Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 2 days of oral dosing with sulindac (200 mg twice a day) or indomethacin (75 mg twice a day) on glomerular filtration rate, urinary excretion of prostaglandin E2, sodium homeostasis, and other renal function parameters were investigated in eight patients with chronic stable impaired renal function. Indomethacin reduced creatinine clearance (from 41.0 +/- 7.9 to 30.3 +/- 6.3 ml/min) and increased serum levels of creatinine and beta 2-microglobulin. Sulindac had no effect on any of these parameters. Both drugs induced depression of urinary prostaglandin E2 excretion; this depression was greater after indomethacin. Urinary sodium excretion fell from 144.4 +/- 18.7 to 85.5 +/- 9.7 mmol/24 hr after indomethacin and from 131.7 +/- 11.6 to 103.4 +/- 13.3 mmol/24 hr after sulindac. Body weight increased 1.2 kg after indomethacin but was not changed by sulindac. Plasma renin activity was reduced from 2.3 +/- 0.8 to 1.7 +/- 0.6 nmol/L/hr by sulindac and from 2.8 +/- 0.8 to 1.5 +/- 0.5 nmol/L/hr by indomethacin. Urinary N-acetyl-beta-glucosaminidase and kallikrein excretion was not changed by either drug. Our data suggest that sulindac affects renal prostaglandin E2 synthesis and sodium excretion in patients with severe renal failure to a lesser extent than does indomethacin. Sulindac still seems to be the drug of choice in this group of patients, but glomerular filtration rate, body weight, and electrolyte balance should be carefully monitored.
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PMID:Acute renal effects of sulindac and indomethacin in chronic renal failure. 388 24

Sixty-one male subjects with mild untreated essential hypertension were classified by renin-sodium profiling as high renin (HR--13 Subjects), normal renin (NR--33 Subjects), or low renin (LR--15 Subjects). The HR subjects reported significantly more symptoms of sensitivity, depression, anxiety, hostility, paranoia, and psychotic thought than LR subjects on the Symptom Checklist (SCL-90). The NR subjects also reported more symptomatology than LR subjects. Similar differences between HR and LR subjects were found with the Cattell 16 Personality Factor Questionnaire (16PF).
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PMID:Psychologic differences between high-, normal-, and low-renin hypertensives. 388 67

Ten patients with hypertension and obesity were studied during a program of weight loss on an unrestricted sodium diet. The study showed that weight loss during the ten month period was accompanied by a significant decrease in urinary aldosterone, tetrahydroaldosterone -3-glucuronide and plasma renin activity values. It was also demonstrated that successful reduction in body weight was associated with a reduction in blood pressure. It is postulated that blood pressure reduction in obese patients during weight reduction may depend on decreases in aldosterone and plasma renin activity. The reduction in levels of tetrahydroaldosterone-3-glucuronide is due to an energy related depression of the glucuronidation process caused by carbohydrate deficiency. It is postulated that the lowered rate of metabolism of aldosterone as measured by the diminished formation of the metabolite tetrahydroaldosterone-3-glucuronide is an important determinant of blood pressure status during weight reduction.
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PMID:Aldosterone studies in obese patients with hypertension. 389 May 39

During normovolemia, nitrous oxide causes mild sympathetic stimulation and direct myocardial depression; these effects offset each other, resulting in only minimal cardiovascular changes. To test the hypothesis that during hypovolemia this balance would change and depression predominate, 10 swine were made hypovolemic (30% blood loss) and then were given 70% N2O (0.25 MAC in swine) or an equipotent concentration of halothane, an agent that does not cause sympathetic stimulation. The alternate anesthetic was given to the same hypovolemic swine on another day. Five minutes after induction of anesthesia during hypovolemia, both N2O and halothane caused significant, physiologically important deterioration of compensation for hemorrhage. Halothane decreased systemic vascular resistance (SVR); N2O was more variable in its action, and SVR did not decrease significantly. Both agents caused similar decreases in cardiac output, mean aortic blood pressure, stroke volume, oxygen consumption, and left ventricular minute work, despite increases in plasma epinephrine concentration and plasma renin activity. No differences were found between groups for any of these variables (P greater than 0.05). Plasma norepinephrine concentration increased only in the N2O group and was greater in that group than in the halothane group. The deterioration of cardiovascular compensation for hemorrhage was expressed metabolically by similar decreases in the two groups in partial pressure of oxygen of mixed venous blood and by increases in blood lactate concentration. Thirty minutes after induction of anesthesia, with stable end-tidal anesthetic concentrations, both groups had some cardiovascular, but no metabolic, recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular actions of nitrous oxide or halothane in hypovolemic swine. 390 22

