Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normothermic cardiopulmonary bypass (CPB) is used in cardiac surgery at some institutions. To compare hemodynamic and hormonal responses to hypothermic (29 degrees C) and normothermic nonpulsatile CPB, 20 adults undergoing coronary artery bypass graft and/or aortic valve replacement were studied. Hemodynamic measurements and plasma hormone concentrations were obtained from preinduction to the third postoperative hour. The two groups were given similar amounts of anesthetics and vasodilators. Systemic vascular resistance increased only during hypothermic CPB, and heart rate was higher at the end of hypothermic CPB. Postoperative central venous pressure and pulmonary capillary wedge pressure were lower after hypothermic CPB. Oxygen consumption decreased by 45% during hypothermic CPB, did not change during normothermic CPB, but increased similarly in the two groups after surgery; mixed venous oxygen saturation (SvO2) was significantly lower during normothermic CPB. Urine output and composition were similar in the two groups. In both groups, plasma epinephrine, norepinephrine, renin activity, and arginine vasopressin concentrations increased during and after CPB. However, epinephrine, norepinephrine, and dopamine were 200%, 202%, and 165% higher during normothermic CPB than during hypothermic CPB, respectively. Dopamine and prolactin increased significantly during normothermic but not hypothermic CPB. Atrial natriuretic peptide increased at the end of CPB and total thyroxine decreased during and after CPB, with no difference between groups. This study suggests that higher systemic vascular resistance during hypothermic CPB is not caused by hormonal changes, but might be caused by other factors such as greater blood viscosity. A higher perfusion index during normothermic CPB might have allowed higher SvO2.
...
PMID:Hemodynamic and hormonal responses to hypothermic and normothermic cardiopulmonary bypass. 156 99

To study the mechanisms of alcohol-induced diuresis, the plasma concentration of immunoreactive atrial natriuretic peptide and arginine vasopressin, serum sodium and osmolality, plasma renin activity and aldosterone, urinary sodium and volume, free water clearance, blood pressure and heart rate were measured in seven healthy men after oral intake of ethanol (1.5 g kg-1 in 6 h). Serum ethanol levels increased to 27 +/- 4 mmol l-1 (mean +/- SD) in 30 min and remained detectable for 14 h. Serum osmolality rose from 280 +/- 10 to 340 +/- 4 mosm kg-1 in 2 hours (P less than 0.01) and was 300 +/- 4 at 14 h (P less than 0.01). Formation of hypotonic urine began after the alcohol intake and resulted in a net loss of 0.9 +/- 0.1 kg water in 2 h. Free water clearance increased from -3.4 +/- 1.4 to 2.8 +/- 1.5 ml min-1 in 2 h (P less than 0.01). Plasma immunoreactive arginine vasopressin decreased from 5.7 +/- 2.1 to 3.3 +/- 1.3 ng l-1 (P = 0.05) in 30 min and increased to 17 +/- 25 and 12 +/- 10 ng l-1 at 6 and 12 h, respectively (P less than 0.05 for both). Plasma immunoreactive atrial natriuretic peptide levels decreased from 17 +/- 9 to the minimum of 11 +/- 3 ng l-1 in 2 h (P less than 0.01) and returned to the initial levels in 6 h. Serum sodium, plasma renin activity and plasma aldosterone increased maximally by 4 +/- 2, 165 +/- 153 and 143 +/- 101% (P less than 0.01 each) during 1-6 h.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Plasma immunoreactive atrial natriuretic peptide and vasopressin after ethanol intake in man. 153 84

Seven normal subjects underwent sequential 20-min infusion of arginine vasopressin (AVP) at 0.5 and 2 ng/(kg.min) and a complete right-side heart hemodynamic evaluation during the study to analyze the effect of this hormone on atrial natriuretic factor (ANF) secretion in humans and to elucidate whether this effect was primary or secondary to the hemodynamic or hormonal changes induced by AVP. Plasma ANF levels increased at the end of the first (P less than 0.05) and second (P less than 0.01) infusion periods. No significant changes in mean arterial, pulmonary artery, right and left atrial pressures were recorded during the study. Cardiac output (P less than 0.05) and heart rate (P less than 0.05) decreased, while total vascular resistances (P less than 0.05) increased with respect to basal values in both infusion periods. Plasma renin activity decreased (P less than 0.01) at the end of the infusion, while plasma aldosterone, epinephrine and norepinephrine showed no significant changes. We conclude that arginine vasopressin increases plasma ANF levels in humans and that this effect cannot be ascribed to hemodynamic or hormonal changes induced by this hormone, suggesting a direct effect of vasopressin on the atrial myocyte.
...
PMID:Arginine vasopressin infusion increases plasma levels of atrial natriuretic factor in humans. 153 5

