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)

Pulmonary endothelial cells and the renin-angiotensin-aldosterone (RAA) system respond to different types of injury (direct or indirect) with variations in their functions. These variations influence the regulatory mechanisms of pulmonary and systemic blood pressure, electrolyte balance and fibrinolysis. Concentration changes of some components of the RAA system and lung plasminogen activator were observed following NdYag laser application to the brain surface in rats. These changes were similar to those observed in cutaneous burn and haemorrhagic hypotension. CO2 laser application did not cause the same changes.
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PMID:Brain surface exposure to CO2 and NdYag laser application: effect on pulmonary endothelium response in the rat. 303 May 14

Hypoxia alters the relationship of aldosterone secretion to plasma renin activity. The potential role plasma electrolytes play in this modification is not clear. This study analyzed the interrelationships among renin, aldosterone, vasopressin (ADH), and plasma electrolytes during 96 h of normobaric hypoxia. Eight ewes were exposed, in discrete experiments, to hypocapnic hypoxia [arterial O2 tension (PaO2) 37-42 mmHg, arterial CO2 tension (PaCO2) 26-28 mmHg] and eucapnic hypoxia (PaO2 40-43 mmHg, PaCO2 28-31 mmHg) by N2 dilution in an environmental chamber. Urine output (24 h) was measured, and arterial plasma samples were collected during the normoxic control period and at 24-h intervals of hypoxia. Plasma Na+, K+, renin, and ADH levels did not change from the normoxic values during either hypocapnic or eucapnic hypoxia. However, urinary aldosterone excretion [critical significance (alpha) less than 0.046] and K+ excretion (alpha less than 0.046) decreased markedly during each type of hypoxia. All sheep developed a pronounced negative K+ balance by 96 h of hypoxia. These data suggest that plasma K+ concentration is preserved by movement of K+ out of the intracellular compartment; this change in K+ distribution may inhibit aldosterone secretion during hypoxia.
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PMID:Hormonal and electrolyte responses of conscious sheep to 96 h of hypoxia. 304 47

It was the purpose of this study to determine whether acute increases of endogenous plasma renin induced by administration of anesthetics cause simultaneous increases of the enzyme in aortic tissue of the rat. Administration of CO2 did not alter plasma or tissue renin. Ether, Innovar and Nembutal increased active plasma renin and had variable effects on the inactive form of the enzyme. Only Innovar, a combination of droperidol and fentanyl, increased aortic renin. The active component of Innovar was shown to be droperidol, which also increased aortic renin in 24 hour nephrectomized animals. The increase of aortic renin was, therefore, independent of changes of circulating active or inactive renin. The increase of tissue renin following droperidol was rapid, suggesting activation of an inactive tissue renin.
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PMID:Independent change of plasma and tissue renin in response to anesthetics. 314 Oct 91

The role of endogenous opioids in systemic and renal circulatory changes during combined acute hypoxemia and hypercapnic acidosis was evaluated in seven conscious female mongrel dogs in rigid sodium balance. Animals were studied 2 wk apart in separate protocols of combined acute hypoxemia (arterial O2 tension = 33 +/- 1 mmHg) and hypercapnic acidosis (arterial CO2 tension = 56 +/- 1 mmHg, pH = 7.19 +/- 0.01) of 40 min duration during 1) naloxone, 5 mg/kg iv bolus followed by an intravenous infusion of 5 mg.kg-1.h-1, and 2) vehicle (5% dextrose in water) alone. Systemic circulatory changes during the combined acute blood-gas derangement including increased mean arterial pressure, heart rate, and cardiac output and decreased total peripheral resistance were comparable between naloxone and vehicle treatments. However, in striking contrast to the brief fall in renal hemodynamic function during combined acute hypoxemia and hypercapnic acidosis with vehicle, naloxone administration during the combined acute blood-gas derangement resulted in a sustained decrease in effective renal plasma flow, glomerular filtration rate, and filtered sodium load and enhanced rise in circulating norepinephrine and epinephrine. Changes in plasma renin activity were comparable between vehicle and naloxone protocols except that plasma renin activity increased from the first to the second 20-min periods of combined hypoxemia and hypercapnic acidosis with naloxone. These observations suggest that endogenous opioids may contribute to preservation of renal hemodynamic function during acute blood-gas derangements, possibly through attenuation of sympathetic nervous system and renin-angiotension activation.
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PMID:Hypoxemia and hypercapnia in conscious dogs: opioid modulation of catecholamines. 327 21

