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)

Hemodynamics, elastic characteristics of the greater arteries and blood renin activity were studied at the different stages of the disease in 23 patients with renovascular hypertension, caused by unilateral stenosis of the renal arteries. In 14 cases electron microscopy of the bioptic specimens of the impaired kidney was performed. It was shown that the peripheral plasma renin activity plays the leading role in the pathogenesis of arterial hypertension in the disease duration up to 3 years. The irreversible changes of the renal juxtaglomerular apparatus and the depression of their renin synthesizing function occur with progressing hypertension, and the secondary pressor mechanisms and factors prevail in the pathogenesis of hypertension. The loss of the arterial elastic properties as well as the depression of the renal hypotensive function may be one of the factors determining the failure of surgery at the late stages of the disease.
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PMID:[Complex clinical and morphofunctional study of vasorenal hypertension]. 702 18

Studies were undertaken in intact rats to characterize the renin response to pentobarbital anesthesia and the mechanisms involved in this response. Aortic and peritoneal cavity cannulas were previously implanted to allow drug infusion, blood sampling and anesthesia to be performed without stress. A sustained 2-3-fold increase in plasma renin concentration (PRC) and a 10-15 mm Hg depression of mean arterial pressure were found in pentobarbital anesthesia. Circulating levels of epinephrine and norepinephrine were unchanged. Sympathetic stimulation by tyramine did not decrease and chronic renal denervation did not abolish the PRC rise by pentobarbital. Phenoxybenzamine given to conscious or anesthesized animals elevated PRC to similar levels. Propranolol was effective in suppressing PRC in anesthetized animals, regardless of the presence or absence of phenoxybenzamine. We concluded that the renin response to pentobarbital anesthesia is unrelated to changes in sympatho-adrenal activity. The response appears to be mediated by beta-adrenergic receptors. It is postulated that pentobarbital-induced relaxation of afferent arterioles or JG cells exposes previously concealed beta-receptor sites which increase the signal for the release of renin.
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PMID:Renin release by pentobarbital anesthesia in the rat: a role for vascular mechanisms. 704 Aug 89

Prazosin is a post synaptic alpha adrenergic blocker effective in hypertension, whose hypotensive effect is unaccompanied by reflex tachycardia or hyperreninemia, nor by other evidence of increased sympathetic activity. We studied the baroreceptor reflex arc as a potential mediator of these effects. Twenty-two essential hypertensive men were treated with prazosin alone versus placebo, and experienced a blood pressure fall (from 114.8 +/- 3.6 down to 101.1 +/- 2.5 mmHg, p less than 0.005) unaccompanied by any change in heart rate, plasma renin activity, or several other indices of sympathetic nervous system activity (plasma dopamine-beta-hydroxylase activity; urinary excretion of free catecholamines and vanillyl mandelic acid; all p less than 0.1). Concomitant with the blood pressure fall, there was a significant depression of baroreflex arc sensitivity, from 11.4 +/- 2.0 ms/mmHg down to 6.6 +/- 1.9 ms/mmHg (p less than 0.05), without an associated change in cardiac vagal inhibition (291.2 +/- 46.2 versus 300.3 +/- 19.2 ms, p greater than 0.1). Baroreflex arc sensitivity depression may in part explain the lack of reflex sympathetic outflow noted during prazosin treatment of hypertension.
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PMID:Prazosin depression of baroreflex function in hypertensive man. 704 70

Experiments were performed to determine the influence of varying inspired oxygen tension on renal prostaglandin E2 (PGE2) excretion, renal hemodynamics, and water and electrolyte excretion in the conscious dog. Hypoxic exposure (PIO2 = 56 torr) resulted in a 13% increase in renal blood flow (RBF), while hyperoxic breathing with PIO2 of 700, 1426, or 2139 torr, all resulted in significant 5--7% decline in RBF, a response that was significantly attenuated compared to the striking renal vasoconstriction caused by hyperoxia in anesthetized dogs. Hyperbaric oxygenation (HBO) (1426 torr O2, 2139 torr O2) was associated with unexpected decreases in urine flow (V) of 61% and 70%, respectively. The antidiuresis and mild hemodynamic adjustments were correlated with a 67% decline in urinary PGE2 excretion (UPGE2 x V) when the dogs breathed 700 torr O2, while exposure to 1426 torr O2 and 2139 torr O2 diminished UPGE2 x V by 92% and 99%, respectively. Plasma antidiuretic hormone (ADH) concentration, measured during exposure to 1426 torr O2, was unchanged. In addition, this nonpharmacologic hyperbaric decline in PGE2 excretion was not associated with any changes in sodium excretion of renin secretion, in contrast to the usual depression of these variables with pharmacologic PG inhibition (indomethacin). The HBO antidiuresis may be a consequence of an increased medullary osmotic gradient secondary to reduced vasa recta blood flow. Alternatively, this antiduresis could occur as a consequence of a lowering of the normal functional antagonism existing between PGE2 and ADH, such that the influence of endogenous ADH is potentiated.
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PMID:Antidiuresis and inhibition of PGE2 excretion by hyperoxia in the conscious dog. 740 49