In this pilot study we investigated the effects of a 4-h infusion of atrial natriuretic peptide (8-33 Met ANP) on hemodynamic, renal, and hormonal parameters in 12 patients with hypertension. Either 8-33 ANP in 5% mannitol (0.7 microgram/min [eight patients] and 1.05 micrograms/min [four patients]) or placebo (5% mannitol) was infused for 4 h on 2 consecutive days in a randomized double-blind crossover design. The plasma levels of ANP were not significantly different between the two doses of ANP and therefore the results from the two doses were combined. Plasma ANP increased from 61 +/- 24 pg/mL to 291 +/- 55 pg/mL after 2 h and to 288 +/- 40 pg/mL after 4 h. ANP caused a significant lowering of systolic blood pressure after 2 h of infusion from 148 +/- 5 mm Hg to 142 +/- 5 mm Hg (P less than .05) and to 128 +/- 6 after 4 h (P less than .01). Two hours after discontinuation of the infusion, systolic blood pressure was 126 +/- 6 and 135 +/- 7 mm Hg 4 h after the end of the infusion. Diastolic blood pressure did not change. Heart rate increased from 69 +/- 3 beats/min to 74 +/- 3 beats/min after 4 h and to 78 +/- 4 beats/min 2 h after termination of the infusion. Cardiac output did not change significantly. Urinary sodium and chloride increased significantly but creatinine clearance did not change. Plasma aldosterone decreased after 2 h of ANP infusion from 9.8 +/- 1.7 ng/dL to 6.7 +/- 0.9 ng/dL (P less than .01) and to 6.5 +/- 1.2 ng/dL after 4 h (P less than .05). Plasma renin activity decreased from 0.81 +/- 0.1 ng angiotensin I/mL/h to 0.57 +/- 0.1 after 2 h of infusion (P less than .05). There were no significant changes in plasma catecholamines or arginine vasopressin. Two patients developed severe hypotension and bradycardia and one of them had a sinus pause of 7.4 sec associated with loss of consciousness. Neither of these two patients had a significant increase in plasma catecholamines in response to the severe hypotension, suggesting that ANP may have inhibited their sympathetic response and increased their sensitivity to vagal cardioinhibitory reflexes. In conclusion, infusion of ANP in hypertensive patients causes prolonged lowering of systolic blood pressure with no change in diastolic pressure and cardiac output.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Effect of atrial natriuretic peptide (8-33-Met ANP) in patients with hypertension. 153 72

Eighteen beagles were chronically instrumented with an anterior third ventricular (A3V) infusion device to analyze, in conscious dogs, the involvement of central atrial natriuretic peptide (ANP) in body fluid and blood pressure control. The dogs' osmotic and body fluid homeostasis was challenged by 24 h water deprivation or blood withdrawal (12 ml/kg body wt) to elucidate possible modifying influences on the release of arginine vasopressin (AVP), angiotensin II (ANG II), and drinking. Three series of experiments were performed: 1) infusion of ANP (500 ng/min) dissolved in artificial cerebrospinal fluid (aCSF) and given for 10 min, 2) infusion of aCSF alone for the same length of time, and 3) time control experiments without infusion. Plasma AVP and ANG II were analyzed by radioimmunoassay, and in several experiments on dehydrated dogs, plasma norepinephrine and epinephrine were additionally determined by high-performance liquid chromatography. Various blood parameters and rectal and ear skin temperatures were measured. Arterial pressure and heart rate were recorded in three animals additionally equipped with carotid loops. Changes in plasma AVP and ANG II induced by dehydration and bleeding were not significantly modified by A3V infusions of ANP and aCSF in comparison to time controls. Blood pressure changes were similar in experiments with A3V ANP infusion and time controls during bleeding and reinfusion. It is concluded that central ANP is not important in the control of vasopressin and renin-angiotensin systems during osmotic and volume challenges in conscious dogs.
...
PMID:Central ANP administration in conscious dogs responding to dehydration and hypovolemia. 153 4

