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)

Left ventricular injection of meglumine diatrizoate caused an initial (1-10 minute) decrease in renal vascular resistance followed by a late (30-minute) increase in renal vascular resistance. The late renal vasoconstrictor response was not blocked by bilateral cervical vagotomy, by renal adrenergic blockade or by renal alpha adrenergic receptor blockade; it was blocked by prior extracellular fluid volume expansion and blockade of the response of the kidney to angiotensin II. There was no effect on intrarenal distribution of blood flow. In the kidney perfused at constant flow, injections of meglumine diatrizoate into the kidney resulted in early renal vasodilation (1-5 minutes) with a return to control renal vascular resistance by 7 minutes; no vasoconstriction was observed. The renal vasodilatation was not abolished by prior treatment with atropine. Vasodilator responses identical to those observed with meglumine diatrizoate were obtained with 4.5% NaCl (equiosmolar to meglumine diatrizoate); no response was obtained with 0.9% NaCl. When given into either the left ventricle or the renal artery, meglumine diatrizoate caused an early reversible depression in renal extraction of para-aminohippurate; both 0.9 and 4.5% NaCl were without effect. The renal vasodilation produced by meglumine diatrizoate initially appears to be caused by its hyperosmotic properties; the late renal vasoconstrictor response appears to be mediated via an activation of the renin-angiotensin system. The depressive effect of meglumine diatrizoate on the renal extraction of para-aminohippurate is not related to its osmotic properties but rather to an effect of the organic iodinated molecule on cellular transport of para-aminohippurate.
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PMID:The renal vascular effects of meglumine diatrizoate. 115 40

A marked increase in preglomerular resistance mediated through the renin-angiotensin system has been proposed as the mechanism for the sustained decrease in glomerular filtration rate seen following release of 24-hour ureteral obstruction. The importance of the renin-angiotensin system in mediating this response was evaluated by determining whole kidney and single nephron function following release of 24-hour ureteral obstruction in rats with normal renal renin content and in rats depleted of renal renin by desoxycorticosterone acetate acetate (DOCA) and saline treatment. The DOCA and saline treatment was effective in reducing renal renin content to less than 10% of the normal values. However, when compared to nonobstructed kidneys, both whole kidney filtration rate and single nephron filtration rate were similarly and significantly reduced in both groups following release of 24-hour ureteral obstruction. Single nephron stopflow techniques were used to determine the net hydrostatic force for filtration. The net hydrostatic force for filtration in control nonobstructed nephrons averaged 37.8 +/- 1.1 mm. Hg, but was significantly decreased to 22.5 +/- 2.2 mm. Hg in the normal renin obstructed kidney and to 18.8 +/- 1.0 mm. Hg in the renin-depleted obstructed kidney. It is concluded that the marked depression in glomerular filtration rate seen following release of 24-hour ureteral obstruction is due to increased afferent arteriole resistance and that the renin-angiotensin system is apparently not important in mediating the response.
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PMID:Influence of renin depletion on renal function after release of 24-hour ureteral obstruction. 124 84

Chronic renal failure was induced in male Wistar rats with 5/6 nephrectomy (group I) and sham-operation was carried in the controls (group II). The results showed that in group I, plasma ANP levels increased progressively as Scr elevated. The plasma levels of renin and angiotensin raised simultaneously as compared with the controls (P < 0.001). At the 20th week after operation, urine volume and Na decreased significantly (P < 0.05) and the number of glomerular ANP receptors decreased significantly at the 12th week (P < 0.05) and 20th week (P < 0.01). Our data suggest that in 5/6 nephrectomized rats: 1. The elevation of plasma ANP level might be partly caused by damage of glomerular receptors. 2. The elevated plasma ANP could not cause its diuretic, natriuretic, blood pressure depression and R-A inhibition effect due to the damage of kidney ANP receptors.
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PMID:[The relationship between plasma atrial natriuretic peptide (ANP) and glomerular ANP receptors in 5/6 nephrectomized rats]. 130 71

