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)

Six patients with essential hypertension underwent a randomized cross over design study to investigate the effect of supplementing a 10 mmol/day sodium diet for a period of 5 days with either 120 mmol sodium chloride (Slow Sodium, Ciba, Horsham, UK) or 122 mmol sodium in the presence of other anions, mainly phosphate (Phosphate, Sandoz, Feltham, UK). With both sodium salts, urinary sodium excretion was increased. The calculated amount of sodium retained was similar for both the sodium chloride and sodium phosphate periods. However, with the addition of sodium chloride to the low-salt diet, there were increases in supine mean blood pressure whereas with the addition of sodium phosphate no change in mean blood pressure occurred. The supine mean blood pressure after supplementation with sodium chloride (119.8 +/- 4.3 mmHg) was significantly greater than that after sodium phosphate (113.3 +/- 4.5 mmHg), similarly, the standing mean blood pressure was greater after addition of sodium chloride than of sodium phosphate (122.3 +/- 4.20 versus 115.4 +/- 3.0 mmHg). With both salts there were similar but non-significant increases in weight and reductions in plasma renin activity (PRA) and plasma aldosterone (PA).
 ...
PMID:A randomized crossover study to compare the blood pressure response to sodium loading with and without chloride in patients with essential hypertension. 318 67

Fischer 344 rats show no spontaneous preference for isotonic sodium chloride (NaCl) solution. These experiments indicate, however, that a strong appetite for this solution may be induced by various methods, including adrenalectomy, administration of a mineralocorticoid hormone, acute depletion of sodium, and treatment with inhibitors of the angiotensin I converting enzyme (ACE). These treatments were also shown to produce the expected changes in the renin-angiotensin-aldosterone system, which thus appears to be involved in the induction of an appetite for NaCl solution in this strain of rat. The intakes of NaCl induced in the Fischer 344 rats by these experimental paradigms are less than those that have been reported in either Sprague-Dawley or Wistar strains in similar paradigms. In the case of sodium depletion, the intake of NaCl solution by Fischer 344 rats appears to be more closely related to the deficit than in the other two strains. Thus, the Fischer 344 strain of rats may be a particularly good model for studies of need-related sodium appetite.
 ...
PMID:Induction of an appetite for sodium in rats that show no spontaneous preference for sodium chloride solution--the Fischer 344 strain. 321 43

The acute administration of ANG II into the brain of experimental animals produces transient pressor effects, a marked increase in drinking, release of the antidiuretic hormone, increase in total peripheral resistance, a diuretic and natriuretic effect and an increase in sympathetic outflow. The chronic administration of ANG II into a cerebrolateral ventricle produces sustained pressor effects only if 0.9% sodium chloride solution is used as the drinking fluid. The hypertension is due to an increase in total peripheral resistance which appears to be due to an increase in intrinsic tone of vascular smooth muscle. In addition there was enhanced responsiveness of the vasculature to norepinephrine and ANG II and a decrease in reflex vasodilatation of the hind limb of ANG II treated dogs. The chronic elevation of ANG II in the CSF plus an increase in NaCl intake produces a low renin, sodium dependent, expanded volume hypertension. Data are presented suggesting that this model of hypertension is induced by the central release of an inhibitor of the Na+,K+-Pump.
 ...
PMID:The central effects of the renin-angiotensin system. 328 Jan 70

