Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The systemic hemodynamic effects of deep hypotension (MAP: 38 +/- 6 mm Hg) induced by sodium nitroprusside (S.N.) were studied in 20 patients who underwent surgery for cerebral aneurysm. The hemodynamic measurements were performed four times.: (1) during the preoperative period, (2) during stable anesthesia just before hypotension, (3) during stable hypotension, (4) 20 minutes after stopping nitroprusside. All patients were mechanically ventilated with a constant tidal volume and rate. Parameters for acid-base balance and Pa O2 were also recorded. Nitroprusside produces arterial and venous dilatation which results in a decrease of afterload and preload. The mean dosage of S. N. was 18 mcg/kg/mn. Systemic vascular resistances decreased by 62 p. cent. Mean arterial pressure decreased by 53 p. cent; it reached 40 mm Hg. Fall in preload resulted in a decrease in pulmonary wedge pressure by 28 p. cent. This fall in preload produced a decrease in stroke index according to Frank-Starling's mechanisms. However tachycardia allowed a rise in cardiac index by 20 p. cent. Increase of pulmonary wedge pressure at 8-10 mm Hg by blood volume expansion maintains stroke index at control level. Under these conditions the elevation of cardiac index is due to tachycardia. Cardiac rhythm disorders (wandering pace-maker, nodal rhythm) are observed in 5 patients after having stopped nitroprusside.
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PMID:[Deep hypotension induced by sodium nitroprusside in neurosurgery. I.--Systemic hemodynamic effects (author's transl)]. 48 87

A 10 mg bolus of the angiotensin blocker saralasin was injected 113 times in 68 subjects with essential or renovascular hypertension. Ninety percent of injections caused a transient increase in blood pressure, which correlated with plasma renin activity (PRA) (r = -0.54); Mean increase at 2 minutes was 21/13.4 mm Hg (P less than 0.001) and was independent of pre-injection control blood pressure, with a rapid decrease to or below control values thereafter. Thirty-seven subjects were studied on successive days before and after furosemide-induced sodium depletion (152 +/- 26 mEq [SE] sodium loss). In the low renin group, sodium depletion did not change PRA or the magnitude of the pressor response to saralasin, but significantly decreased control MAP by 13 mm Hg (P less than 0.01). In normal and high renin patients, MAP was unchanged after diuresis, but PRA increased significantly and the pressor response was attenuated. The net effect of sodium depletion was to reduce the pressor response to saralasin in all renin subgroups by 9 to 12 mm Hg. Saralasin bolus injection, unlike infusion, saturates available vascular receptors only briefly, eliminating prolonged pressor responses.
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PMID:Pressor response to saralasin (1-sar-8-ala-angiotensin II) bolus injection in hypertensive patients. 63 40

On the basis of microsphere distribution, inert gas washout, and standard clearance data, the effects of acute hypoxia and hypercapnia on the kidney were studied in anesthetized, mechanically ventilated rats. Moderate hypoxia (mean PO2, 48 mm Hg) did not significantly change diuresis, GFR, and tubular sodium rejection. Due to a decrease in renal vascular resistance (R) from 40.1 to 31.8 mm Hg ml-1 min, mean renal blood flow stayed constant in spite of a significant drop in mean arterial blood pressure. Hypoxic changes in R were not accompanied by significant changes in intrarenal distribution of blood flow (IDBF). In severe hypoxia (PO2 less than 45 mm Hg) with oliguria and marked arterial hypotension, R was the lowest of all groups (28.8 mm Hg ml-1 min). Hypercapnia did not significantly change the renal excretory parameters, although an increase in R (without change in IDBF), together with a decrease in MAP caused a marked drop in mean renal blood flow. From these studies we conclude: 1) in the anestheized rat, acute hypoxia caused significant changes in intrarenal hemodynamics without changes in excretory function, 2) hypoxic renal vasodilation persists even in severe hypotension with oliguria and anuria, 3) in acute hypoxia and hypercapnia, changes in renal blood flow and renal vascular resistance are not accompanied by significant changes in IDBF.
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PMID:Renal function and intrarenal hemodynamics in acutely hypoxic and hypercapnic rats. 68 25

Cardiac and circulatory function (cardiac output, stroke volume, heart rate, mean arterial pressure = MAP, total peripheral resistance = TPR), further renal function (PAH- and inulin clearance, filtration fraction, urinary excretion, renal sodium- and potassium excretion) were measured on 15 patients undergoing cardiac surgery to whom Dopamine and Orciprenaline were administered in increasing doses of 100 mug - up to 500 mug/min (Dopamine) and 10 mug - to 20 mug/min (Orciprenaline). An infusion of Dopamine up to 250 mug/min caused a dosis-related increase of the cardiac output up to 31% (2P less than 0.001) without essential increasing of the MAP and of the heart rate. Dopamine caused a decrease of the TPR up to 24%. Doses of Dopamine over 250 mug/min cause an increase of the MAP and of the heart rate without a real increase of the cardiac output. Renal function improved under increasing doses of Dopamine, effective renal plasma flow (ERPF) up to 74%, urinary excretion up to 130%, sodium and potassium excretion up to 60% respectively. After administering Orciprenaline in a dosis of 20 mug/min cardiac output increases up to 28%, MAP and heart rate up to 12% and 17% respectively. After the administration of Orciprenaline (20 mug/min) and Dopamine (500 mug/min) frequent extra systoles were observed without any increase of the cardiac output; MAP increased by 12%, TPR decreased by 16% after 20 mug/min of Orciprenaline. ERPF decreased slightly after Orciprenaline. Urinary excretion was reduced by a half.
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PMID:[Comparing studies on the influence of dopamine and orciprenaline on cardiac and renal function of patients after cardiac surgery (author's transl)]. 108 62

