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PubMed1982

Intrapartum hypoxia: the association between neurological assessment of damage and abnormal excretion of ATP metabolites.

A series of 29 newborn infants had been studied after intrapartum hypoxia defined as meconium aspiration, an Apgar score of less than or equal to 6 at 5 min or a peripheral blood pH of 7.2 or less after resuscitation. Two independent sets of techniques were used; one concerned with the critical system in hypoxic damage, the central nervous system, the other assessing the central biochemical events in hypoxia. Both sets of data were assembled, then graded separately and only then combined. In this way detailed neurological assessment has been combined with measurement of urinary excretion of the ATP metabolites, hypoxanthine and xanthine. The essential metabolic consequence of hypoxia is a reduction in the synthesis of the energy currency of cells, ATP. This is associated with an outflow of ATP metabolites from cells. The extent of neurological damage was related to the magnitude of the hypoxanthine and xanthine excretion; neither were closely related to the initial blood pH. Infants who were normal neurologically had normal oxypurine excretion. Infants with neurological abnormalities for less than 48 h had lower excretion than those who were abnormal for more than 48 h. The duration of abnormal oxypurine excretion after an acute episode of hypoxia was studied in two infants with respiratory distress and in two other infants with apnoeic attacks. Severe hypoxia was followed by abnormal oxypurine excretion for at least 40 h after an acute episode. It is justifiable to suggest that abnormalities of oxypurine excretion should indicate intrapartum hypoxia in newborn infants. This excretion should also quantify the metabolic damage.

Adenosine Triphosphate↗
PubMed1993

Beta 2-glycoprotein-1 (apolipoprotein H) excretion and renal tubular malfunction in diabetic patients without clinical proteinuria.

AIM: To compare the urinary excretion of beta 2-glycoprotein-1 with that of two other markers of early tubular disorder in diabetic patients without clinical proteinuria. METHODS: The urinary excretion of retinol binding protein, beta 2-glycoprotein-1, and N-acetyl-beta-D-glucosaminidase was measured in 90 known diabetic patients who had a negative reagent strip test for proteinuria. RESULTS: Among 43 patients with urinary albumin excretion within the reference range, 23 (53%) had raised urinary N-acetyl-beta-D-glucosaminidase activity, five (12%) increased excretion of beta 2-glycoprotein-1, and five (12%) increased loss of retinol binding protein. Among 47 patients with an albumin excretion of 0.9-7.9 mg/mmol creatinine, 42 (89%) had increased urinary N-acetyl-beta-D-glucosaminidase, 23 (49%) an increased output of beta 2-glycoprotein-1, and 16 (34%) a raised excretion of retinol binding protein. The excretion of these markers of tubular defects seldom exceeded two and a half times the upper reference limit and the differences between the findings in the insulin dependent and non-insulin dependent patients with similar albumin excretion were small and insignificant. CONCLUSIONS: In diabetic patients with a negative dipstick test for proteinuria: (a) assay of urinary beta 2-glycoprotein-1 may be a more sensitive test for the detection of impaired tubular reabsorption of protein than measurement of retinol-binding protein; (b) assay of N-acetyl-beta-D-glucosaminidase can detect tubular injury at a time when protein reabsorption remains normal; and (c) impaired renal tubular function may be present in the absence of evidence of glomerular malfunction.

Acetylglucosaminidase↗
PubMed1998

Work stress and recovery measured by urinary catecholamines and cortisol excretion in long distance coach drivers.

OBJECTIVES: To evaluate coach drivers' work stress during work and in the course of recovery from work by measurement of urinary catecholamines and cortisol. METHODS: The urinary excretion rate of adrenaline, noradrenaline, and cortisol of 10 coach drivers was studied during a long distance trip of three days and two consecutive days off. Each driver was asked to provide seven urine samples on the working days and six urine samples on the days off. The second day off was considered as the baseline. RESULTS: An occupationally induced disturbance of the circadian rhythmicity was found for adrenaline and noradrenaline but not for cortisol. The mean excretion rates of adrenaline on the first working day and most samples on all working days were higher than the baseline. For both adrenaline and noradrenaline the mean excretion rates on the first day off were lower than the baseline. For cortisol, the mean excretion rate on all working days was higher than the baseline. A trend towards accumulation of cortisol excretion from the first working day to the third working day was found. A backward shift in peak concentrations was found for adrenaline and noradrenaline on the second working day, as was a forward shift in peak concentration of cortisol on both days off. CONCLUSIONS: Long distance coach drivers showed occupationally induced reactivity in rates of urinary excretion of adrenaline, noradrenaline, and cortisol. After the outward journey the rates of excretion of catecholamines did not return to baseline values. The course of recovery in adrenaline excretion after the journey showed a new phenomenon, which has been called "fatigue debt". It is recommended that longer resting times in shuttle bus trips and fixed days off after these kind of trips should be planned. Extensive future research should be focused on the additional relations between fatigue debt and health complaints.

