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 beta-adrenergic blocking agent, timolol, administered to resting rabbits as an i.v. bolus (0.125 mg/kg) sustained by a 2-hr infusion at 0.0625 mg/kg/hr, caused significant depression of plasma renin activity (PRA) to 49% of the control level. Significant correlations emerged between the fall in mean blood pressure and changes in both heart rate and PRA. Timolol also antagonized isoprenaline-induced renin release. In anaesthetized normal rats, timolol (0.2 mg/kg i.p.) suppressed mean plasma renin concentration (PRC) to 16% of the pre-treatment value. Furthermore, the mean PRC of normal rats, bled immediately after decapitation, to avoid stimulating renin secretion, was reduced by 55% one hr after i.p. injection of timolol. The potency of timolol in this respect was 8 times that of dl-propranolol. Thus, in rabbits and rats, timolol effectively depresses both basal and stimulated plasma renin levels.
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PMID:Suppression of renin release by timolol. 0 74

The effect of timolol versus propranolol on hypertension, hemodynamics, and plasms renin activity was evaluated in 20 men. After two weeks of placebo, 11 men received timolol 30 to 60 mg daily, and nine men received propranolol, 240 to 480 mg daily, for five weeks in a double-blind randomized study. The 20 men then received placebo again for two weeks. Right heart catheterization was performed in all 20 patients after two weeks of the first placebo and after five weeks of timolol or propranolol. Equipotent doses of timolol and propranolol were equally effective in significantly lowering supine and upright systolic and diastolic blood pressure and heart rate recorded on an outpatient basis. Equipotent doses of timolol and propranolol caused similar hemodynamic effects including similar significant depression of cardiac index. Equipotent doses of timolol and propranolol caused similar marked depression of plasma renin activity. The hypotensive action of timolol and of propranolol was unrelated to their effect on plasma renin activity.
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PMID:Effect of timolol versus propranolol on hypertension and hemodynamics. 0 61

Plasma renin activity (PRA) in 40 diabetic patients and 42 healthy controls was investigated using the method of Pickens in modification of Serebrovskaja et al. (1967). PRA was slightly lower in the whole group of diabetes but the difference was not significant. The subgroup of 20 maturity-onset diabetics had significantly lower PRA in comparison with 22 controls of similar age, while PRA in juvenile diabetics did not differ significantly from matched controls. In patients without clinical signs and symptoms of microangiopathy PRA was as high as in the controls. In diabetics with microangiopathy PRA was significantly lower. PRA was also lower in patients with longer duration of the disease. The stimulation of juxtaglomerular apparatus with sodium free diet and diuretic drugs resulted in an increase of PRA both in controls and diabetics. This suggests a functional depression of PRA in diabetic patients. In diabetics with ketoacidosis PRA was higher than in control subjects and decreased after disappearance of ketoacidosis. A high level was recorded in a patient with hyperosmolar coma and a very low level in a patient with polyneuropathy and severe orthostatic hypotension. The possible mechanisms involved in the changes of PRA in diabetic patients are discussed.
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PMID:Plasma renin activity in diabetic patients. 11 36

To investigate whether a direct influence exists between the prolactin suppressive effect of alpha-bromoergocriptine (CB 154) and the aldosterone response to a potassium stimulation, the present study was performed in 7 anephric patients and in 7 non-nephrectomized patients, all on regular haemodialysis. The increase in the plasma potassium concentration between dialysis was used as a stimulus to the adrenals, and was correlated to the increase in the plasma aldosterone concentration (PAC). Plasma samples were obtained during a control period and during a corresponding period of treatment with bromocriptine. Despite a significant fall in the prolactin levels during the bromocriptine treatment, no differences in the aldosterone response to the increasing potassium concentration in the two periods were found neither in the anephric nor in the non-nephrectomized patients. It is concluded that depression of prolactin levels by the dopamine agonist (bromocriptine) has no influence on the ability of the adrenals to react with an increase in aldosterone secretion following potassium stimulation in dialysis patients with and without preserved renin-angiotensin system.
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PMID:Lack of effect of prolactin inhibition by alpha-bromoergocriptine (CB 154) on plasma aldosterone in anephric and non-nephrectomized patients on regular haemodialysis. 19 47

