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 plasma renin activity (RA), the concentration and the ratio of angiotensin (AI) conversion into angiotensin II (AII), and arginine vasopressin (AVP) level were observed in Wistar rats with pulmonary hypertension (PH) induced by extracardiac left-to-right shunting (LRS), hypobaric hypoxia (HH) and shunting plus HH (SHH). In comparison with normal control rats, RA in LRS and SHH rats showed an increasing trend, although no statistical significance appeared (P > 0.05). No change occurred in HH rats. The concentration and ratio of AI conversion into AII were significantly increased in LRS rats (P < 0.05), but decreased in HH and SHH rats (more markedly in HH rats). AVP increased significantly in LRS rats, and also showed an increasing trend in HH and SHH, but no significance was found (P > 0.05). The action of humoral factors in PH formation was discussed.
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PMID:[The changes in plasma renin angiotensin and arginine vasopressin in pulmonary hypertension rats]. 129 43

Six young healthy subjects underwent a 20 day exposure to altitude, at 4930 m (16,174 ft), to evaluate possible plasma and urine digoxin-like immunoreactive substance (DLIS) changes accompanying the altered water and electrolyte balance induced by hypoxia. We studied DLIS, plasma renin activity (PRA), aldosterone, atrial natriuretic peptide (ANP), and arginine vasopressin (ADH) in serial blood and urine samples. An increase in DLIS in plasma (P less than .005) and urine (P less than .01) was found, while aldosterone was decreased (P less than .02). PRA, ADH, and ANP did not change significantly. A trend to a greater loss of sodium through urinary excretion, correlated with urinary DLIS values (r = 0.47, P less than .01), was observed. Data suggest a possible important role of DLIS in adaptive response of human organism to high altitude.
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PMID:Effects of high altitude exposure on plasma and urinary digoxin-like immunoreactive substance. 132 52

In the present study we investigated the effects of an intranasal administration of 25 micrograms alpha-human atrial natriuretic peptide (alpha-hANP) dissolved in 0.2 mL 0.9% saline on renal excretory function, blood pressure (BP), heart rate (HR), and also its interaction with the renal effects of 20 micrograms deamino-d-arginine vasopressin (d-DAVP) in 10 healthy volunteers. After two 30-min control periods plasma concentrations of ANP and cGMP rose significantly from 14.8 +/- 1.8 pmol/L and 5.9 +/- 0.3 pmol/mL to 23.3 +/- 2.3 pmol/L and 6.6 +/- 0.4 pmol/mL (P less than .05), respectively within 30 min after ANP administration. The levels returned to basal values after 60 min. Urinary cGMP excretion initially rose from 17.9 +/- 3.6 to 46.8 +/- 3.7 pmol/30 min and then returned to control values, whereas plasma renin activity and plasma aldosterone concentration decreased significantly after 30 and 60 min (P less than .05). Systolic and diastolic BP declined slightly by 8% and 7%, respectively, while HR remained unaltered. Urine flow rate and sodium excretion increased by 321% and 190%, respectively (P less than .05). These changes were also significant when data were compared with a time-matched placebo study performed on the preceding day with intranasal administration of 0.2 mL 0.9% saline alone. After 48 h the protocol was repeated but 20 micrograms d-DAVP was administered intranasally 120 min before an intranasal application of 25 micrograms alpha-hANP. Within 120 min d-DAVP had reduced urine flow by approximately 50% (P less than .05), while sodium excretion remained unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intranasal application of atrial natriuretic peptide and 1-deamino-d-arginine vasopressin in healthy volunteers. Hemodynamic, hormonal, and renal excretory effects. 132 53

NG-monomethyl-L-arginine (NMA) and nitroarginine have been reported to be competitive inhibitors of the production of endothelium-derived relaxing factor (EDRF). In chronically instrumented conscious rats, we observed that the pressor response of NMA was attenuated by pretreatment with L-arginine but not by pretreatment with D-arginine, phentolamine, or meclofenamate. Inhibitors of the renin-angiotensin system, captopril and [Sar1,Ile5,Thr8]angiotensin II, did not significantly affect the pressor response of NMA, either. Ten to fifteen minutes after bolus administration of 7-15 mg/kg NMA, when baseline blood pressure was virtually restored, the pressor responses of angiotensin II (ANG II), norepinephrine, and arginine vasopressin were significantly potentiated by approximately 30-40% compared with control values. This potentiation was prevented by pretreatment with L- but not D-arginine. It was also observed in conscious rats subjected to ganglionic blockade. Likewise, the pressor responses of ANG II were significantly increased during infusions of 2 and 5 micrograms/min nitroarginine methyl ester (NAME), dosages that raised baseline blood pressure by 6 +/- 2 and 15 +/- 3 mmHg, respectively. During administration of 5 and 50 micrograms/min NAME, hypotensive responses of methacholine and histamine were only modestly attenuated compared with the responses recorded during infusions of phenylephrine, which raised resting blood pressure to comparable levels. Finally, in freshly isolated rat aorta, NMA inhibited basal and stimulated production of guanosine 3',5'-cyclic monophosphate in a manner comparable to reduced hemoglobin, a known inhibitor of EDRF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:NG-monomethyl-L-arginine and nitroarginine potentiate pressor responsiveness of vasoconstrictors in conscious rats. 844 5

