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)

The effect of beta adrenergic blockade on the increase in plasma renin activity produced by acute respiratory acidosis was studied in chloralose anesthetized dogs. Sixteen mongrel dogs were given 4%, 8% and 12% CO2 in room air, successively. Propranolol (2 mg/Kg) was given to 8 dogs prior to CO2 inhalation. The other 8 dogs served as the control group. The response of elevated plasma renin activity during 4% and 8% CO2 inhalation was not different between the control and propranolol groups. However, the increase of plasma renin activity in the control group was greater than that of the propranolol treated group during 12% CO2 inhalation. It is suggested that activation of beta adrenergic receptors is not the sole factor in renin control during acute respiratory acidosis, although these receptors do mediate a significant fraction of the renin response to CO2 inhalation.
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PMID:The effect of beta adrenergic receptor blockade on the renin response to respiratory acidosis. 3 Aug 49

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.
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PMID:Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates. 37 15

Experiments were designed to clarify the factors affecting renin released during in vitro experiments. Kidneys from rat, dog, and pig were used. Experiments were done in which the gas phase was either bubbled through the incubation medium or layered above it. Renin released into the incubation medium disappeared very rapidly when gas was bubbled through the medium. The decline was similar in mediums bubbled with oxygen-CO2 (95%--5%) or nitrogen-CO2 (95%--5%). The half-life of renin activity in the bubbled medium was approximately 15 min in both cases. However, in experiments in which nonbubbled medium was used throughout, renin released into the incubation medium did not disappear after removal of slices. These data are interpreted to mean that the renin released into the incubation medium is inactivated at the air-water interface.
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PMID:Renin inactivation during in vitro experiments. 44 87

The effects of arterial PCO2 on plasma activity was studied in chloralose anesthetized dogs undergoing carefully controlled respiratory acidosis. Plasma renin activity, measured by radioimmunoassay, was enhanced (P less than 0.001) during inhalation of CO2 despite insignificant changes in renal blood flow and arterial pressure. Although underlying mechanism remained to be investigated, activation of sympathetic nervous system and intrarenal effects of CO2 seemed to be involved in this enchancement.
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PMID:The effects of respiratory acidosis on plasma renin activity in the dog. 119 7

In dogs, plasma renin activity (PRA) was increased by anesthesia, by hypercapnia and by extreme hypoxia (paO2 47.6 mm Hg). Relatively moderate hypoxia (paO2 47.6 mm Hg) and artificial respiration had no appreciable influence on PRA. It appears that the sympathomimetic stimulus of CO2 has an important bearing on PRA.
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PMID:[Proceedings: Experimentally induced effects on the plasma renin activity]. 121 77

The present study was undertaken to assess the influence of acute metabolic acidosis on the activity of renin-angiotensin-aldosterone system and renal function in a group of seven one-week-old neonates with mean birth weight of 2164 g (range: 1300-3750 g) and mean gestational age of 34 weeks (range: 28-40 weeks) undergoing oral NH4Cl load. NH4Cl was given in a dose of 2.8 mEq/kg to evaluate renal acidification. Prior to and following NH4Cl administration blood acid-base parameters, plasma urinary electrolytes, creatinine and aldosterone concentration as well as plasma renin activity, glomerular filtration rate, urine flow rate and net acid secretion were measured. NH4Cl administration significantly depressed blood pH (P < 0.05), total CO2 content (P < 0.01) and base excess (P < 0.01) and resulted in a significant elevation of plasma potassium concentration (P < 0.05). Furthermore, NH4Cl ingestion significantly increased urine flow rate, sodium, chloride and net acid excretion. In response to NH4Cl acidosis no consistent change in plasma renin activity and plasma aldosterone concentration could be detected. There was, however, an about 50% increase in urinary aldosterone excretion from the control value of 4.1 +/- 1.2 micrograms/day to 6.8 +/- 2.3 micrograms/day (P < 0.05) after NH4Cl administration. These data suggest that the responsiveness of neonatal adrenals to stimulation by metabolic acidosis is blunted, acidosis therefore, may play a minor role in the neonatal hyperfunction of renin-angiotensin-aldosterone system.
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PMID:Effect of NH4Cl acidosis on the function of renin-angiotensin-aldosterone system in newborn infants. 128 79