In anesthetized vagotomized dogs with renal arterial pressure constant, carotid sinus hypotension (BCO) caused a reflex rise in systemic arterial pressure, a fall in renal blood flow, and a similar increase in renin release from both kidneys. Unilateral alpha-adrenoceptor blockade with phenoxybenzamine resulted in an increase in basal renal blood flow, a depression of basal renin release, and an abolition of the responses to BCO in the treated kidney. The untreated kidney responsed to BCO as before. Nonblocked and alpha-blocked kidneys released similar amounts of renin when renal blood flow was mechanically reduced by aortic constriction. Administration of propranolol to the nonblocked kidney prevented the release of renin but not the hemodynamic changes resulting from BCO. The experiments demonstrated that under certain conditions carotid sinus hypotension produced alpha-adrenoceptor-mediated changes in the kidney sufficient to cause increased renin release. A step in the renin release mechanism subsequent to the alpha-adrenoceptor-mediated changes in sensitive to propranolol.
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PMID:Involvement of renal alpha- and beta-adrenoceptors in release of renin by carotid baroreflex. 21 17

Peripheral beta-adrenergic receptor sensitivity was characterized in 24 patients with essential hypertension and in 13 age-matched normotensive subjects using an isoproterenol hydrochloride bolus dose-response technique. Decreased beta-receptor responsiveness to this exogenously administered beta-agonist was observed in hypertensive patients; for an equivalent chronotropic effect, higher doses of isoproterenol were required in hypertensive subjects than in normal subjects. Among "normal-renin" hypertensive patients, beta-receptor responsiveness was directly related to furosemide-stimulated plasma renin activity (PRA), suggesting that independently stimulated PRA may provide an indirect estimate of endogenous beta-receptor sensitivity. Hypertensive patients whose mean arterial pressure fell at least 10 mm Hg after four weeks of treatment with hydrochlorothiazide had even further depression in beta-receptor responsiveness, whereas receptor sensitivity was unchanged in patients whose blood pressure was unaffected. Thus, it is unlikely that this decreased receptor responsiveness in patients with untreated essential hypertension is a direct consequence of elevated arterial pressure.
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PMID:Peripheral beta-receptor responsiveness in patients with essential hypertension. 22 9

Physiological roles have been suggested for prostacyclin in the cardiovascular system. Prostacyclin was administered by intravenous infusion to unanesthetized rats. Over a 24 hr period, 0.32 mg/kg/day caused only flushing of the ears. Larger doses (0.56 and 1 mg/kg/day) caused hypothermia, behavioral depression, and swelling of the paws. Cumulative dose-response curves for its depressor action were determined in both unanesthetized and anesthetized, vagotomized, ganglion-blocked rats. In unanesthetized rats, the threshold dose was about 0.1 ug/kg/min. Respiratory depression precluded doses larger than 1 ug/kg/min. In anesthetized rats, the threshold dose was about 0.001 ug/kg/min, and the maximally effective dose was about 0.1 micrograms/kg/min. At 0.032 ug/kg/min, blood pressure first fell and then rose slightly. This compensatory rise did not occur in nephrectomized rats, suggesting renin release as the mechanism. Intravenous infusion of 0.1 but not 0.01 ug/kg/min in unanesthetized rats doubled plasma renin activity. In saline-loaded unanesthetized rats, urine volume and urinary sodium excretion were decreased by 0.1 ug/kg/min of prostacyclin.
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PMID:The cardiovascular pharmacology of prostacyclin (PGI2) in the rat. 37 17

