal renin depletion is not essential to the prevention of acute renal failure in the rat.
 ...
PMID:Resistance to acute renal failure afforded by prior renal failure: examination of the role of renal renin content. 115 48

To evaluate the role of the proposed baroreceptor mechanism in the afferent arteriole in regulating renin release, we modified the isolated perfused tubule technique to perfuse afferent arterioles. Arterioles with attached glomeruli were isolated from rabbit kidneys and perfused using standard methods. To stop the arteriolar flow and allow perfusion pressure, as set by a mercury manometer, to be built up in the lumen of the vessel, the glomerulus was sucked into a constriction pipette. The preparation was continuously superfused with Krebs-Ringer solution in the first series of experiment, and a cell culture medium in the second series of experiment. The superfusate droplets were collected under mineral oil with 10-min collection intervals. The renin content of the samples was assayed by radioimmunoassay of the angiotensin I generated. In the two series of experiments we tested the effects of sequential changes in intraluminal pressure on renin release. In the first series of experiments (n = 6) the renin release was 56.3 nGU arteriole-1 min-1 in the first 10 min of sampling. The renin release was then constant for 80 min with an average of 21.6 nGU arteriole-1 min-1. In the last 30 min the renin release was 96.5 nGU arteriole-1 min-1. In the second series of experiments (n = 8) the renin release was 26.5 nGU arteriole-1 min-1 throughout the course of the experiment. These results indicate that under these conditions there is no relation between renin release and intraluminal pressure in afferent arterioles.
 ...
PMID:Lack of effect of intraluminal pressure on renin release from isolated afferent arterioles. 146 16

Male weanling Wistar rats received 200 micrograms/ml of mercury (Hg), as HgCl2, in drinking water for 180 days. At the end of the treatment, systemic arterial blood pressure was augmented, cardiac inotropism was reduced, and heart rate was unchanged. Light and electron microscopical studies of the kidney showed a mesangial proliferative glomerulonephritis in about 80% of the glomeruli. Tubular cells showed reduction of the acid phosphatase activity, which was related to functional abnormalities of the lysosomes. In the 24 hour urine samples of the Hg exposed rats, there was slight reduction of kallikrein activity, but evident proteinuria was not present in all samples. Plasma renin activity was reduced, that of angiotensin I-converting enzyme was augmented, and plasma aldosterone concentrations were unchanged. Mercury was accumulated mostly in the kidney of the Hg treated animals; and the content of Hg in the heart was higher than in the brain. These data show that chronic exposure to Hg acts on the kidney with complex mechanisms of toxicity; these contribute to modify systemic haemodynamics.
 ...
PMID:Renal mechanisms in the cardiovascular effects of chronic exposure to inorganic mercury in rats. 157 Dec 92

The influence of different vasoactive substances on the evolution of HgCl2-induced acute renal failure (ARF) was evaluated in the dog. HgCl2 alone caused a progressive fall in both glomerular filtration (GFR) and renal blood flow (RBF) during the first 3 h of the mercury administration (delta after 3 h: -44% and -39%) and provoked a concomitant stimulation of the renin-angiotensin (RAS) and thromboxane systems. The administration of the thromboxane inhibitor dazoxiben (2 mg/kg i.v. every 2 h) adequately inhibited the activation of the thromboxane system after HgCl2, but could not prevent the fall in GFR and RBF. The continuous intrarenal administration of the Ca2+ entry blocker verapamil (0.005 mg/kg per min) into the left kidney resulted in the prevention of the postmercurial fall in GFR and RBF at the perfusion site. This beneficial effect was immediately lost when the verapamil administration was stopped. Finally, the administration of the converting enzyme inhibitor captopril (300 micrograms/kg every 2 h) resulted in an effective inhibition of the renin-angiotensin system, the prevention of the postmercurial fall in RBF, and the partial attenuation of the fall in GFR. This beneficial effect was immediately lost after the intravenous administration of indomethacin (2 mg/kg). These results indicate that the fall in GFR after HgCl2 can be prevented by vasoactive agents such as captopril and verapamil and point at least in part to a pathophysiological role of the renin-angiotensin system or of an alteration in the equilibrium between renin-angiotensin and prostaglandins. The thromboxane system is seemingly of no major importance.
 ...
PMID:Influence of vasoactive substances on early toxic acute renal failure in the dog. 312 11

