Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chorionic cells are known to produce several protein hormones; among them is prorenin/renin, whose function is unknown at this time. Amnion is contiguous with chorion and plays a part in the mechanism(s) of parturition through increased prostaglandin (PG) production. The purpose of the present study was to determine whether renin has any action on amnion cell PGE2 biosynthesis. Amnion cells in primary monolayer culture were incubated for 16 h with increasing concentrations of renin. Renin induced a concentration-dependent increase in amnion cell PGE2 production (e.g. in picograms of PGE2 per microgram protein/16 h; mean +/- SEM; n = 4; control, 3.01 +/- 0.15; 0.0001 U/mL renin, 9.66 +/- 2.0; 0.001 U/mL renin, 10.36 +/- 1.91; 0.01 U/mL renin, 10.3 +/- 3.36; 0.1 U/mL renin, 13.82 +/- 2.1). Significant stimulation of amnion cell PGE2 by renin is not observed until 2 h of incubation; stimulation continues a further 6 h, with little change in the following 8 h. We tested the possibility that renin's stimulatory effects were due to angiotensin-I (AI) and angiotensin-II (AII) formation by testing the effects of AI and AII directly and that of renin in the presence of saralasin, a potent antagonist of AII action. Saralasin did not inhibit the effect of renin, nor was AI or AII alone (10(-10)-10(-6) M) stimulatory. Thus, we believe that chorionic renin may have a novel role in the regulation of amnion cell PGE2 production that is independent of angiotensin formation.
 ...
PMID:Renin increases human amnion cell prostaglandin E2 biosynthesis. 185 69

The captopril test was performed on 49 children of whom 36 were hypertensive, and the remainder were normotensive but were at risk for developing hypertension because of scarred kidneys secondary to vesico-ureteral reflux. Blood pressure (BP) was monitored in fasting supine patients throughout the duration of the test. Blood was taken for measurement of plasma renin activity (PRA); then captopril (0.7 mg/kg of body weight) was administered orally. A second blood sample was taken for PRA at 90 min postcaptopril. The mean (SEM) PRA at 90 min was 11.90 (4.01) ng/l/s [42.84 (14.44) ng/ml/h] in 7 patients with renovascular disease. In 4 patients with essential hypertension corresponding values were 0.88 (0.38) ng/l/s [3.17 (1.37) ng/ml/h]. Patients with other renal diseases showed variable values. Some individuals had PRA values as high as those of patients with renovascular disease, but the etiology of their hypertension was usually clinically evident. Our preliminary data would suggest that the captopril test may help differentiate between patients with essential hypertension and those with renovascular disease, or may help select patients that should be followed up by more definitive diagnostic procedures.
 ...
PMID:Use of the captopril test to assess renin responsiveness in children with hypertension and renal disease. 186 75

The response to the cold pressor test (CPT) was studied in 49 normotensive (NT) and 73 patients with essential sustained hypertension (HT). Patients were classified as responders when they increased their systolic pressure (SBP) by at least 16 mm Hg or their diastolic blood pressure (DBP) by at least 12 mm Hg. Forty-seven out of seventy-three (64%) increased their mean blood pressure (MBP) by 18.6 +/- 1.4 mm Hg (mean +/- SEM) in response to CPT. In NT subjects 23 out of 49 (47%) were responders (MBP = 16.3 +/- 1.3 mm Hg). In NT, but not in HT, patients, a negative relationship was observed between MBP changes during CPT and age (P less than .001) or basal DBP (P less than .01). There was no relationship between blood pressure response and the presence of a family history of hypertension. A positive correlation was found in HT patients between basal levels of active renin (AR) in the upright position and MBP changes during CPT (P less than .001). Mean plasma AR was 24.2 +/- 3.5 pg/mL in nonresponders v 37.5 +/- 2.9 pg/mL in responders (P less than .001). In HT, but not in NT, patients, blood pressure changes were associated with a simultaneous increase in HR (P less than .01 between delta MBP and delta HR). These results suggest that blood pressure elevation during CPT is a very common reaction in young normotensive subjects especially in those that have the lowest mean blood pressure. Therefore it is unlikely that CPT may be used as a predictor test of future hypertension in this population.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Response to the cold pressor test in normotensive and hypertensive patients. 187 19

