Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilating prostaglandins may be increased in patients with chronic congestive heart failure (CHF) to balance out the effects of vasoconstricting forces. Significant increases in plasma levels of bicycloprostaglandin E2 metabolite (PGEm), a chemically stable degradation product of the vasodilating prostaglandin E2, were found in response to captopril (39.4 +/- 7.8 vs. 46.2 +/- 8.2 pg/ml; p less than 0.01). With chronic captopril treatment bicyclo-PGEm remained elevated for 12 h after the last dose after 1 and 2 months (75.5 +/- 5.5; p less than 0.05 and 72.1 +/- 6.3 pg/ml; p less than 0.05, respectively). Upon readministration of captopril during chronic captopril treatment the significant increase of bicyclo-PGEm in response to captopril was sustained, as were changes in plasma renin activity, angiotensin II, and blood pressure. Plasma catecholamines were unchanged with captopril or decreased slightly, vasopressin remained moderately increased throughout. Taken together, the results suggest that vasodilating prostaglandin E2 production might play a part in captopril's beneficial action in chronic congestive heart failure.
Clin Cardiol 1989 Feb
PMID:Increase in bicycloprostaglandin E2 metabolite in congestive heart failure in response to captopril. 265 80

Nisoldipine, a calcium entry blocker, was given to 10 patients with congestive heart failure. During a 2 month follow-up period, 7 of the 10 patients were readmitted with pulmonary edema; daily furosemide doses were increased (128 +/- 87 to 192 +/- 135 mg/day, p less than 0.01), and plasma creatinine increased (1.5 +/- 0.5 to 1.8 +/- 0.6 mg/dl, p less than 0.05) (all values mean +/- SD). Despite this unfavorable clinical course, nisoldipine caused some beneficial chronic (1 month) hemodynamic effects. It decreased systemic vascular resistance (from 1,781 +/- 229 to 1,306 +/- 345 dynes X s X cm-5, p less than 0.01), decreased mean arterial pressure (from 88 +/- 0 to 74 +/- 4 mm Hg, p less than 0.001) and increased stroke volume index (from 27 +/- 6 to 33 +/- 9 ml/min per m2, p less than 0.02). Heart rate, pulmonary capillary wedge pressure and stroke work index did not change. However, nisoldipine's chronic renal and neurohumoral effects were not as favorable. These were assessed during a 5 hour water load (15 ml/kg body weight of 5% dextrose in water) and compared with the effects of a water load before therapy. Nisoldipine did not change creatinine clearance or sodium excretion, but decreased water excretion (from 58 +/- 35 to 46 +/- 40% of water load in 5 hours). Over this 5 hour study, mean plasma vasopressin was also higher with nisoldipine (1.9 +/- 2.3 versus 2.7 +/- 3.2 pg/ml, p less than 0.05), but mean plasma aldosterone was lower (67 +/- 31 to 47 +/- 27 mg/dl, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1987 Mar
PMID:Chronic renal and neurohumoral effects of the calcium entry blocker nisoldipine in patients with congestive heart failure. 288 Aug 84

The peak hemodynamic effect and hormonal response of the phosphodiesterase inhibitor enoximone (MDL 17,043) were compared with those of dobutamine in 10 patients with severe congestive heart failure. Both agents significantly (p less than 0.05) increased cardiac index, stroke volume index and heart rate. Enoximone tended to decrease mean systemic arterial and pulmonary artery wedge pressures (0.05 less than p less than 0.1), whereas dobutamine did not. Both agents decreased systemic vascular resistance (p less than 0.05). The increase in heart rate was greater with dobutamine than with enoximone (p less than 0.05). Plasma renin activity increased significantly with dobutamine (from 11.3 +/- 13.5 to 17.8 +/- 15.0 ng/ml/hour, p less than 0.01) and with enoximone (from 13.6 +/- 18.3 to 16.6 +/- 18.8 ng/ml/hour, 0.05 less than p less than 0.1). Dobutamine suppressed plasma norepinephrine level (p less than 0.05) and enoximone did not. Neither agent affected the plasma vasopressin level. These data demonstrate a similar acute hemodynamic and hormonal profile for both enoximone and dobutamine. Further, dobutamine, like other beta agonists, provokes renin secretion and may do so to a greater extent than enoximone.
Am J Cardiol 1986 Jul 01
PMID:Comparative hemodynamic and hormonal response of enoximone and dobutamine in severe congestive heart failure. 294 27