In the present study we investigated the in vivo and in vitro renal responsiveness to ANF, and the adaptation of ANF receptors in compensatory renal hypertrophy in the rat. One week after left nephrectomy (UNx), plasma levels of immunoreactive ANF, blood pressure (MAP), hematocrit (Hct), and urine flow rate (V) were unaltered compared to control (C) rats. Baseline GFR and potassium excretion (UKV) were significantly higher, and sodium excretion (UNaV) tended to be elevated in UNx rats. Administered ANF led to similar dose-related decreases in MAP and increases in Hct in UNx and C rats. However, at each dose of infused ANF, absolute values and the increase in GFR and UNaV were higher in UNx than in C rats. Hypertrophied (H) kidneys were removed from UNx and perfused in vitro to determine distribution and density of ANF receptors, responsiveness to ANF, and receptor-mediated organ clearance of 125I-ANF1-28. The density of ANF receptors in cortex, outer medulla, and papilla of H kidneys was not significantly different from that in C kidneys. In H isolated kidneys, ANF led to dose-related increases in GFR, V, UNaV, and UKV that were indistinguishable (P greater than 0.05) from those in C kidneys. Receptor-mediated organ clearance of 125I-ANF1-28 in isolated H kidneys was 2.8 +/- .02 ml/min, a value not significantly different (P greater than 0.05) from that in C kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal receptors and effects of atrial natriuretic factor in compensatory renal hypertrophy. 132 31

The impact of esmolol infusion on hemodynamics, ventricular performance, venous admixture, sympathoadrenal, and renin-angiotensin system responses during sodium nitroprusside (SNP)-induced hypotension was studied in 11 patients undergoing lymph node dissection during general anesthesia with 60% nitrous oxide and fentanyl. Radial arterial and thermistor-tipped pulmonary catheters were employed for hemodynamic monitoring. Arterial and mixed venous blood gas tensions, arterial plasma renin activity (PRA), and plasma catecholamine levels were measured. Derived hemodynamic parameters and venous admixture (Qs/Qt) data were obtained from standard equations. Transesophageal echocardiography (6 patients) was used to assess left ventricular performance using the relationship between end-systolic wall stress (ESWS) and velocity of circumferential shortening (VCFC). After surgical incision, arterial hypotension was induced with SNP alone. Esmolol was infused at each of the following rates in sequence: 200, 300, and 400 micrograms/kg/min. Each esmolol infusion lasted 20 minutes and the SNP dose was adjusted to maintain MAP at 55 to 60 mm Hg. The mean dose of SNP required to induce hypotension was 5.5 micrograms/kg/min +/- 0.5 SE. Compared to prehypotension values, SNP induced significant increases in Qs/Qt and reductions in PaO2, systemic vascular resistance (SVR), and stroke volume index (SVI). Esmolol infusion caused dose-dependent (highest with 400 micrograms/kg/min) reductions in the SNP requirement, heart rate (HR), SVI, Qs/Qt, and PRA, and also led to significant increases in SVR and left ventricular (LV) internal diameter in diastole as well as systole. Furthermore, esmolol infusion was associated with a dose-dependent downward and leftward shift of the ESWS versus VCFC relationship, implying diminished contractility.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Esmolol infusion during nitroprusside-induced hypotension: impact on hemodynamics, ventricular performance, and venous admixture. 134 63

There is general concern that major blood loss during deliberate hypotension could produce severe organ ischemia, but documentation of the magnitude of this response remains obscure. To examine this response, we studied 43 male Sprague-Dawley rats that were divided into seven groups: the control animals received 1 MAC (1.4%) isoflurane only; the hypotensive animals received a 1.4% isoflurane baseline anesthetic and were then rendered hypotensive by either increasing the isoflurane concentration (dISO), or by adding sodium nitroprusside (SNP), or 2-chloroadenosine (2AD) to the baseline anesthetic, decreasing the MAP to 51 mmHg; hemorrhaged animals had hypotension produced in the same manner as for the hypotensive animals, but additionally were bled 20% of estimated blood volume during deliberate hypotension produced with either deep isoflurane (dISOH), sodium nitroprusside (SNPH), or 2-chloroadenosine (2ADH). After a 25-min period of hypotension, or hypotension plus hemorrhage, cardiac output and blood flow to brain, heart, gastrointestinal tract, kidney, and liver were measured with 141Ce-labelled 15-microns microspheres. Hypotension was associated with decreased blood flow to the kidneys in all groups and to the liver in the 2AD group and an increased blood flow to the heart in the SNP and 2AD groups. Hemorrhage decreased blood flow during deliberate hypotension to the brain and the gastrointestinal tract in the dISOH and 2ADH groups and to the liver in the dISOH group. Our results suggest that hemorrhage during deliberate hypotension with dISO or isoflurane plus 2AD may be associated with compromised organ blood flow, whereas blood flow to vital organs is maintained after 20% hemorrhage during isoflurane and superimposed SNP-induced hypotension.
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PMID:The influence of hemorrhage on organ perfusion during deliberate hypotension in rats. 834 11