Cardiac hypertrophy is an adaptive response to an increased load imposed on the myocyte which allows the heart to perform increased work while maintaining normal myocardial fiber stress and shortening in systole. A deleterious consequence of pressure-overload hypertrophy is the prolongation of Ca(2+)-sensitive force inactivation (impaired myocardial relaxation) which is related to intrinsic alterations in cytosolic Ca2+ transport and reuptake in diastole. Additional factors appear to adversely modify myocardial relaxation in the hypertrophied heart, including the imposition of ischemia. There is also evidence that the expression and activity of the cardiac tissue renin angiotensin system (RAS) may be modified in the hypertrophied heart and contribute to diastolic dysfunction. Recent studies have demonstrated the presence of increased cardiac angiotensin converting enzyme (ACE) mRNA expression and activity in animal models of hypertrophy, including the aortic-banded rat with compensatory pressure-overload hypertrophy and rats with post-infarction remodeling. In the beating, isovolumic aortic-banded rat heart, the increased intracardiac activation of angiotensin I to II has been shown to be associated with a dose-dependent depression of diastolic relaxation. Preliminary studies suggest that the depression of diastolic function by angiotensin II in the hypertrophied heart can be prevented by the specific inhibition of cardiac ACE. In addition, the well-recognized susceptibility of the hypertrophied heart to severe ischemic diastolic dysfunction also appears to be favorably modified by the inhibition of cardiac ACE activity. The mechanisms responsible for the adverse effects of angiotensin II on diastolic relaxation in the hypertrophied heart are likely to be complex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic dysfunction in pressure-overload hypertrophy and its modification by angiotensin II: current concepts. 133 63

The direct effect of noradrenaline on renin release from juxtaglomerular (JG) cells in vitro were investigated in a dynamic superfusion system of dispersed rat renal cortical cells. At low concentrations (1-100 nmol/l), noradrenaline stimulated renin release in a dose-dependent manner, while at higher concentrations (0.1-1 mmol/l) it inhibited renin release. The stimulatory effect of 0.1 mumol noradrenaline/l was completely blocked by a beta-adrenoceptor antagonist, propranolol (0.1 mumol/l). When applied at concentrations of 1 mumol/l or 10 mumol/l, noradrenaline had no consistent effect on renin release, although 10 mumol noradrenaline/l had an inhibitory effect in the presence of propranolol (0.1 mumol/l). The inhibitory effect of noradrenaline (0.1 mmol/l) was converted to a stimulatory effect by the addition of an alpha 1-adrenoceptor antagonist (bunazosin, 1 mumol/l), but was not altered by the addition of an alpha 2-adrenoceptor antagonist (yohimbine, 1 mumol/l). These results indicate that low concentrations of noradrenaline directly stimulate renin release from JG cells by the activation of beta-adrenoceptors, while high concentrations of noradrenaline inhibit renin release by the activation of alpha 1-adrenoceptors. Accordingly, a dynamic balance may exist between beta-adrenergic stimulation and alpha 1-adrenergic depression of renin release.
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PMID:A biphasic effect of noradrenaline on renin release from rat juxtaglomerular cells in vitro is mediated by alpha 1- and beta-adrenoceptors. 134 23

Several classes of drugs that modify serotonin (5-HT) neurotransmission are either currently used, or are being evaluated for their potential use in the treatment of anxiety, schizophrenia, and depression. 5-HT1A agonists are considered potential anxiolytics, while some atypical antipsychotics are potent 5-HT2 antagonists (and also have modest dopamine D2 affinity). Furthermore, there is a diverse group of serotonergic drugs that may be effective antidepressants. Secretion of ACTH, corticosterone/cortisol, prolactin, renin, oxytocin and vasopressin are stimulated by activation of different 5-HT receptor subtypes, while other neurotransmitter receptors also influence the secretion of these hormones. We compared the receptor binding profiles of 5-HT anxiolytics, antipsychotics and antidepressants with their endocrine effects. These comparisons could aid in understanding both the therapeutic and side effects of these drugs.
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PMID:Endocrine and receptor pharmacology of serotonergic anxiolytics, antipsychotics and antidepressants. 135 27

The depression of renal function caused by cyclosporin does not generally reflect permanent kidney damage but is caused by a reversible vasoconstriction, with no relevant changes in tubular function. Serum creatinine may remain within the normal range during therapy, but any decline in renal function can be detected by a rise in serum creatinine above the baseline value. Measurements of glomerular filtration rate before and during therapy have shown the degree of renal dysfunction in individual patients to correspond to their rise in serum creatinine. The cause of renal vasoconstriction is uncertain but animal experiments have highlighted several possibilities. These include: (1) albumin leakage with circulatory volume contraction; (2) enhanced Ca mobilization in contractile cells; (3) activation of a renin-like enzyme in vessel walls; and (4) renin accumulation in the renin-producing cells of the afferent arteriole. Such mechanisms, although seeming to operate at different doses, may act in unison at high doses, when renal function is most severely depressed.
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PMID:The effect of cyclosporin on renal function. 150 31

