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)

Numerous community drinking water sources have elevated levels of both sodium and lead. Recently reported studies have indicated that elevated levels of sodium in drinking water may be a facter in the development of elevated blood pressure. The question of how elevated levels of lead may affect sodium induced elevated blood pressure is addressed. The hypothesis is developed which states that elevated levels of lead exposure will not interact with sodium to enhance the development of renin angiotensin aldosterone related hypertension but in fact may even diminish the effects of exposure to elevated amounts of sodium on blood pressure through a depression of plasma renin activity.
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PMID:Does exposure to elevated levels of lead enhance sodium induced hypertension? 51 19

Experiments were conducted to determine whether suppression of the renin-angiotensin-system and inhibition of the tubuloglomerular feedback response offer protection from acute renal failure, as found in chronically-salt loaded animals. The juxtaglomerular renin activity and tubuloglomerular feedback response were inhibited acutely, by saline expansion, or chronically, by DOCA-treatment with saline drinking fluid or salt diet, by high salt diet alone, or by inducing two-kidney Goldblatt hypertension. The chronic pretreatment procedures depressed juxtaglomerular renin to 16, 7, 13 and 4% of control, respectively, inhibited the feedback response to 53, 37, 56, and 38% of control, respectively, but conferred no benefit in the first hours following a nephrotoxin or ischaemia. In contrast, the acute treatment procedure reduced juxtaglomerular renin activity to only 56% and lowered the feedback response to only 71%, but improved renal function after the nephrotoxin, although not after ischaemia. It is concluded that since severe restrictions of renin activity and tubuloglomerular feedback are not protective, neither is primarily involved in generating the functional restrictions early in acute renal failure. The restoration of renal function by saline expansion accompanied only a modest depression of these two systems and suggests that the beneficial effect may result more from volume expansion or diuresis than from suppression of renal renin or inhibition of tubuloglomerular feedback.
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PMID:The early phase of experimental acute renal failure. V. The influence of suppressing the renin-angiotensin system. 57 64

The paper describes a two-month period of study in four bipolar manic-depressive patients in a metabolic ward. Plasma renin activity, packed cell volume, plasma sodium and potassium were determined at intervals. Twenty-four-hour urinary sodium, potassium and creatinine were also estimated daily. Aldosterone production rate was measured on two occasions for each patient. Three of the patients showed at least one episode each of mania and depression during the study, while the fourth patient, who was receiving prophylactic lithium throughout, had one ten-day depressive episode but was otherwise normal. No obvious relationship between mood and plasma renin activity was observed, but the group showed a high resting renin activity, a blunted renin response to posture, and inappropriate aldosterone production rates for the renin activity found. It is postulated that a primary defect in the aldosterone-renin system may be present in bipolar manic-depressive psychosis.
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PMID:Renin and aldosterone relationships in manic depressive psychosis. 59 84

Plasma renin activity (PRA), both in supine and standing position, was investigated in primary and secondary depressed patients. After orthostatic stimulation (standing position) primary depressed patients showed PRA values significantly lower than did those with secondary depression. The authors stress the importance of the peripheral sympathetic system in the control of renin release and discuss the data obtained in the light of some evidence in the literature indicating a possible impairment of transmitter turnover in central and peripheral noradrenergic synapses in the pathogenesis of primary depression.
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PMID:Plasma renin activity in primary and secondary depression. 60 4

The purpose of the study was to determine the early haemodynamic effects of injectable acebutolol and to study in parallel the changes in plasma renin activity (P.R.A.) in 11 patients, most of whom were affected with labile arterial hypertension. The haemodynamic measurements and P.R.A. determinations were carried out before and 5 and 15 mn after very slow intravenous injection of 10 mg acebutolol. The results obtained under these conditions were as follows: 1) Decrease in cardiac index (I.C.). It was particularly significant after 5 mn, since the I.C. decreased from 4.43 to 3.75 1/mm (p less than .01). It was essentially due to a decrease in heart rate, that fell from 90.45 to 77 beats/mn (p less than .001), while stroke volume changed virtually not. 2) Decrease in blood pressure, more marked on systolic blood pressure (110 mm Hg after 15 mn as against 154 mm Hg before injection; p less than .001), associated with a decrease in left ventricular work (4.7 kgm/mn/m2 after 5 mn as against 6.2 kgm/mn/m2 before injection; p less than .001), without significant changes in total systemic arterial resistances. 3) Increase in diastolic pulmonary arterial pressure (10.4 mm Hg after 5 mn against 8.09 mm Hg before injection; p less than .001), testifying to a slight left ventricular myocardial depression. 4) Decrease in supine P.R.A. level (0.72 nanogram/1/mn after 5 mn as against 1.15 nanogram/1/min before injection; p less than .01). A significant correlation was found between this decrease in P.R.A. and that in I.C., testifying to a close parallelism between the inhibition of cardiac beta-1 receptors and that of the receptors involved in renine secretion. 5) The tolerance of injectable acebutolol appeared to us to be excellent.
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PMID:[Hemodynamic effects and effects on plasma renin activity of injectable acebutolol in arterial hypertension]. 76 6