To elucidate the mechanism underlying the sodium retention caused by alpha 1-adrenoceptor blockade in man, a placebo-controlled, randomised, double-blind study has been made of the acute effects of bunazosin an alpha 1-antagonist, on urinary sodium excretion, atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and the renin-aldosterone system in 7 healthy men. A single oral dose of bunazosin 2.0 mg caused a significant reduction (P less than 0.05) in urinary sodium excretion after 0-2 h, 2-4 h, and 4-6 h. The mean values for plasma ANP, AVP, aldosterone, and cortisol concentrations at those times were similar after placebo and bunazosin, and plasma renin activity was significantly increased 2 and 4 h after bunazosin. Pretreatment with oral enalapril 10 mg, an angiotensin converting enzyme inhibitor, did not prevent the bunazosin-induced reduction in urinary sodium excretion. There was a significant positive correlation between the drug-induced changes in blood pressure and urinary sodium excretion. The results suggest that ANP, AVP, and renin-aldosterone may play little role in the sodium retention caused by acute alpha 1-adrenoceptor blockade in man.
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PMID:Acute effect of an alpha 1-adrenoceptor antagonist on urinary sodium excretion, plasma atrial natriuretic peptide, arginine vasopressin, and the renin-aldosterone system in healthy subjects. 135 18

1. The effects of a single oral dose (100 mg) of flosequinan on systemic and regional (forearm, splanchnic and renal) vascular responses to simulated orthostatic stress (lower body negative pressure, LBNP) were investigated in nine healthy male volunteers, in a double-blind, placebo-controlled crossover study. 2. Forty-five minutes after its administration and before LBNP, flosequinan induced a significant decrease in total peripheral and in forearm vascular resistances without any concomitant change in arterial pressure, in heart rate and in the investigated biological parameters (plasma catecholamines, arginine vasopressin and renin activity). 3. After flosequinan and placebo, LBNP induced similar decreases in central venous pressure at all levels of LBNP (-10, -20 and -40 mm Hg) and in pulse pressure at LBNP -40 mm Hg. LBNP-induced increase in forearm vascular resistance was significantly more marked after flosequinan than after placebo at all levels of LBNP, and this was also true for splanchnic vascular resistance but at LBNP -40 mm Hg only. However, inasmuch as the basal values of these two parameters before LBNP were lower after flosequinan than after placebo, their final values after LBNP -40 mm Hg were similar. Finally, LBNP-induced changes in renal vascular resistance, glomerular filtration rate and filtration fraction as well as in plasma catecholamines, arginine vasopressin and renin activity were similar after flosequinan and placebo at all levels of LBNP. 4. Flosequinan affected neither reflex control of heart rate (phenylephrine test) nor non-specific vasoconstrictor responses (cold pressor test). (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flosequinan does not affect systemic and regional vascular responses to simulated orthostatic stress in healthy volunteers. 138 45

During the past 3 decades, groundbased experiments have been performed in order to investigate the effects of increased and decreased gravitational stress, respectively, on the renal response in humans. Experiments that simulate an increase in gravitational load (+Gz) to the subjects (centrifugation, passive head-up titlt [HUT] or lower body negative pressure [LBNP] have clearly demonstrated a decrease in renal sodium and water excretion. Simultaneously, increases in plasma levels of arginine vasopressin (AVP), renin activity (PRA), aldosterone (PA), norepinephrine (NE) and decreases in ANP have been observed. Additionally, experiments that have utilized immersion of seated subjects to simulate a decreased gravitational stress (approximately 0 Gz) have demonstrated that renal water and sodium excretion increases by 100-400% and that plasma AVP, PRA, PA, and NE concentrations are reduced and ANP levels increased. Alternative experimental models conducted to simulate the effects of weightlessness in humans such as head-down tilt (HDT) and lower body positive pressure (LBPP) have yielded less consistent results than those of water immersion (WI) with respect to renal function. However, compared to a seated control HDT clearly induces an increased rate of renal fluid and sodium excretion. The demonstration that central volume expansion during WI is accompanied by an increase in renal fluid and electrolyte excretion and that central hypovolaemia during centrifugation, HUT, and LBNP is accompanied by the opposite effects indicate that changes in central blood volume is an important determinant of the renal functional changes. Results of experiments in humans during weightlessness in space are inconsistent and difficult to interpret. However, they have indicated that a cephalad redistribution of blood and fluid occurs and that this is accompanied by a decrease in total body fluid. Experimental models that, respectively, increase and decrease the gravitational stress in humans constitute promising tools in the investigation of the physiology and pathophysiology of volume regulation.
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PMID:Gravitational stress and volume regulation. 139 44