Intracellular sodium, potassium, and free calcium concentrations were investigated in lymphocytes of 30 patients with essential hypertension and 30 normotensive controls. All subjects were placed on a diet containing 8 to 10 g of sodium chloride per day. Lymphocyte sodium concentration was higher in hypertensive patients than in normotensive controls (19.8 +/- 1.8 vs 18.4 +/- 1.8 mmol/kg wet weight; p less than 0.01), whereas lymphocyte potassium concentration was similar in both groups. Lymphocyte free calcium concentration was also higher in hypertensive patients than in normotensive controls (134.6 +/- 13.2 vs 120.2 +/- 16.4 nmol/L; p less than 0.01). There was a positive correlation between lymphocyte sodium and free calcium concentrations in normotensive controls, in hypertensive patients, and in the subjects combined (r = 0.59, p less than 0.01; r = 0.71, p less than 0.001; and r = 0.70, p less than 0.001, respectively). Lymphocyte potassium concentration was not related to lymphocyte sodium or free calcium concentration in each group. In patients with essential hypertension, intracellular sodium and free calcium concentrations were negatively correlated with plasma renin activity (r = -0.66, p less than 0.001; r = -0.60, p less than 0.001, plasma norepinephrine concentration. These results suggest that a considerable relationship exists between intracellular sodium and free calcium in lymphocytes and that, in essential hypertension, the alteration in cellular metabolism of sodium and calcium may be linked to the renin system but not to blood pressure, age, or adrenergic activity.
 ...
PMID:Intralymphocytic sodium and free calcium and plasma renin in essential hypertension. 329 77

The validity of the captopril test for primary aldosteronism (PA) was tested in patients with surgically verified PA (n = 12) or essential hypertension (EHT, n = 20) with different levels of sodium intakes. The patients were scheduled on 7 days each of three regimes of the prepared diet containing 34, 120 and 340 mEq of sodium chloride per day, and the captopril test was repeated in each period. For the test, captopril (50 mg) was administered orally at 9:00 A.M. after 1 hour of rest in a supine position, and venous blood samples were obtained before and 90 min after drug administration. Plasma aldosterone concentration (PAC; ng/dl) and plasma renin activity (PRA; ng/ml/h) were measured by radioimmunoassay. Under the three different sodium intakes, a PAC/PRA ratio greater than 20 at 90 min after captopril administration was sufficiently sensitive (0.95, 19/20) and specific (0.92, 55/60) to identify PA. Similarly, PA was associated with a PAC above 15 ng/dl 90 min after captopril. There were no complaints associated with the antihypertensive effects of the drug even when patients were sodium-restricted. These results confirmed that the captopril test is safe and useful for screening out-patients for PA, independent of individual differences in sodium intake.
 ...
PMID:Effects of sodium intake on the captopril test for primary aldosteronism. 330 11

An in vitro method has been used to examine whether secretion of renin from the juxtaglomerular apparatus is affected by changes in the sodium chloride concentration of the tubular fluid at the macula densa. Single juxtaglomerular apparatuses were microdissected from rabbits and the tubule segment containing the macula densa was perfused, while simultaneously the entire juxtaglomerular apparatus was superfused, and the fluid was collected for renin measurement. In this preparation, in which influences from renal nerves and local hemodynamic effects are eliminated, a decrease in the tubular sodium chloride concentration at the macula densa results in a prompt stimulation of the renin release rate.
 ...
PMID:Direct demonstration of macula densa-mediated renin secretion. 330 25

Chronic hyperkalemia (6.8 mmol/L [6.8 mEq/L]) was discovered in a boy, aged 13 years 7 months, with short stature, delayed puberty, and normal blood pressure. Additional studies revealed hyperchloremic metabolic acidosis (serum values: sodium ion, 139 mmol/L [139 mEq/L]; chloride, 113 mmol/L [113 mEq/L]; bicarbonate, 18 mmol/L [18 mEq/L]), a normal glomerular filtration rate, a subnormal renal threshold for bicarbonate reabsorption, and normal serum thyroxine, growth hormone, and cortisol values. Renal excretion of potassium ion was subnormal for the prevailing serum concentration of potassium ion but was increased normally by infusion of sodium sulfate. The serum aldosterone concentration was appropriate for a normokalemic subject, despite marked suppression of plasma renin activity (PRA) (supine/upright: aldosterone, 140/580 pmol/L [5/21 ng/dL]; PRA, 0.0/0.03 ng/L X s [0.0/0.1 ng/mL/h]). Treatment with chlorothiazide and sodium chloride resulted in correction of the abnormal electrolyte concentrations and an increase in linear growth velocity. Serum aldosterone concentrations did not change significantly during treatment, even though the PRA had increased (supine/upright: aldosterone, 110/920 pmol/L [4/33 ng/dL]; PRA, 0.89/2.17 ng/L X s [3.2/7.8 ng/mL/h]). In this patient, we conclude that (1) hyperkalemia was due to inadequate renal excretion of potassium ion; (2) the serum potassium ion concentration was the major stimulus to aldosterone secretion before treatment; (3) suppression of PRA was more likely due to hyperkalemia than to extracellular volume expansion.
 ...
PMID:Suppression of plasma renin activity in a boy with chronic hyperkalemia. 330 88

