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)

Systemic hypertension occurs in more than one third of patients having coronary artery bypass graft (CABG) operations. This report describes our studies in 100 consecutive patients undergoing CABG. We found that certain preoperative clinical, angiographic, and biochemical factors predispose to the development of perioperative hypertension. These included a well-documented history of hypertension, an elevated blood pressure the day prior to operation, greater than 50 percent obstruction of the left main coronary artery, and increased levels of dopamine beta hydroxylase (DBH). The hemodynamic pattern of perioperative hypertension was that of an increased systemic vascular resistance which was associated with increased levels of plasma catecholamines and plasma renin activity (PRA). Nitroprusside was shown to be effective in managing CABG hypertension, although other, more specific therapy may be preferable.
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PMID:Systemic hypertension associated with coronary artery bypass surgery. Predisposing factors, hemodynamic characteristics, humoral profile, and treatment. 30 28

Although endothelium-derived prostaglandin I2 stimulates renin release, exogenous endothelium-derived relaxing factor (EDRF) can inhibit it. To characterize the role of EDRF as an endogenous regulator of renin release, we inhibited or stimulated its production in rat renal cortical slices in vitro. Renin concentration in the incubation medium was determined by radioimmunoassay for angiotensin I (Ang I) generation. NG-Monomethyl-L-arginine (LNMMA) (10(-4) M), which blocks EDRF formation, significantly enhanced basal renin release from kidney slices by more than 50% in control medium (40.0 +/- 14.3 ng Ang I/hr/mg/30 min; p less than 0.01) or in medium treated with 1.6 x 10(-5) M meclofenamate (50.8 +/- 8.4 ng Ang I; p less than 0.025). Isoproterenol (10(-5) M)-stimulated renin release (40.0 +/- 14.3 ng Ang I; p less than 0.02) was not modified by LNMMA; addition of L-arginine (10(-5) M), the precursor of EDRF, did not change basal but blocked isoproterenol stimulation of renin. Nitroprusside (10(-5) M) completely reversed melittin-stimulated renin release. Endothelin-1, an endothelium-derived vasoconstrictor, inhibits renin release and stimulates EDRF and prostaglandin synthesis. To determine whether any of the renin-inhibiting effect of endothelin-1 was due to its stimulation of EDRF, we compared the effect of endothelin-1 on cortical slices with and without EDRF inhibition. Endothelin-1 (10(-7) M) decreased renin by 36.7 +/- 10.9 ng Ang I (p less than 0.01) compared with controls, and the response was the same after either LNMMA or hemoglobin treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonprostanoid endothelium-derived factors inhibit renin release. 173 97

The impact of oral captopril, 2 mg . kg-1, on the dose and on the hemodynamic and hormonal effects of nitroprusside was studied in seven patients (Group II). A comparable group (Group I, n = 7) received nitroprusside alone. In both groups, nitroprusside produced comparable decreases in mean arterial pressure, systemic vascular resistance, and right atrial pressure; cardiac output increased because of a significant change in heart rate. Although plasma renin activity increased significantly (compared with control values) in both groups, it was greater (p = 0.01) through the operative period in patients pretreated with captopril. Plasma aldosterone concentration increased in Group I (p = 0.01) but decreased in Group II (p = 0.01). Plasma catecholamine concentrations increased (p = 0.01) with nitroprusside alone but were unchanged in captopril-treated patients. Plasma converting enzyme activity was markedly inhibited (p = 0.001) by captopril. Following cessation of nitroprusside infusion in Group I, rebound hypertension occurred in conjunction with a significant (p = 0.01) increase in systemic vascular resistance; it was associated with elevated plasma renin activity, catecholamines, and aldosterone concentrations. In contrast, captopril-treated patients showed no rebound hemodynamic changes. Nitroprusside dose was less (p = 0.01) with captopril pretreatment (2.1 +/- 0.3 vs. 4.8 +/- 0.9 microgram . kg-1 . min-1). Thus, captopril is a useful adjunct to nitroprusside-induced hypotension.
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PMID:Impact of captopril on hemodynamic and hormonal effects of nitroprusside. 241 94

This study was designed to investigate adrenocorticotropin (ACTH), cortisol, and renin responses to nitroprusside-induced hypotension in adult sheep. Five sheep were surgically prepared with carotid arterial skin loops at least 1 yr before these experiments. After catheterization of the carotid arteries and external jugular veins the sheep were infused with nitroprusside intravenously at rates of 0, 10, 15, or 20 micrograms . kg-1 . min-1 for 10 min. Nitroprusside produced significantly dose-related decreases in mean arterial pressure and increases in heart rate, plasma ACTH and cortisol concentrations, and plasma renin activity. Hematocrit was significantly increased in the 10- and 20-micrograms . kg-1 . min-1 groups during nitroprusside, probably reflecting contraction of the spleen. After the end of the period of hypotension, hematocrit was significantly decreased in all nitroprusside infusion groups, probably reflecting transcapillary movement of fluid into the vascular space. A posteriori analysis of the data suggests that the ACTH response to nitroprusside infusion was better predicted by the nadir in mean arterial pressure and that the renin activity response was better predicted by the initial rate of decrease of mean arterial pressure during nitroprusside infusion.
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PMID:ACTH, cortisol, and renin responses to arterial hypotension in sheep. 301 9