Blockade of the renin-angiotensin system by an angiotensin converting enzyme (ACE) inhibitor or an angiotensin II (Ang II) antagonist is accompanied by a reactive rise in renin release. This rise is generally attributed to interruption of the short feedback loop between Ang II and renin release. Similarly, after the administration of a renin inhibitor, the plasma concentrations of active and total renin are increased and plasma renin activity is suppressed. The aim of the present study was to investigate if a fall in the plasma Ang II level is the unique determinant of the rise in the active renin (AR) level that follows renin inhibition. Six normal male volunteers participated in three successive 240-minute experiments at weekly intervals according to a single-blind randomized Latin square design. For experiment 1, Ang II was infused at 2 ng/kg/min from 0 to 60 minutes and at 4 ng/kg/min from 60 to 120 minutes. For experiment 2, 0.3 mg/kg of the new potent renin inhibitor Ro 42-5892 was injected at 30 minutes followed by infusion at 0.1 mg/kg/hr from 30 to 240 minutes. For experiment 3, Ang II and Ro 42-5892 were administered simultaneously at the same doses as described above. The mean +/- SEM Ang II concentration increased from 10.2 +/- 1.6 to 33.7 +/- 11.2 pg/ml after infusion of exogenous peptide. It decreased from 9.5 +/- 0.9 to 1.4 +/- 0.3 pg/ml after the injection of Ro 42-5892 and increased from 15.6 +/- 2.9 to 37.1 +/- 11.8 pg/ml after the simultaneous infusion of both compounds.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Renin release regulation during acute renin inhibition in normal volunteers. 188 41

Angiotensin II, when given in low doses, raises blood pressure slowly. When tested in vitro on vascular smooth muscle cells, it has mitogenic and trophic effects; it is not known if it has these effects in vivo. Our purpose was to determine whether vascular hypertrophy develops during slow pressor infusion of angiotensin II and, if so, whether it is pressure induced. Three experiments were done in rats infused subcutaneously with angiotensin II (200 ng/kg/min) by minipump for 10-12 days. Experiment 1: Angiotensin II gradually raised systolic blood pressure (measured in the tail) from 143 +/- 2 to 208 +/- 8 mm Hg (mean +/- SEM), significantly suppressing plasma renin and increasing threefold (NS) plasma angiotensin II. There was no loss of peptide in the pump infusate when tested at the end of the experiment. Experiment 2: In the perfused mesenteric circulation, vasoconstrictor responses to norepinephrine, vasopressin, and KCl were enhanced in rats given a slow pressor infusion of angiotensin II, but sensitivity of responses was not altered. This combination of changes suggests that vascular hypertrophy develops during slow pressor infusion of angiotensin II. Experiment 3: Vessel myography was done after angiotensin II infusion with and without a pressor response. Angiotensin II raised systolic blood pressure, increased heart weight, and produced myographic changes of vascular hypertrophy in the mesenteric circulation, increasing media width, media cross-sectional area, and media/lumen ratio. Hydralazine given with angiotensin II prevented the rise of pressure and the cardiac effect but not the vascular changes. Two-way analysis of variance showed that angiotensin II significantly increased media width, media cross-sectional area, and media/lumen ratio, all independent of hydralazine. Thus, although hydralazine inhibits the pressor and cardiac effects of angiotensin II, suggesting a pressor mechanism for the cardiac change, it does not inhibit structural vascular change, which suggests that at least part of the effect has a non-pressor mechanism.
 ...
PMID:Angiotensin II causes vascular hypertrophy in part by a non-pressor mechanism. 202 7