We investigated the relationship of aerobic fitness to the response of volume-regulating hormones to acute simulated microgravity. Six untrained (UT) and six endurance-trained (ET) healthy young males were studied in the head-down tilt (HDT) position of -6 degrees for 4 h. Peak oxygen uptake (VO2peak) and plasma volume (PV) were significantly greater in the ET (VO2peak = 61.7 +/- 1.6 ml.min-1.kg-1 and PV = 53.1 +/- 2.8 ml.kg-1) than in the UT (VO2peak = 38.4 +/- 1.7 ml.min-1.kg-1 and PV = 38.8 +/- 1.0 ml.kg-1). Plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), norepinephrine (NE), renin activity (PRA), and aldosterone (PA) were measured prior to HDT and at minutes 2, 5, 15, 30, 60, 120, 180, and 240 during HDT. PRA and PA significantly decreased during the time of HDT in both groups. The changes in ANP and NE concentrations were not significantly different between the groups nor across time. However, in the ET subjects, the changes in PRA and NE were significantly correlated with the changes in ANP (r = 0.49, P less than 0.01; and r = 0.86, P less than 0.001, respectively); in the UT subjects, the changes in AVP, PRA, and PA were significantly associated with changes in NE (r = 0.34, P less than 0.03; and r = 0.59; and r = 0.53, P less than 0.01, respectively). PV significantly decreased during HDT, and was primarily related to the decrease in PA in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aerobic fitness: I. Response of volume regulating hormones to head-down tilt. 140

Recent studies in our laboratory indicated that a blunted (40-50%) renal excretory response to isotonic intravenous saline loads occurred in conscious, renal-denervated dogs after 70% of the atrial mass was removed. The blunted responses could not be explained by differences in the responses of arterial pressure, renal nerve activity, or by measured changes of plasma immunoreactive atrial natriuretic peptide (iANP), arginine vasopressin (AVP), plasma renin activity (PRA), or aldosterone (Aldo). The present study was designed to determine whether the central nervous system (CNS) was the source of an unidentified substance, which could account for the blunting of the urine excretory response seen in the atrial-resected dogs. Renal denervation was performed in all dogs to eliminate alterations in efferent renal sympathetic nerve activity derived from reflexes activated during volume expansion. Cardiac denervation (CDX) was used to eliminate sensory cardiac afferent nerve activity to the CNS. A group of five renal-denervated dogs was given an isotonic volume load (400 ml/30 min) before and after complete CDX. Plasma AVP was fixed at normal plasma levels of 3 pg/ml by continuous intravenous infusion. Na and H2O excretion were not different in renal-denervated dogs compared with combined renal and cardiac denervation during the 5 h after the saline load. Plasma AVP and Aldo were unchanged with the volume loads, although PRA rose gradually over the 5 h after the saline loads. Plasma iANP increased transiently in the combined renal and cardiac-denervated state rising from a control of 65-120 pg/ml at the end of the load period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Saline diuresis and natriuresis in unanesthetized dogs: a missing atrial factor? 141 4

The purpose of these studies was to determine whether attenuating the increase in arterial and central venous pressure (CVP) during acute hypoxia can augment the renin and arginine vasopressin (AVP) responses to isocapnic hypoxia in chronically instrumented sheep fetuses. Young (122 +/- 2 days; n = 7) and old (133 +/- 1 days, n = 7) fetuses were exposed to hypoxemia (arterial PO2 = approximately 12-13 Torr) without and with attenuation of the increase in mean arterial pressure (MAP) and CVP with the simultaneous infusion of sodium nitroprusside (NP). NP did not attenuate the bradycardia induced by hypoxia. Plasma renin activity did not increase with hypoxia even when the potentially inhibitory effect of increased MAP and CVP was attenuated with NP. The AVP response to hypoxia was greater in the old fetuses. Furthermore, NP did augment the AVP response to hypoxia in the young but not old fetuses. We conclude that increases in MAP and CVP (i.e., baroreceptor input) do not influence the decrease in heart rate and lack of renin responses to acute hypoxia in the sheep fetus and that increased MAP and CVP seems to restrain the AVP response to hypoxia in younger sheep fetuses.
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PMID:Effect of age and blood pressure on the heart rate, vasopressin, and renin response to hypoxia in fetal sheep. 141 1


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