Plasma renin concentration (PRC), renal blood flow (RBF) and renin secretion rate (RSR = renal veno-arterial PRC difference multiplied by renal plasma flow) were measured before and after a period of hypothermic renal ischaemia in seven patients undergoing surgery for renal calculi. After hypothermic (10-15 degrees C) ischaemia (duration 36 to 71 min) the temperature rose to 37 degrees C within 4 min, while RSR decreased transiently in the posthypothermic postocclusive period. Maximal decrease in RSR (-65%) was found 6 min after re-establishment of the renal perfusion, and 30 min later RSR was similar to the prehypothermic, preocclusive value. RBF decreased in the same period, while mean arterial blood pressure and renal oxygen uptake were unchanged. The results are compatible with a reversible depression of the release of renin in the postocclusive, posthypothermic human kidney.
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PMID:Effect of hypothermic renal ischaemia on renin secretion rate in man. 390 52

Studies in our laboratory and by others have repeatedly shown that the mean value of the rate-constant for ouabain-sensitive sodium efflux is reduced and intracellular sodium increased in essential hypertension, but that there is considerable overlap with the normotensive population. There is a significant negative correlation between the rate constant and the diastolic blood pressure. The depression of the rate constant is most marked in those hypertensives with the most suppressed renin/angiotensin systems. Treatment of a population of essential hypertensives with thiazide diuretics returns the rate constant to normal. The serum of hypertensives depresses the rate constant of normal cells in vitro in proportion to the degree of abnormality present in the hypertensive's cells.
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PMID:Factors influencing leucocyte sodium transport in hypertension. 399 43

1. When applied directly to the brain, angiotensin II amide, as either the valine(5) octapeptide, causes rats in normal fluid balance to drink water.2. The drinking response to angiotensin injections is copious, rapid, repeatable within the same test session, and stable over months of testing in the same animal.3. The response is motivationally potent and specific. After injection the animals move directly to the source of water and drink. There is typically no preliminary hyperactivity or subsequent depression. The animals do not eat, gnaw or exhibit other behaviours that are not normally seen during spontaneous drinking. The injections rouse sleeping animals to drink and interrupt eating in animals deprived of food for two days.4. The region of the brain that is most sensitive to angiotensin includes the anterior hypothalamus, the preoptic region, and the septum including the nucleus accumbens.5. Intracranial renin elicited drinking. Bradykinin and vasopressin did not, nor did adrenaline, noradrenaline or aldosterone. In the most sensitive region, sites positive for angiotensin also yielded drinking to carbachol.6. Responses were obtained with 5 ng (ca. 5 p-mole) and occurred reliably with 50 ng angiotensin or more. The dose-response curve for amount drunk rose from 5 to 100 ng and levelled off thereafter. Angiotensin is therefore the most potent dipsogen known and is effective at doses that are reasonably within the concentration range for circulating endogenous angiotensin.7. Injections into the sensitive region of doses of angiotensin that were effective for drinking did not produce peripheral haemodynamic changes in lightly anaesthetized rats.8. This work strengthens the suggestion that angiotensin is a natural hormone of drinking behaviour that participates in extracellular thirst by its release from the kidney and subsequent direct action on a specific chemoreceptive region in the anterior diencephalon and limbic lobe.
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PMID:Drinking induced by injection of angiotensin into the rain of the rat. 432 23