Adult↗
PubMed1977

The excretion of enterotoxin B from nongrowing cells of Staphylococcus aureus 4916.

The physiological conditions for the excretion of staphylococcal enterotoxin B (SEB) by nongrowing cells have been determined. In general, SEB excretion appears to be best when amino acids serve as sources of carbon, nitrogen, and energy. Little toxin was produced in a nitrogen-free medium with glucose as the sole carbon source. Inhibitor studies have shown that most of the toxin excreted by nongrowing cells was the result of de novo protein synthesis. Optimum toxin excretion was also obtained under conditions of aeration, and at or near optimum growth temperature, those conditions at which the cells are metabolically and biosynthetically most active. Levels of cell-associated SEB decreased during toxin excretion. However, these levels of toxin could not account for the high levels of toxin released during excretion. Glucose and several other rapidly fermentable carbohydrates inhibited toxin excretion by as much as 80% under conditions of uncontrolled decrease in pH: however, when the pH was kept at either 6.2 or 7.5 a stimulation of toxin excretion was observed. Protoplast studies have suggested that SEB production does not take place in the absence of an intact cell wall.

Air↗
PubMed1984

Influence of exercise on urea, creatinine, and 3-methylhistidine excretion in normal human subjects.

To evaluate the effects of exercise on net protein catabolism, the losses of urea in sweat and urine and urinary creatinine and 3-methylhistidine (3MH) excretion were determined in eight healthy subjects during cycle ergometer exercise performed at approximately 45% of VO2max for 90 min. The subjects ingested a meat-free diet for 5 days starting 3 days before and continuing for 1 day after the day of exercise. During exercise, total urea excretion (urine + sweat losses) increased 100% above pre- and postexercise values. Thirty percent of the total urea excretion during exercise was in the form of sweat losses. Total protein breakdown (as reflected by urea excretion), however, could account for less than 5% (21 +/- 4 kcal) of total calorie expenditure during the exercise (567 +/- 83 kcal). Urinary creatinine excretion increased by 50% during exercise. Urinary excretion of 3MH also tended to rise, but the ratio of urinary 3MH to creatinine showed no change in response to exercise. We conclude that 1) light to moderate exercise results in an increase in net protein catabolism and an increase in creatinine excretion; 2) sweat losses are an important route for urea excretion during exercise; 3) there is no evidence of a disproportionate increase in breakdown of myofibrillar contractile proteins; and 4) in spite of the increase in the rate of protein catabolism, protein is only a minor source of energy during light to moderate exercise.

Adolescent↗
PubMed1985

Biphasic changes in 3-methylhistidine excretion in humans after exercise.

We previously reported that 3-methylhistidine excretion was increased in human subjects after a strenuous bout of exercise. Because other investigators have not corroborated this finding, we undertook the present study to investigate the conditions that result in decreased and increased 3-methylhistidine excretion in human subjects after exercise. Four experiments were performed: a cross-sectional study comparing 3-methylhistidine excretion in endurance-trained subjects with untrained controls, a longitudinal study of 3-methylhistidine excretion by female basketball players before the start of the season and again during the competitive season, an experiment to determine changes in 3-methylhistidine excretion as a result of 2 h of exercise each day for 7 consecutive days, and a study to determine changes in 3-methylhistidine excretion during 4-h intervals after a strenuous exercise bout. The 3-methylhistidine-to-creatinine ratio was approximately 20% higher for trained than nontrained subjects. In three separate experiments a biphasic change of 3-methylhistidine excretion was observed in response to exercise with an immediate decrease in the 3-methylhistidine-to-creatinine ratio during exercise followed by a prolonged increase. The magnitudes of the negative and positive responses determine whether one observes an increase, no change, or a decrease in the total daily excretion of 3-methylhistidine.