To elucidate the significance of long-term administration of dexamethasone in order to differentiate the 4 types of hyperaldosteronism, blood pressure, serum electrolytes, plasma renin activity (PRA) and diurnal rhythm of plasma aldosterone (PAC) were studied before and after long-term dexamethasone (Dex) administration in patients with aldosterone-producing adenoma (APA), idiopathic hyper aldosteronism (IHA), unilateral adrenal hyperplasia (UAH) and Dex suppressible hyperaldosteronism (DSH). The results were as follows: 1) In APA with ACTH-dependent aldosterone secretion, long-term Dex administration induced a significant depression of PAC associated with an elevation in serum potassium (s-K). In almost all patients with APA, the diurnal rhythm of PAC, parallel to that of ACTH, completely disappeared following Dex administration. 2) In most patients with IHA, PAC was mainly influenced by the renin-angiotensin system. Dex did not affected on s-K, but it induced a slight decrease in PAC in some patients with IHA. 3) In UAH having similar pathophysiological findings of the adrenal cortex as IHA, Dex decreased PAC. 4) In DSH, Dex at a dose of 6 mg/day decreased PAC to normal value in association with normalization of blood pressure and s-K. From these results, hyperaldosteronism inducing a decrease in PAC and an increase in s-K by Dex is possibly diagnosed as APA, while the patients with no change of s-K by Dex may be diagnosed as IHA. Even if PAC is suppressed with Dex and ACTH-independent, the hyperaldosteronism may be UAH. It may be possible that factors other than aldosterone are important to induce hypokalemia in patients with IHA. Furthermore, it is suggested that UAH is a precedent pathophysiological condition of aldosterone-producing adenoma in the adrenal cortex. It is concluded that the measurement of s-K and diurnal rhythm of PAC before and after Dex administration are useful for discriminating APA and IHA.
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PMID:[The long-term administration of dexamethasone for the differentiation of the 4 types of hyperaldosteronism]. 775 Jun 27

To compare the hemodynamic, antiischemic, metabolic, and neurohumoral effects of intravenous esmolol (beta 1 blocking agent) and gallopamil (verapamil-like calcium channel blocker), 14 patients with angiographically proven CAD and reproducible ST segment depression were studied at rest and during exercise under control conditions and after an intravenous bolus injection of esmolol (0.5 mg/kg/1 min, followed by an infusion with 0.2 mg/kg/min) or gallopamil (0.025 mg/kg/3 min). In contrast to gallopamil, esmolol significantly reduced systolic blood pressure (175.7 vs. 160 mm Hg) and heart rate (107.4 vs. 96.9 min-1) during exercise as well as cardiac output (11.57 vs. 9.38 l/min) and significantly enhanced systemic vascular resistance both at rest (1241 vs. 1479 dynes.s.cm-5) and during exercise (805 vs. 947 dynes.s.cm-5). On the other hand, exercise filling pressures and lactate levels (3.66 vs. 3.05 mmol/l) were significantly reduced by gallopamil only. Thus, the significant improvement of exercise tolerance by both esmolol and gallopamil is based on different mechanisms of action: esmolol improves myocardial ischemia by appreciably reducing myocardial oxygen consumption, whereas gallopamil primarily improves oxygen supply and ventricular performance. Plasma catecholamines, atrial natriuretic factor, and aldosterone levels as well as plasma renin activity were identically influenced by esmolol and gallopamil, respectively. A reflex activation of the sympathetic system did not occur.
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PMID:[Anti-ischemia effects of gallopamil and esmolol in an intra-individual comparison in patients with coronary heart disease]. 791 67