The brain influences arterial pressure through central mediation of a variety of neurotransmitters, including norepinephrine, and translates this action into changes in peripheral autonomic tone. Two opposed adrenergic systems have been described in brain: a hypothalamic pathway in which adrenergic receptor stimulation raises arterial pressure and a brainstem pathway related to the baroreflex arc in which adrenergic receptor stimulation lowers arterial pressure. Antihypertensive drugs with primarily central effects, including clonidine and alpha methyldopa, act as alpha 2 adrenoceptor agonists. The central receptor involved in their antihypertensive action is of the alpha 2 type but is located postsynaptically. Activation of this receptor by either clonidine or alpha methylnorepinephrine, a metabolite of alpha methyldopa, engages the depressor pathway in the brainstem and leads to a decrease in norepinephrine release and a reduction in peripheral sympathetic tone. Clonidine and alpha methyldopa share a similar pattern of peripheral effects, including reductions in preganglionic sympathetic nerve traffic, bradycardia, decreases in plasma renin activity, reductions in blood pressure in the supine position and adverse effects such as depression, sedation and bad dreams. Because of the frequency and severity of these side effects, there is an ongoing search for new centrally acting antihypertensive agents which might be better tolerated.
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PMID:Review of therapeutic modalities acting directly via central pathways. 612 82

The antihypertensive effect of a new vasodilator with betablocking properties (SK & F 92657) was investigated in 10 patients with mild to moderate essential hypertension. After a mean treatment period of 26,5 weeks (6,5-49 weeks) blood pressure was significantly reduced, from 168 +/- 22/106 +/- 6 mmHg to 144 +/- 19/94 +/- 12 mmHg (p less than 0.05 and 0.025). The mean dose was 410 mg (100-700 mg). Heart rate decreased slightly from 77 +/- 12 to 70 +/- 8 beats/min. Plasma renin activity and plasma aldosterone showed only minor changes. Nausea, heavy dreams, facial and hand flushing and mild depression were reported as side effects. In most patients the symptoms disappeared without reduction in the dose. In one patient anaemia developed after 7 weeks and treatment with prizidilol was stopped. A slight but statistically significant decrease in haemoglobin concentration of 1.1 +/- 0.6 g/dl was observed in 5 of the 10 patients (p less than 0.02). Thus, a mean dose of prizidilol of 410 +/- 242 mg/day had a mean blood pressure lowering effect of 24/12 mmHg. In 7 of the 10 patients (70%) diastolic blood pressure could be reduced to 95 mmHg or less. However, the observed haematological side-effects should be carefully monitored in further studies and may limit the clinical use of prizidilol.
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PMID:Prizidilol (SK & F 92657), a new vasodilator with beta-blocking properties in the treatment of essential hypertension. 612 80

Expansion of the extracellular fluid volume (ECFV) promotes the release of a small molecular weight (less than or equal to 1,000 Daltons) humoral natriuretic factor. The resulting natriuresis is accompanied by inhibition of renal cortical tissue and red blood cell Na-K-ATPase activity. This transport inhibitor, presumably an acidic peptide derived from a larger precursor molecule, was so far recovered from the serum and urine of rat, dog, and man, and from renal cortical tissue homogenate. Using Sephadex G-25 gel chromatography the inhibitor is eluted in the post-salt fraction IV. Its natriuretic action is demonstrated by bioassay methods, it depresses sodium transport of isolated amphibian membranes and inhibits Na-K-ATPase enzyme activity in vitro. The inhibitor isolated from human urine binds to specific antibodies against digoxin. This natriuretic factor is absent in patients with arterial hypotension and in edematous patients with secondary aldosteronism. In contrast, high inhibitory activity is found in patients with primary aldosteronism, a condition which represents the most classical type of low renin volume-dependent hypertension. Since enzyme inhibition by this humoral endogenous agent probably extends to various Na-K-ATPase-dependent transport systems including vascular smooth muscle fibers, depression of their Na-K pump will raise intracellular concentrations of sodium and calcium and thereby induce vasoconstriction. It is therefore tempting to speculate that the natriuretic hormone plays an important role in the pathogenesis of volume-dependent arterial hypertension.
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PMID:Natriuretic hormone - a circulating inhibitor of sodium- and potassium-activated adenosine triphosphatase. Its potential role in body fluid and blood pressure regulation. 627 45


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