Creatinine↗
PubMed1986

Effects of diets high in refined carbohydrates on renal ammonium excretion in rats.

Ammonium excretion was investigated in spontaneously hypertensive rats (SHR) and normotensive control rats (WKY) ingesting different diets. SHR and WKY on low protein-high sucrose diets surprisingly showed the same ammonium excretion as rats ingesting a higher protein-lower sucrose diet. This was unexpected, because ammonium excretion correlates positively with protein intake. The relatively high ammonium excretion despite low protein intake (approximately 40% of control) was not associated with acidosis, hypokalemia, hypocalcemia, and/or hypomagnesemia. In a follow-up study, where diets were high in refined carbohydrates (sucrose, glucose, and starch) but more equal in protein content compared with a diet high in carbohydrates of a more complex form (grains), ammonium excretion increased significantly. When we examined the factors known to influence ammonium excretion, the only significant positive correlations found were between norepinephrine, epinephrine, dopamine, and ammonium excretion. These correlations still remained significant when only the data from the rats on the diets high in refined carbohydrates, i.e., rats on the same dietary intake of minerals and proteins, were compared. In vitro, we corroborated that catecholamines significantly increased ammoniagenesis from kidney slices. Our data show that diets high in refined carbohydrates augment both ammonium and catecholamine excretion and suggest that these two events may be interrelated.

Ammonia↗
PubMed1995

Effect of insulin on uric acid excretion in humans.

Although hyperuricemia is a frequent finding in insulin-resistant states, insulin's effect on renal uric acid (UA) handling is not known. In 20 healthy volunteers, diastolic blood pressure, body weight, and fasting plasma insulin were positively (and age was negatively) related to fasting plasma UA concentrations, together accounting for 53% of their variability. During an insulin clamp, urine flow was lower than during fasting conditions (1.01 +/- 0.12 vs. 1.56 +/- 0.32 ml/min, P = 0.04), whereas creatinine clearance was unchanged (129 +/- 7 and 131 +/- 9 ml/min, P = not significant). Hyperinsulinemia did not alter serum UA concentrations (303 +/- 13 vs. 304 +/- 12 microM) but caused a significant decrease in urinary UA excretion [whether expressed as absolute excretion rate (1.66 +/- 0.21 vs. 2.12 +/- 0.23 mumol/min, P = 0.03), clearance rate (5.6 +/- 0.8 vs. 7.3 +/- 0.8 ml/min, P = 0.03), or fractional excretion (4.48 +/- 0.80 ml/min vs. 6.06 +/- 0.64%, P < 0.03)]. Hyperinsulinemia was also associated with a 30% (P < 0.001) fall in urine Na excretion. Fractional UA excretion was related to Na fractional excretion under basal conditions (r = 0.59, P < 0.01) and during the insulin period (r = 0.53, P < 0.02). Furthermore, the insulin-induced changes in fractional UA and Na excretion correlated with one another (r = 0.66, P < 0.001). Physiological hyperinsulinemia acutely reduces urinary UA and Na excretion in a coupled fashion.

Adult↗
PubMed2003

Lack of biliary lipid excretion in the little skate, Raja erinacea, indicates the absence of functional Mdr2, Abcg5, and Abcg8 transporters.

The ABC transporters bile salt export pump (BSEP; encoded by the ABCB11 gene), MDR3 P-glycoprotein (ABCB4), and sterolin 1 and 2 (ABCG5 and ABCG8) are crucial for the excretion of bile salt, phospholipid, and cholesterol, respectively, into the bile of mammals. The current paradigm is that phospholipid excretion mainly serves to protect membranes of the biliary tree against bile salt micelles. Bile salt composition and cytotoxicity, however, differ greatly between species. We investigated whether biliary phospholipid and cholesterol excretion occurs in a primitive species, the little skate, which almost exclusively excretes the sulphated bile alcohol scymnolsulphate. We observed no phospholipid and very little cholesterol excretion into bile of these animals. Conversely, when scymnolsulphate was added to the perfusate of isolated mouse liver perfusions, it was very well capable of driving biliary phospholipid and cholesterol excretion. Furthermore, in an erythrocyte cytolysis assay, scymnolsulphate was found to be at least as cytotoxic as taurocholate. These results demonstrate that the little skate does not have a system for the excretion of phospholipid and cholesterol and that both the MDR3 and the two half-transporter genes, ABCG5 and ABCG8, have evolved relatively late in evolution to mediate biliary lipid excretion. Little skate plasma membranes may be protected against bile salt micelles mainly by their high sphingomyelin content.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed1983

Cardiorenal hemodynamics and sodium excretion in rats with myocardial infarction.