Abnormalities of renin release and of venous distensibility have been described in essential hypertension. We have postulated that decreased venous distensibility could contribute to the blunted renin response to upright posture in hypertension. Stiffer veins might prevent venous pooling in the lower extremities, which in turn might affect the stretch on cardiopulmonary mechanoreceptors, thereby influencing the reflex release of renin. We investigated this hypothesis in the present study of 47 patients with mild hypertension and 26 (male) healthy volunteers of similar age and race. To induce isolated changes in the stretch of cardiopulmonary mechanoreceptors, systemic hemodynamics were measured before and after thigh cuff inflation at 60 mm Hg for 30 minutes. Cardiac output was determined by dye dilution. Before the intervention, variable thigh cuff pressures were used to measure venous pressure volume with mercury-in-Silastic strain gauge plethysmography. Venous distensibility was diminished in hypertension, as evidenced by a shift in the calf venous volume/pressure curve toward the pressure axis. During the 30-minute experiment, the hypertensive subjects had less blood pooling in their legs in response to thigh cuff inflation, as compared with the control subjects. The hemodynamic and renin responses reflected this diminished effect of thigh cuff inflation on venous return. The smaller increase of renin in the hypertensive group was associated with a smaller fall in the stroke index and right atrial pressure; the reflex rise in the heart rate was also decreased. By pooling blood in the lower extremities, thigh cuff inflation simulates upright posture. It is customary to classify the renin status of hypertensive patients according to the renin response to upright posture.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Decreased venous distensibility and reduced renin responsiveness in hypertension. 352 19

The authors have studied the effects of Nitrendipine, orally given in a dose of 20 mg, once a day for 30 days, in patients with mild to moderate hypertension. Twelve patients initially entered the study but four of them discontinued the treatment during the first week, because of unwanted side-effects: headaches, palpitation, sensations of burning skin. The remaining eight patients underwent a comparative evaluation at the end of a placebo period (DO) and at the end of the active treatment (D30), including successively: an automatic blood pressure recording with a Bard-Sentron device for 3 hours, then a determination of plasma renin activity, aldosterone and catecholamines, and finally a measurement of the blood pressure with a mercury manometer, at rest and during a standardized exercise on an ergometric bicycle. At D30, the Nitrendipine tablet was given one hour after the beginning of the automatic recording. The blood pressure measured with the mercury manometer (i.e. approximately 2 hours after the dose of Nitrendipine) significantly decreased from D0 to D30, at rest and during exercise, respectively from 161.5/104.6 to 132.8/82.5 mmHg and from 210.0/116.8 to 190.0/95.6 mmHg. The automatic recording provided, at D0, a mean blood pressure value of 152.4/90.6 mmHg; at D30, this mean value was as high as 142.6/90.7 mmHg during the hour preceding the dose of Nitrendipine (NS) and as high as 129.2/78.6 mmHg during the 2nd hour following the intake of the tablet (p less than 0.01). Plasma aldosterone and plasma renin activity significantly (p less than 0.05) increased from D0 to D30, whereas catecholamines did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Evaluation of the antihypertensive effect and tolerability of a new delayed-action calcium channel blocker: nitrendipine, prescribed as a single daily dose of 20 mg]. 381 62

The new angiotensin converting enzyme inhibitor enalapril (MK-421), was given in a single daily dose of 20 mg to 53 patients with uncomplicated essential hypertension. Its effects were compared with those of a placebo given to 47 patients on a double-blind randomized basis. The blood pressure was measured in all patients by a physician, using a mercury sphygmomanometer, and by an automatic device in the absence of the physician. After 15 days of treatment, enalapril induced a significant reduction in systolic blood pressure (161.4 +/- 13 versus 145.1 +/- 15, p less than 0.001) and in diastolic blood pressure (103.3 +/- 6 versus 92.9 +/- 8, p less than 0.001) measured by the physician. The magnitude of the fall in blood pressure was identical after 30 days of active treatment. The reduction in blood pressure induced by enalapril was similarly detected by both methods of measurement, despite the fact that blood pressure values were higher when measured by the physician. A placebo effect was observed with the physician's values that was not present with the automatically recorded values. A very significant correlation between blood pressure values obtained by these two methods was observed. However, among nine of 53 patients treated with enalapril, a difference in the decrease of blood pressure of 10 mm Hg or more was noted between the two methods of measurement. The decrease in blood pressure occurred with no change noted in the pulse rate or orthostatic hypotension. Plasma renin activity increased after treatment. No changes were observed in creatinine clearance and plasma electrolyte levels.
 ...
PMID:Antihypertensive effect of enalapril as first-step treatment of mild and moderate uncomplicated essential hypertension. Evaluation by two methods of blood pressure measurement. 608 55