Studies investigating the antiischemic action of converting enzyme inhibitors (CEIs) in patients with coronary artery disease (CAD) have, after single dosing, provided evidence for mechanisms of action such as coronary vasodilation and reduction of myocardial oxygen-consumption due to pre- and afterload reduction. Measurements of exercise-induced ST-segment depression and exercise duration as criteria for clinical efficacy have revealed contradictory findings. Patient characteristics, which may be important for a satisfactory response to CEI treatment, have yet to be identified. Patients with ischemic left ventricular dysfunction may benefit from CEI therapy. Neurohumoral factors, e.g., plasma renin activity and atrial natriuretic peptide, may also be relevant. The anti-ischemic efficacy of CEIs given as monotherapy has not yet been convincingly demonstrated. The protective effect of CEI treatment with regard to ventricular enlargement after myocardial infarction seems to be established; however, data on mortality are still outstanding.
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PMID:Current concepts: converting enzyme inhibitors in coronary artery disease. 160 Mar 33

Thirty patients undergoing resection of arteriovenous malformations with deliberate hypotension were randomized to receive 1 of 3 hypotensive agents. Anesthesia was maintained with isoflurane and nitrous oxide in all patients. Mean arterial pressure was reduced 20% to 60-65 mm Hg with use of either isoflurane (less than or equal to 4%), sodium nitroprusside (less than or equal to 8 micrograms.kg-1.min-1), or esmolol (less than or equal to 24 mg/min). Esmolol was associated with a decrease in cardiac output from 6.2 +/- 1.3 to 3.8 +/- 0.8 L/min, which, because of a 22% increase in systemic vascular resistance, far exceeded the reduction in mean arterial pressure. Systemic vascular resistance increased despite a 32% decrease in plasma renin activity. In contrast, with sodium nitroprusside or isoflurane, the decrease in mean arterial pressure was associated with decreases in systemic vascular resistance of similar magnitude, with no change in cardiac output. Plasma renin activity levels increased 48% with sodium nitroprusside and 126% with isoflurane. Heart rate increased 13% with sodium nitroprusside, remained unchanged with isoflurane, and decreased 23% with esmolol. Although esmolol may be used as a primary hypotensive agent, the potential for marked myocardial depression must be recognized. The differences in pharmacologic properties for the different hypotensive agents suggest that combinations of these agents may provide a pharmacologic profile superior to either agent alone.
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PMID:Deliberate hypotension in patients with intracranial arteriovenous malformations: esmolol compared with isoflurane and sodium nitroprusside. 167 24

The antiischemic efficacy of the converting enzyme inhibitor (CEI) benazepril was investigated in a randomized, placebo-controlled double-blind study with intraindividual crossover in 11 normotensive patients with angiographically proven coronary artery disease. Bicycle ergometry and 24-h ambulatory ECG were performed before and after 2-week treatment with placebo and benazepril, respectively. Plasma concentrations of atrial natriuretic peptide (ANP) and plasma renin activity (PRA) were measured before each exercise test. Maximal exercise-induced ST-segment depression was not significantly influenced by benazepril therapy (placebo 2.09 +/- 1.22 mm, benazepril 1.91 +/- 1.00 mm). Systolic blood pressure/heart rate (SBP/HR) product at maximum workload remained almost constant with 253 +/- 43 with placebo and 253 +/- 39 with benazepril treatment. The number of anginal attacks and ischemic episodes detected by ambulatory ECG were not significantly reduced. PRA increased significantly from 2.18 +/- 3.76 to 9.62 +/- 8.49 ng/ml/h after benazepril (p less than 0.005), whereas plasma concentrations of ANP remained unchanged (28.04 +/- 12.39 vs. 26.73 +/- 11.09 pg/ml). Therefore, measurement of ST-segment depression with exercise in 11 normotensive patients with coronary artery disease produced no evidence of an antiischemic action for the CEI benazepril 10 mg twice daily (b.i.d.) for 2 weeks, but an improvement was observed in six patients.
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PMID:Converting enzyme inhibition in coronary artery disease: a randomized, placebo-controlled trial with benazepril. 171 85


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