The release of vasopressin, renin, and catecholamines by the fetus during either maternal or fetal hypotension was examined in chronically catheterized fetal lambs. Nitroprusside was infused intravenously for 1 h into seven pregnant ewes (maternal hypotension) or nine fetal lambs (fetal hypotension); the rates were adjusted to achieve a 15 to 30% decrease in mean blood pressure. During maternal hypotension, mean +/- SE vasopressin in maternal plasma increased from 1.2 +/- 0.2 pg.ml-1 to 208 +/- 153 pg.ml-1 and plasma renin activity increased from 1.5 +/- 0.3 ng.ml-1.h-1 to 6.6 +/- 1.6 ng.ml-1.h-1. Fetal vasopressin and plasma renin activity also increased during the same interval from 1.1 +/- 0.3 to 16.9 +/- 7.5 pg.ml-1 and 3.7 +/- 1.1 to 10.5 +/- 2.85 ng.ml-1.h-1, respectively; but no changes were observed in fetal blood pressure, heart rate, or acid base status. During fetal hypotension, mean vasopressin in fetal plasma increased from 4.3 +/- 3.4 pg.ml-1 to 1054 +/- 772 pg.ml-1, plasma renin activity increased from 5.7 +/- 2.2 ng.ml-1 to 22.2 +/- 7.1 ng.ml-1.h-1, and total catecholamines from 174 +/- 58 pg.ml-1 to 810 +/- 416 pg.ml-1. There was no change in fetal heart rate, acid base status, osmolality, or sodium concentration. The fetus became and remained hypertensive for at least 1 h after the end of infusion. This prolonged hypertension was associated with elevated levels of vasopressin and plasma renin activity. Peak vasopressin levels were proportional to the total nitroprusside dose in both the ewe and fetus (maternal r = 0.796, fetus r = 0.870).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma vasopressin, renin, and catecholamines during nitroprusside-induced maternal and fetal hypotension in sheep. 304 42

Three techniques for deliberate hypotension (mean arterial pressure, 60 to 70 mmHg) were prospectively compared in adults undergoing posterior spine fusion. Patients received either IV sodium nitroprusside, sodium nitroprusside with oral captopril pretreatment, or IV nitroglycerin. Patient groups were comparable in age, sex, weight, baseline hemodynamic and laboratory parameters, duration of surgery, and duration of hypotension. Absolute blood loss was significantly less in the group receiving nitroglycerin; however, there were no differences between groups when corrected for operative exposure (milliliter per spine segment exposed). Nitroprusside was effective in producing target blood pressure in all patients. Nitroglycerin was ineffective in two patients and two other patients required greater than 20 micrograms/kg/min. Both groups receiving nitroprusside developed significant postinfusion increases in arterial pressure. Blood pressure fell significantly after induction of anesthesia in patients receiving captopril. Cardiac index, heart rate, pulmonary capillary wedge pressure, intrapulmonary shunt, and arterial blood gases were comparable and did not change significantly in any group. Systemic vascular resistance fell during infusion in all groups and remained depressed after infusion in patients receiving nitroglycerin. Plasma renin activity was significantly increased in the group receiving captopril due to loss of feedback inhibition of renin release and rose significantly during infusion in those patients receiving nitroprusside alone. There were no complications. Nitroprusside with and without captopril pretreatment was associated with postoperative increases in arterial pressure, although not to hypertensive levels, probably due to loss of captopril activity after single-dose administration. The use of nitroglycerin was limited by lack of potency. There was no demonstrable clinical advantage for any of the three techniques.
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PMID:Comparison of intravenous nitroprusside, nitroprusside-captopril, and nitroglycerin for deliberate hypotension during posterior spine fusion in adults. 315 22