1. The effects of external medium calcium concentration, the ionophore A(23187) and lanthanum on the rate of renin release in vitro were studied with particular emphasis on results obtained from isolated superfused glomeruli of rat kidneys.2. The response to reduction in superfusate calcium concentration from 2 mM was a graded and reversible increase in the rate of renin release. An increase in release was detectable at 0.2 mM calcium; a threefold increase was found 36 min after a change from 2 mM calcium to calcium-free superfusate. A similar relative increase in release resulted from reductions from 0.1 mM to zero calcium, but the absolute amounts of renin released were greater in this latter series. Renin release from kidney cortical slices similarly increased in response to calcium-free incubation medium.3. The effects of A(23187) on renin release were modest. Changing from 2 mM calcium during control periods to calcium-free Ringer with A(23187) added caused an attenuated and more delayed increase in release than the change to calcium-free Ringer without ionophore. This difference in response was abolished when glomeruli were superfused with 0.1 mM calcium during the preceding 1 hr control period. There was no significant difference in renin release from glomeruli exposed to calcium-free EGTA-Ringer with and without A(23187) in the 2 mM calcium series; in the 0.1 mM calcium series the increase in release following a shift to calcium-free EGTA-containing superfusate with A(23187) added was significantly greater than in the absence of the ionophore.4. Addition of lanthanum (1 or 0.05 mM) to calcium-containing as well as calcium-free superfusate resulted in a significant depression of renin release. Subsequent removal of the lanthanum did not restore the rate of release unless EGTA was added; in the latter case a massive increase in renin release occurred resulting in a marked depletion of the remaining renin content of the glomeruli.5. It is concluded that calcium influences renin release by a direct action on the juxtaglomerular cells. The data support the previous suggestion that basal renin release is a function of active, calcium-dependent cell volume regulation - swelling causing an increase in the release; and further suggest that membrane-bound calcium has a direct effect on the cell membrane permeability to renin.6. The results exclude that calcium-stimulated exocytosis is responsible for basal renin release from the juxtaglomerular cells adhering to isolated glomeruli.
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PMID:Studies on the mechanism of renin release from isolated superfused rat glomeruli: effects of calcium, calcium ionophore and lanthanum. 41 32

The renal response to left atrial balloon inflation in normal dogs was compared with that in dogs with chronic congestive heart failure (CHF). CHF was induced by the production of an aortocaval fistula below the level of the renal arteries. CHF dogs showed elevated left ventricular end-diastolic pressure, enlarged hearts, a depression of myocardial contractility, pulmonary edema, ascites, and peripheral edema. They also showed significant decreases in urine flow, creatinine clearance, para-aminohippurate clearance, sodium and potassium excretion, fractional sodium excretion, osmolar clearance, arterial blood pressure, and heart rate. Balloon distension of the left atrium evoked a significant increase in urine flow and free-water clearance in the normal group. The reflex nature of this response was indicated by its blockade after bilateral cervical vagotomy. In contrast, the CHF group did not exhibit significant changes in urine flow or free-water clearance during balloon inflation. Plasma antidiuretic hormone (ADH) was significantly elevated in the CHF group; however, balloon distension reduced plasma ADH in both groups of dogs. Plasma renin activity was significantly elevated in the CHF dogs and was not changed by balloon distension in either group of dogs. It is concluded that animals with high-output CHF do not exhibit the atrial-diuretic reflex in spite of their ability to reduce ADH levels by atrial distension.
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PMID:Renal effects of left atrial distension in dogs with chronic congestive heart failure. 43 20

We have investigated in eight healthy persons the effect of a single intranasal dose of 40 microgram DDAVP on plasma renin activity (PRA) in the upright posture. During normal sodium intake there were no differences in the PRA values between the time-control and DDAVP studies. However, during sodium restriction in four subjects with higher initial PRA, DDAVP induced a 40% decrease, lasting no longer than 45 minutes. There was no change in PRA after DDAVP in the other four subjects with much lower initial levels. Although no major or consistent suppressive influence could be demonstrated in the present study, in certain persons with highly stimulated initial PRA levels a transitory slight depression may be expected after a pharmacological dose of DDAVP.
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PMID:Effect of DDAVP on plasma renin activity in man. 48 97


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