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)

Eight normotensive subjects were studied in a randomized crossover trial of a high calcium diet (1800 mg of calcium/day) for a week against a low calcium diet (200 mg of calcium/day) for a further week. The subjects were placed on a diet containing 200 mg of calcium/day throughout the study and the high calcium diet was achieved by supplementing the low calcium diet with calcium glubionate and galactogluconate. Sodium and potassium intake were kept constant throughout the study. Twenty-four hour urinary sodium, potassium, calcium and phosphate were measured daily. In spite of a highly significant increase in calcium excretion from the low to the high calcium diet (P less than 0.0001), there was no increase in sodium or change in potassium excretion with the increased calcium intake. A transient but significant fall in urinary sodium excretion was observed up to the fourth day of the high calcium diet (P = 0.021). Twenty-four hour urinary phosphate excretion fell significantly on the high calcium diet (P less than 0.0001). Body weight, blood pressure, plasma renin activity, aldosterone, plasma creatinine and serum ionized calcium did not change. These results suggest that a short-term increase in calcium intake in normotensive subjects does not increase urinary sodium and potassium excretion.
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PMID:Effect of increasing calcium intake on urinary sodium excretion in normotensive subjects. 375 41

Phosphate depletion (PD) adversely affects myocardial function but its influence on blood pressure is not well elucidated. In this study we evaluated whether PD influences blood pressure and/or affects its hormonal regulation or the peripheral vascular response to pressor agonists. Mean arterial pressure (MAP) in PD rats was lower than in normal animals, whereas heart rate was not significantly different between the two groups. Cardiac index (CI) in PD rats was lower and systemic vascular resistance (SVR) was higher than in controls. Plasma norepinephrine (NE) in the resting state and during the stress of immobilization was significantly greater in PD rats than in controls. Base-line plasma renin activity was also significantly higher in PD rats and increased similarly in the two groups of rats after administration of isoproterenol. Bolus injections of NE or angiotensin II produced a smaller rise in MAP in PD rats than in controls. Reduced responsiveness to NE was also demonstrated in isolated hind-limb preparation from PD rats. When NE was infused to achieve a rise in MAP of 30 mmHg, the dose required in PD was higher than in controls. Treatment with indomethacin did not affect the response in MAP to NE. The content and affinity of both alpha- and beta-receptors in PD hearts were not different from those of control hearts. The contents of PiATP, and AMP in the mesenteric vessels of PD rats were significantly lower than in control animals. These data show that PD leads to reductions in MAP, arteriolar response to pressor agents, and CI with appropriate compensatory rise in NE but with inadequate compensatory increase in SVR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of phosphate depletion on blood pressure and vascular reactivity to norepinephrine and angiotensin II in the rat. 388 79

The interaction between mouse submaxillary gland renin and a statine-containing, iodinated substrate analog inhibitor was studied. The compound, 1 (Boc-His-Pro-Phe-(4-iodo)-Phe-Sta-Leu-Phe-NH2, Sta = (3S,4S)-4-amino-3-hydroxy-6-methyl-heptanoic acid), a statine-containing analog of the renin substrate octapeptide, was a competitive inhibitor of cleavage of synthetic tetradecapeptide renin substrate by mouse submaxillary gland renin, with a Ki of 6.2 x 10(-10) M (pH 7.2, 37 degrees C). Titration of the partial quenching of the tryptophan fluorescence of the enzyme by 1 revealed tight binding with a dissociation constant less than 3 nM and a binding stoichiometry of one mole 1 per mole enzyme. The time course of tight binding of 1 to mouse renin appeared to be fast, with kON greater than or equal to 1.3 x 10(6) s-1 M-1. The UV difference spectrum generated upon binding of 1 to mouse renin had two prominent features: a strong, broad band that had a minimum at 242 nm with delta epsilon (242) = -19,500 cm-1 M-1, and a triplet of enhanced bands centered at 286 nm with delta epsilon (286) about +1100 cm-1 M-1. The strong, broad, negative band was similar to the difference between the UV absorbance of 1 in methanol and in 0.1 M citrate phosphate pH 7.2. A structure-activity correlation for analogs of 1 showed some moieties of 1 that are important for potent inhibition of mouse renin. The inhibition data for these compounds versus human kidney renin suggested that the solution of the crystal structure of 1 bound to mouse renin will provide useful information for the design of inhibitors of human kidney renin.
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PMID:Interaction of mouse submaxillary gland renin with a statine-containing, subnanomolar, competitive inhibitor. 391 10