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

Licorice can induce a hypermineralocorticoid syndrome. Current literature usually refers to the effects of sweets containing glycyrrhizin, but little is known about the consequences of a prolonged intake of "pure licorice". We administered graded daily doses of dried, aqueous extract of licorice root, containing 108, 217, 380 and 814 mg of glycyrrhizin, to 4 groups of 6 healthy volunteers of both sexes for 4 weeks. No significant effects occurred in groups 1 and 2. After 2 weeks, side effects leading to withdrawal from the protocol occurred in a female in group 3 (headache), a male with a family history of hypertension in group 4 (arterial hypertension), and a female also taking oral contraceptives in group 4 (hypertension, hypokalaemia and peripheral edema). In group 4, transient reduction in kalaemia and increase in body weight were found after 1 and 2 weeks, respectively. A depression of plasma renin activity occurred in groups 3 and 4. In healthy subjects, only the highest doses of licorice led to untoward effects. These were favoured by subclinical disease or oral contraceptives, and were less common and pronounced than what has been reported after the intake of glycyrrhizin taken as such or as a flavouring agent in confectionery products.
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PMID:Effects of prolonged ingestion of graded doses of licorice by healthy volunteers. 807 87

We have previously shown that transdermal nitroglycerin may induce an increase in the activity of the adrenergic and the renin-angiotensin-aldosterone systems (SRAA) in patients with chronic stable angina pectoris (SA); when the activation of these systems is more pronounced, the antianginal effect of this drug seems to be reduced. The aim of this study was to evaluate the antianginal efficacy of transdermal nitroglycerin administration (TTS-NG 10 mg.24 h-1) in combination with an ACE inhibitor without sulphydryl groups (BNZ, benazepril 10 mg b.i.d.) in respect to placebo, or to TTS-NG or BNZ administered as monotherapy. Twenty-four patients (21M, 3F) were admitted to this multicentre, randomized, double-blind, latin square, placebo-controlled study. Patients received all the treatments (placebo, TTS-NG, BNZ and BNZ + TTS-NG) each for one week; at the end of each week patients performed two exercise tests 2 and 22 h post-dosing. Two hours post-dosing, exercise duration at 1 mm ST depression was significantly increased in respect to placebo during TTS-NG (P < 0.05) and TTS-NG + BNZ (P < 0.05) treatments. Two hours post-dosing, exercise duration at peak exercise was also increased in respect to placebo during TTS-NG (P < 0.05) and TTS-NG + BNZ (P < 0.05); 22 h post-dosing the increase in exercise duration was significant only during TTS-NG + BNZ treatment (P < 0.05) in respect to placebo, but not during TTS-NG given alone. Rate-pressure product at 1 mm ST depression was significantly increased 2 h post-dosing during TTS-NG treatment (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of transdermal nitroglycerin in combination with an ACE inhibitor in patients with chronic stable angina pectoris. 813 70

In healthy women we have studied the effects of potassium depletions of different degrees on the generation of some bioregulators of hydro-saline balance. The study has been performed on 20 women in normal potassium balance (N group) and 20 women submitted to potassium depletive treatment by dietary and pharmacological means. On the basis of different patterns of treatment we have obtained three groups i.e. KD1 (n = 8), KD2 (n = 6) and KD3 (n = 6) with potassium cumulative deficit of 160 +/- 43, 198 +/- 22 and 214 +/- 54 mmol, respectively. The renal function was assessed by the clearance method during induced hypotonic polyuria and subsequent moderate antidiuresis induced by low dose infusion of lysine-8-vasopressin. The urinary PGE2, 6-keto-PGF1 (6KPGF) and TxB2 were determined by the RIA method. Moreover, the basal PRA and urinary aldosterone were determined before the renal functional exploration. The data obtained in both KD2 and KD3 groups where renal hypokalemic dysfunctions occurred--indicate that hypokalemia stimulated renin secretion and inhibited the reactivity of renal prostanoid production to the polyuric stimulus. However, in the KD3 group--where the circulating levels of renin, and probably of angiotensin II were the highest--the hypokalemic depression of the synthesis of 6KPGF and TxB2 precursors was attenuated while the synthesis of PGE2 was still inhibited.
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PMID:Studies on renal function in healthy women with different degrees of induced potassium depletion. 1) Hormonal changes relevant to salt and water balance. 815 5


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