The relation between left ventricular function and renal excretion of sodium (Na+) was studied in rats with myocardial infarction (MI) and varying degrees of left ventricular dysfunction. Three groups of rats were defined: 1) control sustained no infarct, 2) small to moderate infarcts involved 10-40% of the left ventricular circumference, and 3) large infarcts involved greater than 40%. In conscious rats, Na+ excretion was measured after administration of saline load by gavage. Four hours after the load, rats with large MI excreted less than one half the amount of Na+ excreted by control rats, whereas rats with small to moderate MI excreted an intermediate amount. In a second group of anesthetized rats, Na+ excretion, renal hemodynamics, and ventricular performance were determined before and after acute intravenous volume expansion with a balanced salt solution. Rats with small to moderate MI demonstrated minimal impairment in ventricular pumping ability but excreted less Na+ after volume expansion than did control rats. However, rats with large MI demonstrated marked impairment in left ventricular performance and exhibited the least natriuretic response to volume loading. Glomerular filtration rate and renal plasma flow failed to increase with volume expansion in both groups of rats with MI. Thus Na+ excretion in response to acute volume loading was diminished in rats with large MI and markedly impaired cardiac performance but was also reduced in rats with small to moderate MI and minimal changes in ventricular pumping capacity.

Animals↗
PubMed1985

Renal and extra-renal excretion of calcium in the marine teleost, Gadus morhua.

The calcium turnover, with particular emphasis on the routes and rates of excretion, was investigated in the Atlantic cod, Gadus morhua. A very rapid internal redistribution of injected 45Ca was demonstrated, with the decline in the plasma concentration conforming to the power function f(t) = 8.83% X t-0.585. The clearance for 45Ca and [3H]inulin were both linearly correlated to urine flow and showed a ratio (Cca/CIn) of 2.6:1. Likewise a linear correlation between the renal and extra-renal excretion of 45Ca could be demonstrated with a ratio of 1:0.47, indicating that the renal route of excretion is of major importance in this species. The renal excretion of calcium was estimated to be 4.2 mumol X kg-1 X h-1 and the total calcium excretion to be 6.2 mumol X kg-1 X h-1. Calculations are presented, suggesting that the balance between intake and excretion of calcium can be explained in terms of growth of the animal, which would allow for an increase in the amount of body calcium of approximately 5 g X yr-1. It is also concluded that because about two-thirds calcium is excreted via the renal route, the kidneys may be the most important site for the regulation of calcium excretion in the cod.

Animals↗
PubMed1985

Effect of aldosterone on potassium excretion during potassium chloride infusion in sheep.

Experiments were performed on normal mature ewes to quantitate the effect of acute variations in aldosterone activity on renal K excretion. Six-hour clearance studies were performed on three sheep. Treatments were control (no infusion), infusion of KCl (140 meq in 2 h) alone or with superimposed infusions of aldosterone (20 micrograms/h), or infusion of aldosterone antagonist potassium canrenoate (100 mg/h). During KCl infusion there were simultaneous increases in plasma K, K excretion, and Na excretion. Aldosterone treatment diminished the increase in plasma K and in Na excretion but increased the rate of K excretion. Canrenoate had opposite effects. The rate of change of K excretion relative to the change in plasma K was 417 for aldosterone and 102 microeq/min per meq/l for canrenoate treatments, P less than 0.05. Before KCl infusion aldosterone decreased the rate of Na excretion and the salivary Na-to-K ratio but did not alter plasma K or K excretion. Aldosterone has a potent kaliuretic action in sheep when plasma K is elevated.

Aldosterone↗
PubMed1991

Sodium excretion and renal precession of sodium over inulin.