26 hypertensive patients groupded according to the severity-index and the WHO-index were treated with pindolol (monotherapy, 15 mg daily). The response of blood pressure depression was statistically significant, although not always sufficient when judged by clinical parameters. Plasma renin activity responded variably to the treatment in different patients and different groups. In 18 patients a statistically significant increase of serum potassium could be observed. No major side effects of therapy were encountered.
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PMID:[Pindolol as an antihypertensive agent]. 83 51

Defective potassium excretion with clinical acidosis, associated with fixed moderate sodium wasting, has been found to be a common abnormality in lead nephropathy. Lead poisoning has been shown by others to be associated with depression of the renin-aldosterone system and of sodium and potassium activated adenosinetriphosphatase (ATPase). Since these hormonal defects may contribute to the hyperkalemia and are reversible, lead poisoning should be treated aggressively. Management also requires proper regulation of dietary sodium, correction of acidosis, limitation of dietary potassium, and minimal use of antihypertensive agents, as well as the administration of allopurinal for urate control.
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PMID:Hyperkalemia and acidosis in lead nephropathy. 94 Oct 56

The pathogenesis of paradoxical hypertension after resection of coarctation of the aorta was investigated by comparing the course of seven children undergoing repair of coarctation with five acyanotic children undergoing elective cardiovascular surgery. During the first 24 hours after surgery, all coarctation patients demonstrated a rise in systolic blood pressure (35 +/- 15.5 mm Hg; P less than 0.001), a significant depression in cold pressor test response, and only a slight elevation in plasma renin activity. In the next 24-72 hours, coarctation patients developed a rise in diastolic blood pressure (26.8 +/- 10.6 mm Hg; P less than 0.001), plasma renin activity (22.9 +/- 10.2/ml/hr; P less than 0.001) and fluid retention. By contrast, control patients had no significant postoperative changes. Abdominal pain occurred in five coarctation patients during the period of maximal plasma renin activity. The data suggest that the sympathetic nervous system may be responsible for the initial phase of hypertension after coarctation resection and that the renin angiotension system plays a major role in the second phase of hypertension and in the pathogenesis of mesenteric arteritis.
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PMID:Pathogenesis of paradoxical hypertension after coarctation resection. 94 70

A marked decrease in the nuclear size in the adrenal medulla and a slight increase in the nuclear volume of the zona glomerulosa was found in the Inactin anaesthetized Wistar rat. The nuclear volumes in the zona fasciculata did not show any alteration. The influence on the activity of the cells in the adrenal medulla is supposed to be due to a depression in the central nervous system by Inactin. The slight activation of the zona glomerulosa is attributed to stimulation of the renin-angiotensine-system by an Inactin induced change in renal function. A failing dose dependent effect is taken as a sign of compatibility of the administered drug.
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PMID:[Morphokinetic reactions in the adrenal gland of the albino rat after anaesthesia with inactin (author's transl)]. 94 7

Suppression of renin release by beta-adrenoceptor blocking drugs has been advocated as the prime blood pressure lowering mechanism of these agents. The present report casts doubt on this proposition in three ways. In the first study, involving 22 patients with borderline hypertension, patients with elevated plasma renin levels showed normalization of the blood pressure after pharmacological autonomic blockade with intravenous atropine, propranolol and phentolamine, the time course of the pressure fall being such as to exclude suppression of renin release as the antihypertensive mechanism. It is clear that in patients with mild hypertension and high plasma renin levels, the elevation of blood pressure is maintained by a neurogenic mechanism, the elevated plasma renin having no direct role in sustaining the higher blood pressure. In two additional studies involving 21 patients in all with mild to moderately severe essential hypertension, to whom propranolol was administereed by mouth for 1--3 months, two findings were of interest:1) patients with low-renin essential hypertension showed a good antihypertensive response to propranolol, and 2) in some patients a dosedependent dissociation of the renin and blood pressure lowering action of propranolol could be demonstrated. These findings militate against the assumption that propranolol selectively lowers the blood pressure in "renin-dependent" hypertension, and strongly suggest that the antihypertensive action of this drug is not mediated by depression of plasma renin activity.
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PMID:Dissociation of the renin lowering and antihypertensive actions of propranolol. 103 70


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