Twenty-seven patients with mild to moderate essential hypertension were randomized to receive therapy with either hydrochlorothiazide or diltiazem. After a placebo run-in period of 2 weeks, patients received increasing doses of either drug for 14 weeks. Those in whom hypertension was effectively controlled continued for 26 weeks of total treatment. Those not controlled, i.e. blood pressure greater than 140/90 mm Hg or less than 10 mm Hg reduction of pressure, were unblinded and crossed over to therapy with both drugs. Eleven of 14 patients (79%) were effectively treated with diltiazem alone, and 8 of 13 patients (62%) were effectively treated with hydrochlorothiazide alone. Supine blood pressures fell from 152 +/- 5/97 +/- 1 to 142 +/- 4/87 +/- 3 mm Hg in the 11 patients treated with diltiazem, from 152 +/- 2/99 +/- 1 to 134 +/- 3/88 +/- 2 mm Hg in the 8 patients treated with hydrochlorothiazide, and from 151 +/- 4/104 +/- 3 to 140 +/- 5/92 +/- 1 mm Hg in the 8 patients who received both drugs (p less than 0.01 for each group). Diltiazem patients had significant increases in alkaline phosphatase and urinary magnesium. Hydrochlorothiazide patients had increases in serum uric acid, serum globulin, CO2 content, and plasma renin activity. Serum potassium, serum chloride, urinary osmolality, and urinary calcium decreased after treatment with hydrochlorothiazide. Patients receiving both drugs had increases in serum glucose, serum BUN, serum uric acid, serum globulin, and CO2 content. These patients had decreased serum chloride and urinary calcium. Diltiazem monotherapy was comparable to hydrochlorothiazide in efficacy of lowering blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal-metabolic consequences of antihypertensive therapy with diltiazem versus hydrochlorothiazide. 332 Jul 20

Our studies were designed to optimize a system for studying renin release in vitro. Our rat kidney slices (400 micron) were cut coronally on a vibratome, and the medullary tissue was dissected from each slice. Previous investigators obtained kidney slices by slicing sagittally, parallel to the cortical surface, with a hand-held microtome. Slicing on a vibratome and removal of the medulla ensured that the slices were of uniform thickness, weight (18.3 +/- 0.52 mg; n = 24), and renin content. Furthermore, one kidney can provide approximately 30 renal slices whereas the previous methods provided only two slices per kidney. The slices were placed in siliconized vials containing a Krebs-Ringer solution (pH 7.4) at 37 degrees C for 30 min. The Krebs-Ringer solution was decanted and replaced with fresh Krebs-Ringer solution for a 30-minute preincubation period. At the end of the 30-min preincubation period, a 0.2-ml sample was taken for the determination of renin release, and the remaining medium was decanted. Fresh Krebs-Ringer solution and the test substances were subsequently added for the incubation period. Throughout the experiment, the vials were maintained at 37 degrees C, and each vial received a gas mixture of 95% O2-5% CO2 via plastic tubing connected to a needle that was inserted into the snap-cap of each vial but did not bubble the medium. The old (bubbling) method for the bioassay of renin yielded values for renin release that were low and had large interexperimental variation (0.23 +/- 0.04 to 1.9 +/- 0.3 ng angiotensin I (AI)/mg kidney/hr; n = 24).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An improved method for the measurement of renin release from coronal, vibratome-cut kidney slices. 352 Jan 49