We investigated whether the anionic component of an orally administered sodium salt can influence the salt's capacity to increase blood pressure. In five men with essential hypertension in whom blood pressure was normal with restriction of dietary sodium chloride to 10 mmol per day (0.23 g of sodium per day), oral administration of sodium chloride for seven days, 240 mmol per day (5.52 g of sodium per day), induced significant increases in systolic and diastolic blood pressures, of 16 +/- 2 and 8 +/- 2 mm Hg (mean +/- SEM), respectively (P less than 0.05). An equimolar amount of sodium given as sodium citrate induced no change in blood pressure. Replacing supplemental sodium chloride with an equimolar amount of sodium as sodium citrate abolished the increase in blood pressure induced by sodium chloride. Both salts induced substantial and comparable sodium retention, weight gain, and suppression of plasma renin activity and plasma aldosterone, but supplemental sodium chloride increased plasma volume and urinary excretion of calcium, whereas sodium citrate did not. These preliminary findings demonstrate that the anionic component of an orally administered sodium salt can influence the ability of that salt to increase blood pressure, possibly by determining whether the salt induces an increase in plasma volume. Our observations in a small group of men with salt-sensitive hypertension will require confirmation in larger numbers of patients of both sexes.
 ...
PMID:"Salt-sensitive" essential hypertension in men. Is the sodium ion alone important? 330 53

We have suggested that the renal tubular signal for renin release is related to alterations of sodium chloride cotransport in the TALH. Renin release is inhibited by increased sodium chloride transport and stimulated by interrupted sodium chloride transport. Because of the different affinities of the carriers for sodium and chloride, chloride rather than sodium is rate limiting for this cotransport process. Consequently, renin release is related to alterations of chloride delivery rather than sodium delivery to the TALH. The reduction of PRA by selective chloride loading and by short-term infusion of chloride salts is related to increased chloride delivery to the loop and hence increased chloride transport. Alternatively, chlorpropamide and antidiuretic hormone may inhibit renin release by increasing chloride delivery to the loop. Stimulation of renin release may likewise be related either to decreased chloride delivery and hence decreased transport in the loop (hypochloremia related to selective chloride deprivation) or to an intrinsic alteration in the transporting capacity of the loop (loop diuretics, potassium depletion, glucocorticoid deficiency, Bartter's syndrome). The intermediate steps between alterations of sodium chloride transport in the TALH and renin release remain to be defined.
 ...
PMID:Renal tubular chloride and renin release. 331 41

Ten patients in heart failure of various etiologies underwent a placebo-controlled study to determine the effect of indomethacin (150 mg daily by mouth) on urine volume, sodium chloride excretion, glomerular filtration rate, renal prostaglandins, as well as plasma renin and aldosterone concentrations before and after administration of 40 mg frusemide by mouth. None had hyponatremia and plasma renin levels were within normal limits, but prostaglandin synthesis inhibition by indomethacin significantly reduced urine volume (-50%), sodium excretion (-70%) and glomerular filtration rate (-50%), as well as the urinary excretion of prostaglandin E2 (-80%) and 6-keto-prostaglandin F1 alpha (-70%). Frusemide-induced diuresis was halved by indomethacin. The suppression of renal prostaglandin excretion induced by inhibition of cyclooxygenase was not much influenced by frusemide. Plasma renin and aldosterone concentrations after indomethacin administration were not significantly raised by frusemide. The results indicate that renal prostaglandin synthesis is of great importance in the pathophysiology and treatment of mild to moderate heart failure.
 ...
PMID:[Indomethacin and furosemide in patients with cardiac insufficiency. Kidney function, the renin-angiotensin system and renal prostaglandins]. 331 42


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