The effects of hypotension on systemic and renal hemodynamics, plasma renin activity (PRA), and renin secretion rate (RSR) were determined in dogs anesthetized with sodium pentobarbital plus chloralose. Renal blood flow (RBF) was determined with microspheres (15 micron) and with an electromagnetic flowmeter connected to an extra-corporeal circuit from the femoral artery to the renal artery. Hypotension was induced by nitroprusside infusion, which decreased peripheral resistance, and by hemorrhage, which reduced cardiac output. RSR increased in both forms of hypotension, but the increase following hemorrhage was greater than that after nitroprusside. Thus, when the mean arterial pressure (MAP) was reduced to 75 mmHg, RSR increased from 470 +/- 26 units/min to 990 +/- 12 units/min with nitroprusside and from 415 +/- 13 units/min to 1,509 +/- 21 units/min following hemorrhage. At MAP of 50 mmHg, RSR increased to 1,541 +/- 64 units/min with nitroprusside and to 2,254 +/- 98 units/min following hemorrhage. Nitroprusside increased renin secretion not only by an increase in sympathetic beta adrenergic activity through the baroreceptor reflex, but also by its direct vasolidatory effect in the renal circulation. In hemorrhagic hypotension, the increase in renin secretion was accompanied by renal vasoconstriction. The greater increase in RSR following hemorrhage than after nitroprusside at given levels of hypotension may be explained by a stronger beta adrenergic activation, the activation of prostaglandin and kallikrein systems, a lower microvascular pressure level, and/or smaller pulse pressure and lower sodium load in the macula densa. The comparison of renin secretion at the same degree of hypotension induced by different hemodynamic alterations serves to elucidate the mechanisms of renin secretion.
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PMID:Effects of experimental hypotension on hemodynamics and renin secretion rate. 388 73

A 30 year old man with metastatic embryonal carcinoma became hypertensive during vinblastine, bleomycin, and cisplatin therapy. Three months after completion of therapy, accelerated hypertension occurred (blood pressure 210/140 mm Hg). Nitroprusside failed to control the hypertension, but captopril resulted in a prompt and sustained normalization of the blood pressure. The plasma renin activity was markedly elevated before therapy. Renal biopsy disclosed "onionskin" narrowing of the interlobular arteries and fibrin thrombosis of a majority of the afferent arterioles. A form of drug-induced renovascular hypertension is suggested.
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PMID:Renal vascular lesions after chemotherapy with vinblastine, bleomycin, and cisplatin. 618 79

The effect of acute nitroprusside-induced hypotension on plasma renin activity, catecholamine, and vasopressin concentrations was examined in eight chronically catheterized, conscious ewes. Nitroprusside was infused intravenously for one hour at rates adjusted to achieve a 20% decrease in mean blood pressure (dose range: 14-50 mg, or about 5.8-18.5 micrograms X kg-1 X min-1). During hypotension, renin activity increased from 1.39 +/- 0.49 to 3.92 +/- 1.38 ng X ml-1. h-1, catecholamine concentrations remained unchanged, and vasopressin increased from 1.7 +/- 0.4 to 110 +/- 52.7 pg/ml. A significant positive correlation was obtained between total nitroprusside dose and peak vasopressin level (r = 0.749, P = 0.015). No significant change in arterial-blood pH, PO2, PCO2, plasma osmolality, or sodium concentration were observed throughout the experiment, thus eliminating the possibility of osmolar or hypoxic stimuli for the increased renin activity and vasopressin release. The magnitude of vasopressin release found in our studies implies that it plays a more important role than renin in defense against acute hypotension. In addition, the authors experiments suggest that variation in vasopressin release may be responsible for the variation of the dose of nitroprusside required to maintain hypotension.
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PMID:Plasma renin, catecholamine, and vasopressin during nitroprusside-induced hypotension in ewes. 633 63

Activation of the sympathetic nervous system, manifested by an increase in heart rate and circulating plasma norepinephrine, can occur in normal subjects when they are given vasodilators. The extent to which this activation occurs in patients with congestive heart failure (CHF) and whether this activation could account for the hemodynamic rebound sometimes observed following abrupt withdrawal of nitroprusside in such patients are unclear. We prospectively and retrospectively studied the effects of nitroprusside on plasma norepinephrine in 38 patients with CHF to determine if acute vasodilator therapy activates this vasoconstrictor system during or following such treatment. Thirty-six of these patients also had plasma renin activity (PRA) measured and plasma arginine vasopressin was measured in 12 patients. Baseline supine plasma norepinephrine (714 +/- 72 pg/ml, +/- SEM), PRA (15 +/- 2 ng/ml/hr), and arginine vasopressin (10 +/- 1 pg/ml) were increased at least twofold in the CHF patients. Nitroprusside (96 +/- 11 micrograms/min) was infused for 63 +/- 5 minutes after achieving an optimal hemodynamic response: cardiac index increased (2.01 +/- 0.08 to 2.67 +/- 0.1 L/min/m2, p less than 0.001), pulmonary artery wedge pressure decreased (25 +/- 1 to 16 +/- 1 mm Hg, p less than 0.001), mean arterial pressure decreased (83 +/- 1 to 72 +/- 1 mm Hg, p less than 0.001), and heart rate was unchanged. Plasma norepinephrine (632 +/- 43 pg/ml), PRA (18 +/- 3 ng/ml/hr), and arginine vasopressin (11 +/- 1 pg/ml) did not change significantly for the group during peak effect of the vasodilator.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The acute response of plasma norepinephrine, renin activity, and arginine vasopressin to short-term nitroprusside and nitroprusside withdrawal in patients with congestive heart failure. 635 44


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