When the function of the renin system is inhibited, blood pressure becomes more dependent on changes in sodium and water balance. Diuretics alone and sodium restriction alone are additive to converting enzyme inhibitor therapy. However, it is not known if these two ways of reducing sodium balance are additive in the presence of established converting enzyme inhibition. We therefore performed a double-blind crossover study of the effects of moderate sodium restriction in 21 patients with essential hypertension who were already being treated with the combination of a converting enzyme inhibitor and a diuretic. After 1 month of captopril (50 mg twice daily) and hydrochlorothiazide (25 mg once daily) therapy, with their usual sodium intake, average supine blood pressure was 147/96 +/- 5/3 (SEM) mm Hg 2 hours after treatment. Patients then reduced their sodium intake to around 80-100 mmol/day for the remainder of the study. After 2 weeks of sodium restriction, they entered a double-blind, randomized, crossover study of Slow Sodium (100 mmol sodium/day) compared with Slow Sodium placebo, while continuing sodium restriction and the above treatment. During the double-blind study, after 1 month of treatment with captopril (50 mg twice daily), hydrochlorothiazide (25 mg once daily), and Slow Sodium placebo, supine blood pressure 2 hours after treatment was 138/88 +/- 4/2 mm Hg (24-hour urinary sodium 104 +/- 11 mmol). After 1 month of captopril (50 mg twice daily), hydrochlorothiazide (25 mg once daily), and Slow Sodium tablets, supine blood pressure 2 hours after treatment was 147/91 +/- 5/2 mm Hg (p less than 0.05; 24-hour urinary sodium 195 +/- 14 mmol).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Sodium restriction in hypertensive patients treated with a converting enzyme inhibitor and a thiazide. 204 42

The effects of oral zofenopril pretreatment were investigated in a chronic closed-chest pig model of ischemia and reperfusion. Pigs (25-35 kg) were pretreated orally with zofenopril (15 mg/day) on the 2 days prior to ischemia, which was evoked by the inflation of a catheter balloon in the left anterior descending coronary artery over 45 minutes. The catheter was then removed and the myocardium was reperfused. After 2 weeks, infarct properties were assessed by signal averaging of the body surface electrocardiogram and the inducibility of malignant ventricular tachyarrhythmias was tested with a programmed electrical stimulation protocol. A significant increase in the pressure-rate product (43 +/- 11%, mean +/- SEM), indicating the oxygen demand of the heart, was prevented by zofenopril (19 +/- 8%, p less than 0.05). Zofenopril reduced the peak efflux of adrenaline (1302 +/- 213 vs. 3201 +/- 760 pg/ml; p less than 0.05), noradrenaline (402 +/- 54 vs. 902 +/- 282 pg/ml; p less than 0.05), and of the adenosine catabolites inosine and hypoxanthine (56 +/- 4 vs. 78 +/- 9, pg/ml; p less than 0.05) in the coronary venous effluent. The efflux of the cytoplasmatic enzyme creatine phosphokinase was not significantly reduced after zofenopril (p = 0.08). No difference in plasma renin levels between the groups were found. After 2 weeks, late potentials were found only in the surviving animals from the untreated group, i.e., the voltage vector magnitude was more reduced, and a prolongation of the QRS duration and of the terminal low-amplitude part of the high-frequency QRS were found.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The effects of oral pretreatment with zofenopril, an angiotensin-converting enzyme inhibitor, on early reperfusion and subsequent electrophysiologic stability in the pig. 207 80