Fifteen patients with congestive heart failure (New York Heart Association III) were randomly assigned to treatment with either captopril or ramipril, a newly developed angiotensin converting enzyme inhibitor. Both groups were similar with respect to baseline hemodynamic measurements and plasma levels of norepinephrine, renin and vasopressin. The group receiving ramipril showed hemodynamic changes comparable to the group receiving captopril on the seventh day of treatment. The stroke volume index increased by 20% versus 21%, respectively, and the total peripheral resistance decreased by 13% versus 20%, respectively. The decrease in blood pressure and the tendency to decrease heart rate were similar in both groups. All patients had reactive hyperreninemia during therapy with the converting enzyme inhibitor. The resting elevated plasma norepinephrine decreased in both groups significantly, whereas vasopressin did not change. The hemodynamic improvement was more pronounced and comparable in both groups during exercise. Thus, ramipril is equally effective compared with captopril in the treatment of patients with severe congestive heart failure.
Am J Cardiol 1987 Apr 24
PMID:Ramipril and captopril in patients with heart failure: effects on hemodynamics and vasoconstrictor systems. 295 24

Eighteen patients with essential hypertension were separated into 2 groups, renin-unresponsive and renin-responsive, on the basis of their plasma renin response when challenged by furosemide and upright posture. The response to acute infusion of hypertonic saline solution (1.4% saline solution at a rate of 0.3 ml/min/kg over 60 minutes) was then studied. In the renin-unresponsive group, peak rate of fractional excretion of sodium and peak urine flow after saline loading were 7.6 +/- 0.7% and 476 +/- 34 ml/hour, respectively, and peak value of atrial natriuretic polypeptides (ANP) was 784 +/- 140 pg/ml. In the renin-responsive group, the values were 3.1 +/- 0.4%, 194 +/- 29 ml/hour and 115 +/- 33 pg/ml. Both fractional excretion of sodium, urine flow and ANP response were significantly higher (p less than 0.01) in the renin-unresponsive group. Moreover, a highly significant relation (r = 0.82, p less than 0.01) was observed between fractional excretion of sodium and ANP levels in all hypertensive patients. The degree of saline-induced natriuresis was not related to blood pressure, heart rate, endogenous creatinine clearance, antidiuretic hormone or preexisting level of aldosterone. Plasma renin activity changed little in either group during saline infusion, but tended to be higher at all times in the renin-responsive patients. The present findings suggest that the enhanced secretion of ANP is an important determinant for exaggerated natriuresis observed in patients with renin-unresponsive hypertension.
Am J Cardiol 1987 Sep 15
PMID:Role of atrial natriuretic polypeptides for exaggerated natriuresis in essential hypertension. 295 44

One of the important factors in outer space is the absence of gravity (OG). During longterm missions, this factor is responsible for the larger number of anatomical and physiological changes that astronauts experience. The cardiovascular system undergoes these changes with severe intensity, which is part of an adaptation process to the new environmental conditions. The modifications observed in both the anatomy of the cardiovascular system and its hemodynamics occur in two phases. The first phase begins when the astronauts enter into Earth orbit or in interplanetary trajectory and extends until the second or fourth day of the mission. It is characterized by an important shifting of fluids from the lower extremities to the cephalic regions which produces an increase of the venous return and the preload, the heart rate is increased, the blood volume in the thorax is also increased, the cardiac chambers become dilated, and by reflex action, the antidiuretic hormone diminishes, diuresis increases and leads to a virtual state of dehydration. Clinically, the first stage is manifested by headache, dizziness, space disorientation, nausea, anorexia, projectile vomiting, sweating and pallor. This constalation of data is known as "The Space Adaptation Syndrome". The second phase begins at the end of the first phase and finishes toward the fortieth or fiftieth day of the mission.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Inst Cardiol Mex
PMID:[Behavior of the cardiovascular system in outer space]. 295 26

In patients with congestive heart failure, atrial natriuretic factor may serve as a counter-regulatory hormone, offsetting the vasoconstrictive and volume-retentive effects of the sympathetic nervous system, the renin-angiotensin-aldosterone system and vasopressin. Indeed, the plasma levels of atrial natriuretic factor and the vasoconstrictor hormones are often simultaneously elevated in these patients. It is not known, however, whether atrial natriuretic factor remains responsive to sudden reductions in atrial pressure in patients with chronic heart failure, or is unresponsive like the vasoconstrictor systems. To examine this issue, the plasma concentrations of atrial natriuretic factor and the vasoconstrictor hormones were measured in 20 normal subjects and 12 patients with chronic congestive heart failure during incremental lower body negative pressure, an intervention that lowers atrial pressure. In the normal subjects, incremental lower body negative pressure at -10, -20 and -40 mm Hg decreased central venous pressure and pulse pressure. At maximal lower body negative pressure, plasma atrial natriuretic factor levels decreased from 51 +/- 5 to 27 +/- 3 pg/ml (p less than 0.01), whereas increases occurred in plasma levels of norepinephrine (194 +/- 11 to 385 +/- 70 pg/ml, p less than 0.01), renin activity (1.4 +/- 0.2 to 3.9 +/- 0.1 ng/ml per h, p less than 0.01) and vasopressin (1.3 +/- 0.1 to 6.4 +/- 2.4 pg/ml, p less than 0.05). In the patients with congestive heart failure, lower body negative pressure also reduced central venous pressure. Baseline plasma atrial natriuretic factor levels were markedly elevated, averaging 438 +/- 138 pg/ml, and decreased to 317 +/- 87 pg/ml at maximal lower body negative pressure (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1988 Jun
PMID:Responsiveness of atrial natriuretic factor to reduction in right atrial pressure in patients with chronic congestive heart failure. 296 39