Changes in arterial pressure commonly accompany respiratory adaptations. The purpose of this study was to determine, in awake dogs (n = 6), the degree to which small acute decreases in arterial pressure affect ventilation and acid-base balance. Mean arterial pressure (MAP) was reduced by 6 +/- 2, 10 +/- 3, and 16 +/- 2% by intravenous infusion of sodium nitroprusside for sequential 20-min periods. In another experiment, the ventilatory response to hypercapnia was determined during MAP reduction of 16 +/- 3%. Step reductions in MAP were accompanied by increases in minute ventilation (maximum increase 152 +/- 75%) and step reductions in arterial PCO2 (PaCO2; maximum reduction -4.8 +/- 0.8 Torr). Although eupneic PaCO2 threshold was lowered during MAP reduction, ventilatory sensitivity to CO2 remained unchanged. Despite the lowered PaCO2, arterial [H+] remained constant (acid-base balance was maintained) as a result of a concurrent decrease in strong ion difference. Plasma renin activity increased during MAP reduction (93 +/- 39%) and may have contributed to the increase in minute ventilation, inasmuch as angiotensin II can stimulate respiration by a central mechanism. Evidence is provided that nitroprusside is unlikely to be a primary factor in these hypotensive responses. We conclude that relatively modest decreases in MAP have a consistent stimulatory effect on respiratory control. Therefore it is important to take into account effects of small changes in MAP when interpreting mechanisms for respiratory responses in awake animals.
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PMID:Ventilation is stimulated by small reductions in arterial pressure in the awake dog. 144 3

The control of aldosterone secretion may be altered during acute changes in arterial blood gases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 +/- 2.0 ng.ml-1.h-1), ACTH (96 +/- 32 pg/ml), and ALDO (10 +/- 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 +/- 69 pg/ml) and ALDO (to 33 +/- 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 +/- 14 pg/ml) and ALDO (to 30 +/- 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 +/- 2 ng.ml-1.h-1), ACTH (to 397 +/- 114 pg/ml), and ALDO (to 41 +/- 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (less than 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (Po2 approximately 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.
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PMID:Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats. 283 42

The object of this study was to assess the effect of moderate acute hypoxemia on plasma concentrations of atrial natriuretic factor (ANF), arginine vasopressin (AVP), plasma renin activity (PRA) and urinary excretion of prostaglandin E2 (UPGE2V). Eight volunteers were exposed for 2 hours to a gas mixture containing 10% O2, 4.5% CO2 and 85.5% N2. Hypoxia increased diastolic blood pressure and free water clearance. Hypoxia did not change the AVP, PRA or UPG2V, although increased ANF from 17.7 +/- 3.4 pg/mL to 27.2 +/- 1.7 pg/mL (p less than 0.005) at 120 minutes. ANF changes were closely associated with the rise in blood pressure.
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PMID:Effect of moderate hypoxemia on atrial natriuretic factor and arginine vasopressin in normal man. 296 34

Acute hypoxia has been reported to induce a decrease in aldosterone levels despite no change or increases in plasma renin activity and ACTH. Converting enzyme inhibition and/or mild hypokalemia have been suggested as possible mechanisms for this dissociation. We studied 15 patients with chronic obstructive pulmonary disease (COPD) who used continuous ambulatory O2 therapy (home O2). Group A (n = 10) had O2 discontinued for 30 min before exercise to induce hypoxemia; Group B (n = 5) had O2 continued for 30 min (time control). Discontinuation of home O2 in Group A resulted in a significant fall in Pao2 from 77 +/- 6 to 51 +/- 2 torr. Arterial CO2 tension decreased and the pHa increased slightly. Renin, angiotensin II, plasma potassium, and sodium did not change during hypoxemia, whereas ACTH increased significantly. Despite this, aldosterone decreased from 26 +/- 5 to 18 +/- 2 ng/dl. Group B (time control) did not exhibit significant changes in hormones over 30 min, indicating that the effects observed in Group A were specific to O2 discontinuation. Exercise in Group A induced significant increases in ACTH, potassium, and aldosterone. We conclude from these data that acute hypoxemia in patients with COPD results in a decrease in aldosterone not related to converting enzyme inhibition, ACTH, or plasma potassium.
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PMID:Renin-angiotensin II-aldosterone and ACTH-cortisol control during acute hypoxemia and exercise in patients with chronic obstructive pulmonary disease. 300 60


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