The aim of this study was to examine the contribution of the renin angiotensin system to the antinatriuresis that follows acute volume depletion. Four groups of six dogs each were studied. The first group was exposed to saline expansion (8% body weight) (SE). The second group was exposed to acute volume depletion (2% body weight) followed in one hour by saline expansion (AVD). The third and fourth groups were similar but in dogs treated with high doses of captopril (SE + C and AVD + C). Dogs were anesthetized with phenobarbital. Control measurements were made for 30 minutes before and 60 minutes during saline expansion. Glomerular filtration rate (inulin), renal blood flow (para-aminohippuric acid) and mean arterial pressure were similar in the four groups during the experiment. The increase in fractional sodium excretion from the control period to the end of saline expansion was in the SE group from 0.6 +/- 0.2 to 6.4 +/- 1% and in the SE + C group from 1.1 +/- 0.3 to 8.5 +/- 1.3%. In contrast, in the AVD group it only rose from 0.8 +/- 0.2 to 3.5 +/- 0.7% and in the AVD + C group from 1.3 +/- 0.4 to 4.1 +/- 0.6%. Therefore, the increment in sodium excretion during saline expansion was significantly lower in dogs exposed to acute volume depletion, independent of the treatment with captopril. The blunted natriuresis cannot be explained by differences in GFR, RBF or MAP. These results suggest that renin angiotensin system is not the responsible agent of the sodium retention that follows acute volume depletion.
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PMID:Role of angiotensin II in the antinatriuresis that follows acute volume depletion. 148 79

The effect of 1-deamino-8-D-arginine vasopressin (DDAVP) on mean arterial pressure, pulse rate (PR), plasma renin activity (PRA), plasma factor VIIIc and von Willebrand factor were studied in a case of persistent lithium-induced nephrogenic diabetes insipidus (LINDI). 20% decrease in MAP, 22% increase in PR, 100% in PRA, and release of coagulation factors (2- to 3-fold) were noticed after infusion of 0.3 micrograms/kg DDAVP. Urinary prostaglandin (PG) E2 were enhanced. The treatment of this LINDI by PG synthesis inhibitor (PSI) combined with a low osmotic diet (LOD) led to a 51% fall in urine volume, 57% in free water clearance and 75% in sodium clearance. Urinary osmolality rose by 42% but remained low, probably in part because of the LOD. Urinary PGE2 was about one fifth of the initial high value. The results argue for (1) an end-organ resistance to DDAVP confined to the kidneys in LINDI and (2) an effectiveness of indomethacin combined with an LOD.
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PMID:Normal hemodynamic and coagulation responses to 1-deamino-8-D-arginine vasopressin in a case of lithium-induced nephrogenic diabetes insipidus. Results of treatment by a prostaglandin synthesis inhibitor (indomethacin). 149 Jun 62

Calvasculin, an EF-hand protein with a molecular mass of 11 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, is present abundantly in bovine aorta (Watanabe, Y., Kobayashi, R., Ishikawa, T., and Hidaka, H. (1992) Arch. Biochem. Biophys. 292, 563-569). This protein is synthesized constitutively by bovine aortic smooth muscle (BASM) cells and rat embryo fibroblast 3Y1 cells in culture. We discovered that calvasculin was secreted by BASM cells and 3Y1 cells. Immunofluorescence staining of BASM cells showed a granular distribution for calvasculin that was typical of a secreted protein. This protein bound with an extracellular matrix protein, 36-kDa microfibril-associated glycoprotein (36-kDa MAP), in a Ca(2+)-dependent manner in vitro. A stoichiometry analysis showed that the 36-kDa MAP bound 2.2 calvasculin eq/mol of protein. Solid-phase binding assays indicated a preferential affinity of native calvasculin for 36-kDa MAP among the extracellular matrices in a Ca(2+)-dependent manner. These results suggest that calvasculin, intracellular Ca(2+)-binding protein, is released to the extracellular space and binds with 36-kDa MAP.
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PMID:Calvasculin, an encoded protein from mRNA termed pEL-98, 18A2, 42A, or p9Ka, is secreted by smooth muscle cells in culture and exhibits Ca(2+)-dependent binding to 36-kDa microfibril-associated glycoprotein. 151 51


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