We studied the effects of alpha-human atrial natriuretic factor (alpha-h-ANF) on diuresis, glomerular filtration rate (GFR), natriuresis, atrial blood pressure (BP), heart rate (HR) and plasmatic levels of aldosterone, renin activity (PRA), antidiuretic hormone (ADH) in 21 patients with congestive heart failure (CHF), (NYHA, class IV) and 15 healthy volunteers. Three different doses (25, 50 and 100 micrograms) of alpha-h-ANF were administered; each subject received only one dose. Protocol was as follows: 2 periods of 30 minutes each before alpha-h-ANF administration; 2 periods of 15 minutes and 3 of 30 minutes each after it. Aldosterone, PRA, ADH and plasmatic level of ANF were measured by radioimmunoassay. In patients with CHF 25 and 50 micrograms of alpha-h-ANF produced a significant increase in diuresis, GFR, and natriuresis but no modification of BP. On the contrary BP decreased significantly after 100 micrograms of alpha-h-ANF, without changes in renal function. In healthy volunteers the effects of alpha-h-ANF appeared simultaneously and to same degree after each dose. Both in patients and healthy subjects alpha-h-ANF administration had little effect on aldosterone, renin and ADH secretion. The effects of alpha-h-ANF in patients with CHF may be caused by a lowered receptor sensitivity due to a high level of ANF and to their different haemodynamic status.
G Ital Cardiol 1988 Jul
PMID:[Hemodynamic and renal effects of synthetic atrial natriuretic factor (alpha-h-ANF) in patients with congestive heart failure]. 297 92

The vasodilator 8-bromo-guanosine 3':5'-monophosphate (8-bromo-cGMP) effectively counteracts vasopressin-induced coronary artery constriction in a supported perfused working rabbit heart. In this preparation, the coronary arteries remain in contact with the beating heart. The obtuse marginal artery and portions of the left anterior descending coronary artery were deprived of endothelium. Perfusion was carried out with Krebs-Henseleit solution, oxygenated with a disposable infant oxygenator. The internal diameter of large coronary arteries was determined by color arteriography (injection of patent blue dye and gated photography). The effect of vasopressin with and without the addition of 8-bromo-cGMP on cardiac performance (cardiac output, left ventricular systolic pressure, left ventricular end-diastolic pressure, maximal rate of rise in left ventricular pressure [dP/dtmax], mean aortic pressure) and large coronary vessel and total coronary vascular resistance was determined in nine experiments. In addition, changes in coronary sinus partial pressure of carbon dioxide (PCO2) and pH were observed. Vasopressin alone caused a significant decline in coronary flow, myocardial oxygen consumption and coronary sinus pH. Cardiac performance declined, probably because of myocardial ischemia. Large coronary vessel and total coronary vascular resistance rose. The vasodilator 8-bromo-cGMP strongly inhibited the vasoconstrictor action of vasopressin, counteracted the increase in large and total coronary vascular resistance, prevented the fall in myocardial oxygen consumption and eliminated changes in pH or PCO2 of coronary sinus effluent. Because of the elimination of myocardial ischemia by 8-bromo-cGMP, cardiac performance was normalized.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1986 Aug
PMID:Effect of 8-bromo-cyclic guanosine monophosphate (cGMP) on coronary artery constriction in isolated rabbit hearts. 301 62

The response to ramipril, 10 and 20 mg on consecutive days, in 9 patients with severe (New York Heart Association functional class III or IV) chronic congestive heart failure was measured. Hemodynamic cannulae were placed more than 2 days before ramipril administration to ensure a stable baseline. Dietary sodium (40 mmol daily) and potassium (80 mmol daily) were constant before and during the study, and maintenance doses of digoxin and furosemide (80 to 1,000 mg daily) were continued unchanged. Ramipril induced pronounced, sustained decreases in angiotensin converting enzyme activity, angiotensin II and aldosterone levels, and a reciprocal increase in plasma renin activity. Plasma catecholamines, antidiuretic hormone and cortisol levels were not altered. Urinary sodium and potassium excretion diminished, plasma sodium decreased and plasma potassium increased. Plasma urea and creatinine levels increased. Ramipril treatment resulted in a decrease in systemic arterial pressure that was sustained for 24 hours, a decrease in heart rate and an increase in cardiac index, but little change in pulmonary artery pressure or right atrial pressure. Three patients were drowsy after ramipril administration, and 1 patient had a marked, temporary reduction in urine output. It was concluded that ramipril is a potent, long-acting angiotensin converting-enzyme inhibitor that is likely to be beneficial in patients with severe cardiac failure.
Am J Cardiol 1987 Apr 24
PMID:Acute hemodynamic, hormonal and electrolyte effects of ramipril in severe congestive heart failure. 303 25


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