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)

Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age- and sex-matched controls (p less than 0.02). PGF 2 alpha--excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p less than 0.001), while the increase in PGF 2 alpha-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167% +/- 11, SEM) than in the normotensive (386% +/- 46) group (p less than 0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.
 ...
PMID:[Reduced urinary prostaglandin E2-excretion and diminished responsiveness of plasma renin activity in patients with essential hypertension (author's transl)]. 45 71

In an attempt to provide information about the role of RAAS in development of late hyponatremia in low-birthweight neonates, simultaneous measurement of plasma renin activity, (PRA), plasma aldosterone concentration (PA), and urinary aldosterone excretion (UAE) was made using RIA methods along with determination of Na and K balance weekly up to the 6th week of life. Seven healthy male infants with mean birthweight of 1580 g, range: 1160-1850 g, and mean gestational age of 31 weeks, range: 30-32 weeks, were selected for the study. Due to the increased urinary Na loss, negative Na balance developed in the first 2 weeks followed positive balance thereafter. PRA, PA, and UAE increased tremendously from the initially high values of 18.2 +/- 4.1 ng/ml/hr, 1.7 +/- 0.5 ng/ml, and 2.6 +/- 0.4 microgram/day, mean and SEM, to their maximum of 78.6 +/- 18.1 ng/ml/hr, p less than 0.01, 6.8 +/- 3.7 ng/ml, p less than 0.05, and 26.4 +/- 2.9 microgram/dayp less than 0.01, in the 3rd week, respectively. Later on, gradual declines occurred, however, PRA, PA, and UAE remained highly elevated even at the 6th week with values of 45.5 +/- 15 ng/ml/hr, 1.6 +/- 0.5 ng/ml, and 14.5 +/- 1.4 microgram/day, respectively. It is suggested that late hyponatremia of premature infants is due to tubular unresponsiveness to aldosterone and not to inadequate response of RAAS to stimulation.
 ...
PMID:Postnatal development of renin-angiotensin-aldosterone system, RAAS, in relation to electrolyte balance in premature infants. 48 53

It has been shown that despite an effect of minoxidil to increase PRA, plasma levels of aldosterone do not change. We observed similar findings in seven hypertensive patients undergoing treatment with minoxidil; PRA activity increased markedly, whereas the plasma aldosterone concentration showed no consistent change. The aldosterone MCRs in these patients increased by 41% in response to minoxidil, from 1110 +/- 91 to 1570 +/- 180 (SEM) liters/day; this appeared to explain why plasma aldosterone levels did not increase in parallel with renin activity. Hepatic blood flow (estimated from the clearance of indocyanine green) in a group of patients receiving minoxidil was greater than that in an otherwise comparable group (P less than 0.02). This increase in hepatic perfusion may, at least in part, have accounted for the increase in aldosterone MCR.
 ...
PMID:Minoxidil increases aldosterone metabolic clearance in hypertensive patients. 51 74

The role of endogenous angiotensin II in the regulation of the circulation was investigated by infusion of [sar1],[ala8]-angiotensin II, a competitive antagonist of angiotensin II, into fetal sheep with chronically-maintained intravascular catheters. The thesis considered was that angiotensin II may have a greater role in the fetus than in the adult since the autonomic nervous system does not develop fully until late in gestation. Fetal cardiac output and its distribution to various organs and actual blood flows to fetal tissues were determined by the radionuclide-labelled microsphere technique. Intravenous infusion of [sar1], [ala8]-angiotensin II at a rate of 13.95-42.15 microgram/min per kg fetal body weight increased plasma renin activity from a control value of 8.9 +/- 1.6 to 18.9 +/- 3.9 ng/ml per h (SEM). Mean arterial blood pressure fell significantly from a control level of 47 +/- 1.6 to 41 +/- 1.1 mmHg. Blood flow to the unbilical-placental circulation decreased from 239 +/- 27.0 to 198 +/- 20.2 ml/min per kg, but the calculated vascular resistance in the umbilical-placental circulation did not change. Although cardiac output did not change, blood flow to the peripheral circulation, which includes the fetal skin, muscle and and bone and constitutes 75 +/- 0.9% of the total fetal body weight, increased as did flow to the thyroid and adrenal circulations. Endogenous angiotensin II appears to be important in maintaining blood flow to the umbilical-placental circulation by maintaining fetal arterial blood pressure. Angiotensin II exerts this effect by mediating a tonic vasoconstriction primarily in the peripheral circulation.
 ...
PMID:Effects of endogenous angiotensin II on the fetal circulation. 55 Nov 14