Renal excretory patterns for inulin and 22Na were measured in rats after simultaneous injection into a renal artery. In normal rats, the excretion of 22Na was much faster than inulin. This is referred to as "precession of sodium" and showed that some of the excreted 22Na had bypassed the intratubular route. During water diuresis, 65% of excreted 22Na was excreted before inulin. The quantity of 22Na preceding inulin (0.10 +/- 0.03% of the amount injected) increased eightfold during infusion of atrial natriuretic peptide (ANP). In saline diuresis, 45% of excreted 22Na (1.47 +/- 0.39% of the amount injected) preceded inulin, but precession was not affected by ANP. In rats with a nephrotic syndrome, 13% of excreted 22Na (0.34 +/- 0.12% of the amount injected) preceded inulin during saline diuresis and increased to 1.66 +/- 0.53% of the amount injected during the infusion of ANP. Precession of sodium was completely abolished in kidneys with papillary necrosis, suggesting that 22Na entered the tubular lumen in the inner medulla. These experiments demonstrate that, in rats, a large fraction of excreted sodium enters the tubules by a route other than filtration. The quantity of sodium entering the tubules by this route shows a 10- to 15-fold variation under conditions that modify the rate of sodium excretion.

Animals↗
PubMed1994

What is responsible for the diurnal variation in potassium excretion?

Potassium excretion exhibits a diurnal pattern, with most excretion occurring close to noon in humans. Each component of the K+ excretion rate [urinary K+ concentration ([K+]) and flow rate] was measured and back-calculated to reflect events in the cortical collecting duct (CCD). Our purpose was to determine to what extent each component contributed to this diurnal variation in each 2-h portion of the day. In humans, K+ excretion rose threefold from nadir (0600 h) to peak (1200-1400 h), 18 h after the principal intake of K+. The variation in K+ excretion was due almost exclusively to changes in [K+] in the terminal CCD ([K+]CCD) rather than via changes in flow rate. In rats, the bulk of K+ excretion occurred shortly after eating. Both components of K+ excretion rose after meals; the rise in the [K+]CCD (3.3-fold) predominated at earlier times, and the rise in flow rate occurred later and was primarily a result of a higher rate of excretion of urea. The rise in [K+]CCD did not correlate with aldosterone levels or administration. A very large rise in the [K+]CCD only occurred in the presence of bicarbonaturia; the transtubular potassium concentration gradient was now close to 15 in the morning and evening.

Acetazolamide↗
PubMed1997

Low urine flow reduces the capacity to excrete a sodium load in humans.

Recent studies in rats suggest that vasopressin and the resulting urinary concentrating activity reduce the capacity of the kidney to excrete sodium. The present study investigates the influence of the level of hydration on the excretion of a sodium load in humans. Eight healthy male volunteers (18-35 yr) were studied twice, in random order, under either low (LowH) or high (HighH) hydration. They drank throughout the study either 0.25 (LowH) or 2.0 ml water/kg body wt (HighH) every 30 min. After 1 h equilibration, urine was collected for 2 h before (basal) and 10 h after the NaCl load (5 g NaCl in 250 ml, infused intravenously over 30 min). Differences in excretory patterns between LowH and HighH were mostly confined to the first 4 h after the load. The increase in Na excretion after the load was more intense under HighH than under LowH (+ 10.9 +/- 2.6 vs. + 5.8 +/- 2.7 mmol/h in the first 4 postload h; P < 0.001). Under HighH, urine flow rate (V) increased markedly (+ 41%), with little change in urinary Na concentration (UNa), whereas under LowH, V declined slightly and UNa rose significantly (+ 33%). The capacity to raise UNa seemed to reach a maximum at approximately 280 mM. In both conditions, the changes in UNa observed after the load were positively correlated with basal UNa. After the load, urea excretion increased under HighH and decreased under LowH, whereas K excretion was unaffected in either condition. These results show that sodium excretion is facilitated by an abundant water supply. The less efficient sodium excretion occurring at low V is probably due to the influence of vasopressin on water, urea, and sodium movements across the collecting ducts. These observations suggest that, in everyday life, a low water intake could limit the capacity to excrete sodium. Whether this could contribute to salt-sensitive hypertension remains to be evaluated.

Adult↗
PubMed1981

Effect of glucose on renal excretion of electrolytes in the rat.