K+ depletion of two kinds was induced in two groups of rats by selective dietary restriction for up to 5 weeks. Complete metabolic studies for H+, K+, Na+ and Cl- were carried out daily during weeks 1, 3 and 5. In control rats of group A (receiving K+ with sodium chloride), plasma pH (7.47) and HCO3- (25 mmol/l), as well TA (titratable acid)--HCO3- and NH+4 urinary excretion rates, were stable, while balances were nil for K+ and slightly positive for Cl-. In K+-deprived rats of group A receiving sodium chloride, a progressive metabolic alkalosis developed (plasma pH reached 7.57 and HCO3- 35.8 mmol/l by 5 weeks), and TA--HCO3- and NH+4 urinary excretion rates were not different from controls. Plasma K+ fell progressively from 4.20 to 2.20 mmol/l, with negative K+ balance. Balances for Na+ and H2O were highly positive and plasma renin activity and aldosterone decreased by week 5. Hypochloraemia developed with positive Cl- balance. In control rats of group B (receiving K+ with neutral sodium phosphate), a slight metabolic alkalosis developed, and TA--HCO3- excretion rate was increased compared with control rats of group A.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective dietary potassium depletion and acid-base equilibrium in the rat. 391 25

A twelve-year-old girl with persistent hyperkalemia, metabolic acidosis, normal blood pressure and glomerular filtration rate, and short stature (first percentile for height) was studied using metabolic balance techniques. Prior to therapy with hydrochlorothiazide (HCTZ), urinary potassium and acid excretion were low and urine pH was inappropriately high at 5.8. HCTZ (25 mg orally per day) (1 mg/kg) was then started and rapidly corrected her serum electrolytes. The therapy with HCTZ was associated with a diuresis, a decrease in urine pH to 4.8, and concomitant increases in potassium, titratable acid (TA) and ammonium excretion. The increase in TA excretion was explicable, in part, to the decrease in urine pH and, in part, to the considerable increase in phosphate excretion (from 56 to 81 mmol/d). Plasma renin activity and plasma aldosterone increased markedly following HCTZ but urinary prostaglandin E (PGE) excretion was unchanged. These observations suggest that administration of HCTZ in this setting increases hydrogen ion secretion. It is unclear whether this effect is a direct consequence of HCTZ at the level of the tubule or is secondary to some other action of HCTZ. However, it is clear that this effect is not related to an alteration in PGE excretion.
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PMID:The Spitzer-Weinstein syndrome: one form of type IV renal tubular acidosis and its response to hydrochlorothiazide. 395 73

1. Recently it has been shown that injection of angiotensin II into the anterior diencephalon causes the rat to drink water. In the present experiments the dipsogenic action of a number of other substances including substances related to angiotensin was tested.2. Injection of 0.001 Goldblatt u. renin into the angiotensin-sensitive region causes the water-replete rat to drink. Drinking is slower in onset and continues for longer than after injection of angiotensin II.3. Synthetic tetradecapeptide renin substrate and angiotensin I were as effective as angiotensin II at causing water-replete rats to drink.4. beta-aspartic acid(1)-valine(5)-angiotensin II was also fully effective; but the D-arginine substituted octapeptide was much less effective.5. The (2-8) heptapeptide retained about 50% of the dipsogenic activity of the octapeptide, whereas the absence of phenylalanine at the other end of the peptide chain in the (1-7) heptapeptide results in an inactive compound.6. The (3-8) hexapeptide and the (4-8) pentapeptide, both of which have phenylalanine at the end of the chain, and the (1-4) and (5-8) tetrapeptide fragments of angiotensin II showed only a slight action on intake of water.7. Kallikrein, bradykinin, adenosine-3'5-cyclic phosphate, vasopressin and oxytocin caused no drinking when injected into the angiotensin-sensitive region.8. It is concluded that the requirements for the dipsogenic activity of angiotensin are the same as those for its other biological actions with the qualification that the precursor peptides are also active, presumably because they give rise to angiotensin II locally.
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PMID:The effect on drinking of peptide precursors and of shorter chain peptide fragments of angiotensin II injected into the rat's diencephalon. 432 62