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on fluid-regulating hormones during exercise, 10 healthy men underwent upright leg cycle exercise on land and with WI. Venous plasma renin activity and plasma venous concentrations of atrial natriuretic peptide, plasma aldosterone, and arginine vasopressin were determined at exercise intensities corresponding to approximately 40, 60, 80, and 100% peak oxygen consumption (VO2) and at minutes 1 and 5 of seated rest recovery within each environment. Peak VO2 did not differ on land and with WI. Atrial natriuretic peptide concentration was higher (P less than 0.05) and plasma renin activity was lower (P less than 0.05) in water than on land at 40% peak VO2 through minute 5 of recovery. Plasma aldosterone and arginine vasopressin concentrations were lower (P less than 0.05) in water at peak exercise and at minutes 1 and 5 of recovery. Osmolality and plasma sodium and potassium concentrations during exercise were similar in water and on land. The results indicate that WI alters the circulating levels of several hormones involved in fluid and electrolyte regulation during exercise. These hormonal alterations can best be explained by stimulation of low-pressure baroreceptors and atrial stretch due to increased central blood volume with head-out WI.
...
PMID:Fluid-regulating hormones during exercise when central blood volume is increased by water immersion. 153 5

Hyponatremia is common following subarachnoid hemorrhage and has alternatively been attributed to either the inappropriate secretion of antidiuretic hormone or natriuresis causing intravascular volume contraction. We prospectively studied body sodium and intravascular volume regulation in 19 patients, beginning within 3 days after acute aneurysmal subarachnoid hemorrhage occurred, in order to determine the impact of hypervolemic therapy on both hyponatremia and volume contraction and to ascertain whether humoral factors account for hyponatremia. Serial measurements of plasma arginine vasopressin, atrial natriuretic factor, renin activity, aldosterone, and catecholamines were correlated with body sodium and fluid balance, change in blood volume, serum sodium concentration, and osmolality. Six patients (32%) developed hyponatremia, but only 2 had a negative sodium balance. In most patients, levels of atrial natriuretic factor were elevated, while plasma renin activity and aldosterone concentrations were generally suppressed. Plasma arginine vasopressin levels were not suppressed during hypo-osmolality and did not correlate with serum osmolality in hyponatremic patients. Only 1 patient had a decrease in blood volume, which was associated with marked rises in aldosterone and plasma renin activity, but normal serum sodium and plasma atrial natriuretic factor levels. We conclude that following subarachnoid hemorrhage: (1) Hypervolemic therapy prevents volume contraction but not hyponatremia, (2) humoral factors may favor both sodium loss and water retention, and (3) arginine vasopressin regulation is disturbed and may contribute to hyponatremia.
...
PMID:Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage. 153 78

The objective of this study was to investigate the role of the renal nerves in the pathogenesis of salt-induced hypertension in sinoaortic-denervated uninephrectomized rabbits. Twelve rabbits were divided into two groups. Sinoaortic-denervated uninephrectomized rabbits with intact renal nerves (sham group: n = 6) and without renal nerves (RDN group; n = 6). In both groups, 2 days of 154 meq/l NaCl loading was followed by 10 days of 1,700 meq/l NaCl loading. We administered 154 meq/l or 1,700 meq/l NaCl intravenously at every 8 h. Serial changes in mean arterial pressure (MAP) and heart rate (HR) were recorded using a microcomputer system. We chronologically measured hematocrit, serum osmolality, serum sodium, potassium, and chloride concentration, serum creatinine, plasma renin activity, plasma aldosterone, plasma norepinephrine, plasma arginine vasopressin, and plasma atrial natriuretic peptide. Urine volume and body weight were recorded every day, as were urinary concentrations of sodium, potassium, and chloride. The basal value of MAP in the sham group was significantly higher than that in the RDN group (on day -2, 111 +/- 1 mmHg for sham, 99 +/- 2 for RDN, P less than 0.001). Hypertonic saline loading induced an elevation of blood pressure in the sham group (126 +/- 2 mmHg on day 4, 127 +/- 2 on day 7, 124 +/- 4 on day 10). There were no significant changes in the response to salt loading in the RDN group. In the sham group, the retention of sodium was significant compared with that in the RDN group on day 5, and this difference was maintained until the end of the experiments.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Renal nerves contribute to salt-induced hypertension in sinoaortic-denervated uninephrectomized rabbits. 159 Apr 68