Glucose ingestion or infusion increases calcium and magnesium excretion in the human. To assess the role of renal tubular glucose reabsorption and of the parathyroid glands in this phenomenon, we performed standard two-phase clearance experiments in fed, volume-expanded male Sprague-Dawley rats. When compared with a group of animals receiving only 0.9% NaCl (group I), animals infused with glucose (group II) excreted significantly more calcium at any given level of sodium excretion (delta FECa, 1.95 +/- 0.24 vs. 0.69 +/- 0.18, P < 0.001). Normoglycemic hyperinsulinemia (group III) did not reproduce this increase in calcium excretion. In the group given phloridzin during sustained hyperglycemia (group IV), calcium excretion was well below that of control animals at any given level of sodium excretion. The glycosuric-hyperglycemia group (group V) used to assess the effect of glycosuria seen in group IV responded with a striking calciuria (delta FECa, 3.31 +/- 0.43, P < 0.001, compared with group IV). TPTX animals responded to glucose in the same way as intact animals (delta FECa, 4.8 +/- 0.5 vs. 2.18 +/- 0.3 in TPTX saline controls, P < 0.001). Magnesium excretion in all groups followed the same pattern as calcium. We conclude that renal tubular glucose reabsorption is essential for glucose to augment calcium and magnesium excretion. The presence of the parathyroid glands was not required for this phenomenon to occur.

Animals↗
PubMed1982

Relationship between plasma potassium concentration and renal potassium excretion.

To study the relationship between extracellular potassium concentration and renal excretion of potassium, seven chronically adrenalectomized dogs were maintained on a constant intravenous infusion of aldosterone (50 micrograms/day), and constant sodium intake (30 meq/day ) while they received four levels of potassium intake--10, 30, 100, and 200 meq/day--for 7-10 days each. At the conclusion of each level of intake, plasma potassium and renal excretion as well as other variables known to influence potassium excretion were measured. There were minimal changes in arterial pH, mean arterial pressure, extracellular fluid volume, or glomerular filtration rate at any level of potassium intake. The values for plasma potassium and renal potassium excretion attained at each level of intake were: 3.13 +/- 0.24 and 10 +/- 2; 4.18 +/- 0.18 and 21 +/- 6; 4.31 +/- 0.11 and 66 +/- 10; and 4.75 +/- 0.10 meq/liter and 170 +/- 16 meq/day, respectively. Under these experimental conditions in which the levels of aldosterone, sodium intake, arterial pH, arterial pressure, extracellular fluid volume, and glomerular filtration rate remain constant, plasma potassium concentration appears to have a week effect on renal potassium excretion below the normal level of plasma potassium (approx. 11 meq/day change in excretion for each milliequivalent per liter change in concentration). Above the normal level, however, plasma potassium concentration has a powerful effect, 260 meq/day per milliequivalent per liter. The characteristics of the relationship between plasma potassium and renal potassium excretion make it ideally suited for controlling potassium excretion in response to greater than normal potassium intake.

Adrenalectomy↗
PubMed1985

Alpha 2-adrenoceptor antagonism of vasopressin-induced changes in sodium excretion.

Alpha 2-adrenoceptor agonists attenuate vasopressin-mediated changes in water excretion. The effects on sodium excretion, however, are unclear. We therefore utilized the nonrecirculating isolated perfused rat kidney to study the direct effects of vasopressin and alpha 2-adrenoceptor stimulation on sodium and water excretion in the absence of systemic regulatory systems. The perfusate was a Krebs-Henseleit solution (3.5 g/100 ml Ficoll; 1.0% albumin; 36 degrees C) containing prazosin (30 nM) and propranolol (100 nM) to prevent effects of alpha 1- and beta-adrenoceptor stimulation. Vasopressin (10 microU/ml) produced a significant (P less than 0.05) decrease in both water and sodium excretion. Potassium excretion was not significantly altered. Alpha 2-Adrenoceptor stimulation with l-epinephrine (28 nM) reversed (P less than 0.05) the effects of vasopressin on water and sodium excretion. To confirm that this attenuation was mediated by alpha 2-adrenoceptors, an alpha 2-adrenoceptor antagonist, yohimbine, was administered. Yohimbine (300 nM) blocked the effects of epinephrine on sodium and water excretion (P less than 0.05). The adenosine P-site agonist, SQ 22,536 (100 microM), which mediates its effects through inhibition of adenylate cyclase, produced the same reversal as that of epinephrine on vasopressin-mediated changes. Thus alpha 2-adrenoceptor stimulation antagonized the effects of vasopressin on both water and sodium excretion at the renal level. A corollary to this conclusion is that the function-specific activation of renal adenylate cyclase determines the effect of alpha 2-adrenoceptor stimulation.

Adenine↗