The metabolic and cardiovascular side-effects of intravenous infusions of therapeutic doses of beta 2-adrenoceptor agonists salbutamol and rimiterol have been determined in four healthy male subjects. There were dose-related increases in plasma glucose, renin activity, serum insulin and heart rate, and significant hyperlactataemia and ketonaemia. There were dose-related decreases in plasma potassium, phosphate and corticosteroids and significant hypocalcaemia and hypomagnesaemia. The effects of equivalent molar amounts of salbutamol and rimiterol were similar. Whichever drug is used, special care is required with patients who may have abnormal glucose tolerance, potassium depletion, or be predisposed to lactic acidosis. Rimiterol may be preferable for infusion because of its short plasma half-life.
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PMID:Metabolic and cardiovascular side effects of the beta 2-adrenoceptor agonists salbutamol and rimiterol. 610 76

Ultrastructural features of juxtaglomerular cells have been correlated with plasma and kidney analyses from non-hibernating, hibernating and awakening ground squirrels. Juxtaglomerular cells in kidneys from hibernating animals show signs of increased activity. Plasma samples from hibernating animals show a significant increase in magnesium. Kidney analyses from hibernating animals, show glycogen increases and lactate and inorganic phosphate decrease significantly. Adenosine triphosphate remains the same. Maintenance of high-energy phosphates in the hibernating kidney is essential to maintaining sodium transport and osmotic pressure. This coupled with a functional renin-angiotensin system regulates water and electrolyte balance.
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PMID:Ultrastructure of juxtaglomerular cells correlated with biochemical parameters in a hibernator. 614 44

Studies were performed in anesthetized dogs (n = 5) to determine the effects of synthetic atrial natriuretic factor on renal function and renin release. Intrarenal infusion of synthetic atrial natriuretic factor (ANF) (0.3 microgram X kg-1 X min-1) resulted in a transient increase in renal blood flow (126 +/- 8 to 148 +/- 11 ml/min). The duration of this transient vasodilation was 3.1 +/- 0.4 min. Continued infusion was followed by a slight decrease in renal blood flow (126 +/- 8 to 117 +/- 8 ml/min) and an increase in glomerular filtration rate (23.1 +/- 3.5 to 30.7 +/- 1.9 ml/min), with filtration fraction thus being increased (0.19 +/- 0.04 to 0.27 +/- 0.03). These hemodynamic alterations were associated with increases in fractional sodium excretion (0.6 +/- 0.2 to 5.8 +/- 0.8%), fractional potassium excretion (30.8 +/- 9.4 to 56.3 +/- 7.4%), fractional lithium excretion (32.2 +/- 7.1 to 60.3 +/- 5.7%), and fractional phosphate excretion (8.7 +/- 3.5 to 41.6 +/- 11.7%). Intrarenal infusion of synthetic ANF markedly suppressed renin secretion rate (295.5 +/- 84.6 to 17.2 +/- 10.6 ng/min) despite a slight reduction in arterial pressure (123 +/- 9 to 118 +/- 9 mmHg). Our studies demonstrate that synthetic ANF results in a marked natriuretic response that is in part mediated by an increase in glomerular filtration rate. The increase in fractional lithium and phosphate excretion suggests that this factor may also have an action on proximal tubule reabsorption. Further, these studies demonstrate that synthetic ANF markedly inhibits renin secretion.
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PMID:Effects of synthetic atrial natriuretic factor on renal function and renin release. 623 39

The effect of the anion associated with sodium loading on the development of hypertension in the Dahl salt-sensitive rat was determined. For 5 weeks rats were fed a diet containing normal or high concentrations of sodium chloride or high concentrations of sodium provided as a mixture of sodium bicarbonate, phosphate, and amino acids. After 1 week on these diets and until the end of the study the rats receiving high concentrations of sodium chloride had higher systolic blood pressures than the rats in the other two groups. There were no statistically significant group differences in plasma volume, arterial pH, or plasma concentrations of Na+, K+, Cl-, Ca2+, or creatinine, or in renomedullary prostaglandin E2 production. Compared to the animals receiving normal concentrations of sodium chloride, those receiving high concentrations of sodium chloride or amino acids showed decreased plasma renin activity and plasma aldosterone concentrations. Thus, the anion ingested with sodium alters the development and severity of hypertension in the Dahl salt-sensitive rat.
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PMID:Salt-sensitive hypertension: contribution of chloride. 632 3


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