Hemodialysis-associated skeletal muscle cramps are generally ascribed to a reduction in plasma volume, but during this procedure, it is not known how volume contraction results in cramps. To elucidate this mechanism, we compared responses to one hour of 60 degrees head-up tilt in 8 patients who cramped during no more than one-sixth of their dialyses and in 8 patients who cramped at least half the time. Age and recumbent blood pressure were similar in each group, but more patients with frequent cramps had diabetes underlying their renal failure (p = 0.013) and had been dialyzed for less than 3 years (p = 0.020). Baseline plasma renin activity and plasma norepinephrine and arginine vasopressin concentrations were similar in both groups, except plasma renin activity in one patient with frequent cramps, which was 15 times higher than in the other patients. After tilting, systolic blood pressure fell an average of 17% in patients who cramped infrequently (p = 0.0031) but only 10% in frequently cramping patients. The ratio of tilt/recumbent norepinephrine levels exceeded 1.5 in 7 patients with frequent cramps but was less than this in 6 patients who cramped infrequently (p = 0.020). One of the 2 infrequently cramping patients with a ratio above 1.5 was the only individual to have a normal renin response to tilt. We propose that cramps are prone to occur during hemodialysis in patients whose sympathetic nervous system response to volume stress is partially intact but is not modulated by concurrent activation of the renin-angiotensin system.
...
PMID:Response to head-up tilt in cramping and noncramping hemodialysis patients. 159 45

L-158,809 (5,7-dimethyl-2-ethyl-3-[[2'-(1H-tetrazol-5yl)[1,1']-bi- phenyl-4-yl]-methyl]-3H-imidazo[4,5-b]pyridine) is a potent, competitive and specific antagonist of AT1 subtype of angiotensin II (AII) receptors in in vitro radioligand binding and functional isolated tissue assays. The present study was carried out to characterize the in vivo pharmacology of this potent AII receptor antagonist. In conscious, normotensive and anesthetized pithed rats, L-158,809 inhibits AII (0.1 microgram/kg i.v.) elevations in blood pressure without altering pressor responses to methoxamine or arginine vasopressin. In conscious rats, the relative potencies (ED50) were 29 micrograms/kg i.v. and 23 micrograms/kg p.o. Duration of action with single i.v. or p.o. doses exceeded 6 hr in rats. In similar experiments using rhesus monkeys, the potencies of L-158,809 were 10 micrograms/kg i.v. and approximately 100 micrograms/kg p.o. In these rats and monkeys, L-158,809 was 10 to 100 times more potent than DuP-753 (losartan) and approximately 3 times more potent than the metabolite, EXP3174. AII-induced elevation of plasma aldosterone in rats was also inhibited by L-158,809. Unlike angiotensin converting enzyme inhibitors, L-158,809 did not potentiate the hypotensive responses to i.v. bradykinin. L-158,809 was antihypertensive in high renin hypertensive rats (aortic coarction) and volume-depleted rhesus monkeys. The maximum hypotensive responses with acute doses of L-158,809 were equal to those with an angiotensin converting enzyme inhibitor in these renin-dependent animal models. From these in vivo data, L-158,809 is a selective AII receptor antagonist with high potency, good p.o. absorption, long duration and antihypertensive efficacy equal to angiotensin converting enzyme inhibition after single doses.
...
PMID:In vivo pharmacology of L-158,809, a new highly potent and selective nonpeptide angiotensin II receptor antagonist. 162 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---