Pepstatin, a specific inhibitor of pepsin, cathepsin D (E), renin, etc., was used in a new method to demonstrate the sites of enzymes. Pepstatin (Pst) was covalently attached to glutathione (GSH), using a dicyclohexylcarbodiimide, and CH3Hg+ was then put in the residue of SH for electron microscopic observation. Pst-GS-HgCH3 thus obtained was nonisotopical, had a very low molecular weight (about 1,200 daltons), and still almost completely retained its inhibitory activity. Sections of rat liver (less than 1 mm3 thick), prefixed by glutaraldehyde, were incubated in the prepared reaction medium. Cathepsin D, located in the lysosomes, was demonstrated by this compound, but when the sections were preincubated with pepstatin, this was not the case. These results demonstrate that mercury-labeled pepstatin is a useful reagent for the histochemical staining of acid proteases for electron microscope.
 ...
PMID:Electron microscopic visualization of cathepsin D using mercury-labeled pepstatin as an enzyme inhibitor. 715

Many patients with essential hypertension respond to a high dietary sodium intake with a rise in blood pressure. Experimental evidence suggests that the renal hemodynamic response to sodium determines, at least partially, this rise in blood pressure. Our aim was to clarify the role of the renin-angiotensin system in the renal and systemic adaptation to a change in dietary sodium. We studied changes in mean arterial pressure (MAP) (millimeters of mercury), effective renal plasma flow (ERPF), body weight, and immunoreactive renin in 17 patients with essential hypertension and 15 normotensive control subjects, randomly crossing over between a 3-week sodium-restricted (50 mmol/24 h) and a sodium-replete (200 mmol/24 h) diet period. In addition, the effects of renin inhibition by remikiren (600 mg, single oral dose) were studied during the high sodium period. In normotensive control subjects, high sodium intake had no effect on MAP or body weight, whereas ERPF increased (490 +/- 19 to 535 +/- 21 mL/min, P < .05) and immunoreactive renin decreased (32 +/- 6 to 14 +/- 1 pg/mL). In hypertensive subjects, high sodium intake induced a heterogeneous response of MAP (median change, 2.6 mm Hg; range, -4.7 to +21.2; P = NS) and ERPF (median change, 21 mL/min; range, -33 to +98; P = NS). Body weight increased from 81.3 +/- 1.9 to 82.5 +/- 2.0 kg (P < .05), and immunoreactive renin decreased from 18 +/- 3 to 10 +/- 1 pg/mL (P < .05). Interestingly, the patients with a distinct rise in MAP showed a blunted ERPF response to high sodium intake (r = -.70, P < .01) and an increase in body weight (r = .76, P < .001). Moreover, the increase of ERPF was more pronounced in patients with a larger fall in immunoreactive renin (r = .77, P < .001). After administration of remikiren, a heterogeneous response in ERPF was observed: the patients with the blunted ERPF response to high sodium intake showed the largest ERPF rise (r = .70, P < .01). The remikiren-induced rise in ERPF correlated (r = .68, P < .01) with the fall in MAP (114 +/- 2 to 110 +/- 2 mm Hg). In conclusion, in patients with essential hypertension a rise in blood pressure in response to high sodium intake appears to partially be the result of insufficient renal vasodilatation. This seems to be due to an inadequate (intrarenal?) renin-angiotensin system response to increased sodium intake.
 ...
PMID:Does the renin-angiotensin system determine the renal and systemic hemodynamic response to sodium in patients with essential hypertension? 895 5


1 2 3 Next >>