In 15 patients with severe chronic left ventricular failure, plasma renin activity (PRA) ranged widely, from 0.2--39 ng/ml/hr. The level of PRA was unrelated to cardiac output (CO) or pulmonary artery wedge pressure (PWP), but was slightly negatively correlated with mean arterial pressure (MAP) (r = -0.45) and systemic vascular resistance (SVR) (r = -0.40). After infusion of the angiotensin converting enzyme inhibitor teprotide (SQ 20,881) PWP fell from 26.3 +/- 1.3 (SEM) to 20.3 +/- 1.4 mm Hg (P less than 0.001), CO rose from 3.94 +/- 0.23 to 4.75 +/- 0.31 l/min (P less than 0.001), MAP fell from 87.5 +/- 3.8 to 77.9 +/- 4.1 mm Hg (P less than 0.001) and SVR from 1619 +/- 148 to 1252 +/- 137 dyne-sec-cm-5 (P less than 0.001). The fall in MAP and in SVR was significantly correlated with control PRA (r = 0.68 and r = 0.58, respectively). When subjects were divided on the basis of control PRA the hemodynamic response to teprotide was greatest in the high renin group. PRA rose after teprotide (8.7 +/- 3.4 to 37.9 +/- 7.7 ng/ml/hr, P less than 0.05) but plasma norepinephrine fell (619.1 +/- 103.6 to 449.7 +/- 75.7, P less than 0.05). The renin-angiotensin system thus appears to have an important role in the elevated SVR in some patients with heart failure. Chronic inhibition of converting enzyme should be explored as a possible therapeutic approach.
 ...
PMID:Role of the renin-angiotensin system in the systemic vasoconstriction of chronic congestive heart failure. 69 45

Five normal subjects took a low sodium diet for four days on two occasions, one with and one without added bromocriptine 2.5 mg three times a day by mouth. Daily measurements of urinary electrolytes and the concentrations of plasma renin (PRC), angiotensin II (AII), aldosterone, 18-hydroxycorticosterone, cortisol, electrolytes and prolactin were made in both phases of the study. Deprivation of sodium without bromocriptine resulted in progressive and highly significant increases in the plasma concentration of aldosterone from 230 +/- 50 to 418 +/- 44 (SEM) pmol/l, 18-hydroxycorticosterone from 627 +/- 138 to 1420 +/- 478 pmol/l, PRC from 108 +/- 38 to 166 +/- 14 muU/ml and AII from 16 +/- 3 to 29 +/- 4 pmol/l. Similar changes were found during bromocriptine administration despite suppression of prolactin secretion. Sodium deprivation together with bromocriptine resulted in increases in the plasma concentrations of aldosterone from 230 +/- 47 to 416 +/- 72 pmol/l, 18-hydroxycorticosterone from 630 +/- 99 to 1629 +/- 552 pmol/l, PRC from 105 +/- 12 muU/ml and AII from 14 +/- 3 to 26 +/- 5 pmol/l. Plasma cortisol did not change either in response to sodium deprivation or bromocriptine. Mean cumulative negative sodium balance was 101 +/- 14 mmol on bromocriptine and 118 +/- 14 mmol in the control period. We conclude that prolactin is not necessary for the steroidogenic response to sodium deprivation in man.
 ...
PMID:Bromocriptine: lack of effect on the angiotensin II and aldosterone responses to sodium deprivation. 69 48

Minoxidil-induced sequential changes in plasma renin activity, urinary aldosterone and norepinephrine excretion were assessed in 11 patients with severe hypertension receiving propranolol or oxprenolol, chlorthalidone and spironolactone. Blood pressure with this treatment alone averaged 175 +/- 7/114+/-4 mm Hg (mean +/- SEM). Addition of minoxidil in a dose of 5 to 35 mg/day (mean 16 mg/day) reduced blood pressure within one week to 125+/-5/87+/-3 mm Hg. Plasma renin, urinary aldosterone and norepinephrine increased two- to threefold initially, but returned to baseline within two weeks and remained unchanged during a mean follow-up of 6.8 months. In 6 patients beta-blocking drugs were then progressively reduced and withdrawn without adverse effects, though blood pressure and heart rate increased slightly in 5 patients who required readministration of minimal doses of beta-blockers. Neither renin nor urinary aldosterone or norepinephrine excretion changed significantly after discontinuation of beta-blockade. Thus, the stimulating effect of minoxidil on renin, aldosterone and norepinephrine secretion lasts less than 3 weeks. With long-term minoxidil treatment the need for beta-blockade is markedly reduced, and these drugs may even become unnecessary in some patients.
 ...
PMID:[Long-term minoxidil therapy: renin, aldosterone, noradrenaline and the need for beta blockers]. 71 7