The captopril test was performed in 49 children of whom 36 were hypertensive, and the remainder were normotensive but at risk for developing hypertension because of scarred kidneys secondary to vesicoureteral reflux. The blood pressure was monitored in fasting supine patients throughout the duration of the test. Blood was taken for measurement of plasma renin activity (PRA), then captopril (0.7 mg/kg body weight) was administered orally. A second blood sample was taken for PRA measurement 90 min after captopril administration. The mean PRA at 90 min was 11.90 +/- (SEM) 4.01 ng/l/s (42.84 +/- 14.44 ng/ml/h) in 7 patients with renovascular disease. In 4 patients with essential hypertension, the corresponding value was 0.88 +/- 0.38 ng/l/s (3.17 +/- 1.37 ng/ml/h). Patients with other renal diseases showed variable values. Some individuals had PRA values as high as those of patients with renovascular disease, but the etiology of their hypertension was usually clinically evident. Our preliminary data would suggest that the captopril test may help differentiate between patients with essential hypertension and those with renovascular disease or may help select patients that should be followed up by more definitive diagnostic procedures.
 ...
PMID:Use of the captopril test to assess renin responsiveness in children with hypertension and renal disease. 208 87

Atrial natriuretic factor (ANF) may play a role in the regulation of the changes of blood volume and vascular reactivity during pregnancy and when pregnancy is complicated by hypertension. Reports of plasma ANF levels during pregnancy are conflicting. We have prospectively studied plasma ANF levels during pregnancy in 25 women, and compared these with 20 age-matched non-pregnant women. Five women developed hypertension during pregnancy and a further five who remained normotensive had insulin-dependent diabetes mellitus. Plasma ANF was 6.8 +/- 1.2 (mean +/- SEM) and 6.3 +/- 0.9 pmol/l during weeks 8-15 and 24-31 of normal pregnancy (n = 15; vs non-pregnant levels (4.0 +/- 0.6 pmol/l) P less than 0.05, n = 20). Levels were 4.3 +/- 0.8 and 3.9 +/- 0.4 pmol/l during weeks 16-23 and 32-39. In the diabetic patients and in the group who developed hypertension levels were at no time different from the uncomplicated pregnancy group. Serum aldosterone increased as pregnancy progressed, but plasma renin activity remained unchanged. As plasma ANF was not different between those who did, and those who did not develop hypertension, early measurement of it will not predict who will and who will not develop hypertension during pregnancy.
 ...
PMID:Plasma atrial natriuretic factor levels during normal pregnancy and pregnancy complicated by diabetes mellitus and hypertension. 214 May 86

Because the role of systemic hormones in the pathophysiology of edema in acute renal disease remains incompletely understood, we compared the levels of atrial natriuretic factor (ANF) and plasma renin activity (PRA) in patients with acute glomerulonephritis (AGN), nephrotic syndrome (NS), and normal individuals during salt deprivation and salt loading. Sixteen patients with AGN (10 males) and nine patients with NS and hypoalbuminemia (7 males) were studied on admission, and after recovery (12 AGN patients) or remission (4 NS patients). Eighteen normal controls were each studied after five days on a low (20 mEq Na/day), regular (120 mEq Na/day) and high (300 mEq Na/day) dietary salt intake. Patients with AGN and NS had comparable edema (AGN 2.8 +/- 0.53 kg; NS 3.36 +/- 0.47 kg; SE) and urinary Na excretion (mean +/- SEM: AGN 0.97 +/- 0.11 mEq/hr; NS 1.06 +/- 0.16 mEq/hr), but AGN patients had five times higher ANF (AGN 27.2 +/- 4.06 fmol/ml; NS 5.51 +/- 1.02 fmol/ml; P less than 0.001) and six times lower PRA ng/liter.sec levels (AGN 0.187 +/- 0.047; NS 1.144 +/- 0.222; P less than 0.001) than NS patients. The degree of edema was correlated with ANF levels in AGN patients (P less than 0.001) but not in NS patients. There was a strong exponential negative correlation (r = -0.773, P less than 0.0001) between ANF and PRA, in which AGN patients and Na-restricted controls were located in the opposite ends of the volume sensing-response, and NS patients in the middle, alongside controls with regular Na intake.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Atrial natriuretic factor in the acute nephritic and nephrotic syndromes. 214 29


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>