33 blood and urinary components were titrated in 11 men 5 days before a marathon race (42 km), just before the start of the race, 1/4 hour after the arrival, the following day and 5 days after the race. On arrival, or/and the following day, even still 5 days later, we observed an increase of: natremia, kaliemia, blood proteins, hematocrit, aldosteronemia, plasma renin activity, uricemia, creatininemia, blood cortisol, myoglobinemia, blood lactic acid, total enzymatic CK activity, enzymatic ASAT activity, urinary elimination of creatinin, urea and 3 methylhistidine. On the contrary, a decrease of plasma total CO2 and blood testosterone levels were observed. These biochemical modifications are the consequence of hydro-mineral losses, muscular necroses, alteration of energetic metabolism with increase of the protein catabolism.
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PMID:[Changes in several plasma and urinary components in marathon runners]. 357 35

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3-6.9 mmol/l), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mmol/l), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/h), high plasma aldosterone level (32-100 ng/dl), and normal glomerular filtration rate (131 ml/min/1.73 m2). During the hyperkalemic period, urine was highly acidic (pH 4.6-5.0), urinary NH4 excretion (10-13 microEq/min) and urinary net acid excretion (19-24 microEq/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, the maximal tubular HCO3 reabsorption was markedly diminished (19.8 mmol/l glomerular filtrate), and the fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized was 20%. Urine minus blood PCO2 increased normally during NaHCO3 infusion (31 mm Hg), and the urinary pH remained maximally low (less than 5.3) when the buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while the urinary pH remained maximally low (4.9-5.2), the maximal tubular HCO3 reabsorption returned to normal values (24.8 mmol/l glomerular filtrate), and FE HCO3 at normal plasma HCO3 was 1%. Nasal insufflation of 1-desamino-8-D-Arginine Vasopressin (dDAVP) resulted in an acute normalization of the renal handling of K and in an increase in net urinary acid excretion. We conclude that: the effect of dDAVP on renal handling of K may be explained by the reversal of the distal chloride shunt and/or an increase in luminal membrane conductance to K; the distal acidification seems to be normal which in the event of distal chloride shunt impairing distal hydrogen secretion might be explained by the presence of systemic acidosis which is a potent stimulus of hydrogen secretion, and metabolic acidosis in the steady state was accounted for by the diminution of bicarbonate reabsorption and ammonia production in the proximal tubule secondary to chronic hyperkalemia.
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PMID:Pseudohypoaldosteronism type II: proximal renal tubular acidosis and dDAVP-sensitive renal hyperkalemia. 377 34

We describe a patient who developed persistant hypokalemia after renal transplantation that was initially attributed to diuretics and/or steroids. However after stopping the diuretic, the patient continued to have urinary losses of potassium (less than 30 mEq/day) at a time when the serum potassium was only 2.4 mEq/l and high urinary chloride (33 mEq/day) suggesting that the diuretics were not responsible for the hypokalemia and the metabolic alkalosis. The results of these simple laboratory tests and the presence of persistent severe hypokalemia prompted additional studies (peripheral renin activity; plasma aldosterone levels; and CT scan) that led to the diagnosis of left adrenal gland adenoma. Surgical removal of the adrenal adenoma led to the normalization of the serum potassium and a fall in the total CO2 content in plasma. To our knowledge this is the first report of a case of hypokalemia secondary to primary hyperaldosteronism in a renal transplant recipient.
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PMID:Hypokalemia secondary to primary hyperaldosteronism in a renal transplant recipient. 390 9

Studies were conducted in anesthetized dogs to examine the influence of the renal sympathetic nerves on renal hemodynamic and renin responses during controlled hypercapnia. The dogs were subjected to unilateral denervation and tested for their responses to hypercapnia induced by inhalation of 15% CO2 in air. Simultaneous measurements of the responses from both the denervated and innervated kidneys allowed an assessment of the influence of the renal nerves on the responses during acute hypercapnia. The data indicate that reductions in renal blood flow and glomerular filtration rate and increases in renin of the renal vein during respiratory acidosis are dependent, in part, on the presence of intact renal nerves. Other factors, however, are probably also present.
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PMID:The influence of renal sympathetic nerves on renal hemodynamic and renin responses during hypercapnia in dogs. 391 20


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