Plasma renin activity (PRA) was measured during the administration of clonidine (0.1 mg twice daily) to 11 patients with essential hypertension. After eigth weeks a trend toward an increase in PRA was noted. This increase was significant in "low renin" subjects (less than 1 ng Al/ml/hr, n = 7) in whom PRA (ng/ml/hr +/- SEM) rose from a control value of 0.7 +/- 0.1 to 2.0 +/- 1.1 at one week, 5.6 +/- 2.1 at four weeks, and 4.4 +/- 1.0 at eight weeks (p less than 0.05). In contrast, in a small group of "normal renin" patients (n = 4), PRA did not change significantly but tended to decrease on clonidine therapy from 9.2 +/- 3.4 at control to 3.3 +/- 2.0 at one week, 3.4 +/- 0.6 at four weeks, and 4.7 +/- 1.7 ng Al/ml/hr at eight weeks. Plasma renin substrate and serum and urinary electrolytes did not change significantly in either group and blood pressure reduction was comparable in the two groups. A strong negative correlation (r = -0.84, p less than 0.001) was found between changes in creatinine clearance and changes in PRA. Previous studies have implicated alpha-adrenergic receptors as the site of clonidine actions on blood pressure and renin release. The observed renin stimulation during chronic administration of clonidine to "low renin" patients with essential hypertension may imply an altered intrarenal alpha-receptor function in "low renin" essential hypertension.
 ...
PMID:Renin stimulation during clonidine therapy in "low renin" essential hypertension. 72 16

We studied the relative rates of release of active and inactive renin by the kidney in anesthetized pigs. Renin concentration was determined in arterial and renal venous plasma as follows: (1) before and after stimulation of renin release with isoproterenol or furosemide, (2) after suppression of renin release by extracellular fluid volume expansion, and (3) after administration of propranolol or indomethacin. Inactive renin was activated by dialysis of plasma at pH 3.3 for 24 hours. Renin concentration was estimated by radioimmunoassay determination of angiotensin I after a 3-hour incubation with excess homologous renin substrate. Following isoproterenol, the release of active renin increased from 8 +/- 4 (SEM) to 58 +/- 34 ng/min, and inactive renin increased from 53 +/- 33 to 321 +/- 136 ng/min. Similarly, furosemide stimulated the release of both active and inactive renin. Both forms of renin were suppressed by propranolol or indomethacin. Although changes in renin release following volume expansion were not statistically significant, the direction of change for both forms of renin was similar. Following logarithmic conversion of the rate of release, the plot of active vs. inactive renin formed a straight line. Values for active renin as a percentage of the total renin in simultaneously drawn arterial and renal venous plasma samples were not different. Thus, under the conditions of these experiments, release of active and inactive renin appears to be controlled by similar mechanisms. Both stimulation and suppression of renin release result in parallel changes in release of the two forms. Data on relative amounts of active renin in arterial and renal venous plasma suggest that there is no systemic conversion of the two forms.
 ...
PMID:Release of active and inactive renin by the porcine kidney. 75 31

In patients with chronic renal failure (CRF) (CCr less than 20 ml/min), we have previously demonstrated greater rates of Na excretion (ex) when Na intake was nearly all NaHCO3 as compared to NaCl (both 200 mEq Na daily). Chloride (Cl) wasting on NaHCO3 (with severe Cl restriction) occurred, however, and may in part explain the results. To avoid Cl restriction in 6 patients with CRF (CCr 10-15 ml/min) on an estimated 10 mEq Na and Cl diet, electrolyte ex was compared on NaCl supplements of 200 mEq/day versus a daily mixture of NaHCO3 (100mEq) and NaCl (100 mEq). Periods on NaCl and the mixture lasted 4 days (order randomized) separated by re-equilibration to baseline weight (wt). Mean +/- SEM ex of Na, Cl, HCO3 mEq/day and CCr and deltawt (lbs) are compared below for the 4th day of NaCl vs NaHCO3 intake. (see article). Also there were no significant differences in K excretion, blood pressure, or plasma renin activities. Mean serum HCO3 increased from 21.2 to 25.8 mEq/l (day 1 vs 5, P less than 0.01) reflecting the net positive HCO3 balance on the mixture indicated above. Thus increments of Na intake above a fixed NaCl intake were excreted similarly whether given as NaCl or NaHCO3. Greater Na ex on NaHCO3 may depend on severe Cl restriction and/or higher serum HCO3 levels. If dietary NaCl intakes are near maximum tolerance, NaHCO3 supplementation should be accompanied by reductions in NaCl intake to maintain Na balance,
 ...
PMID:NaHCO3 and NaCl tolerance in chronic renal failure II. 83 32


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