Publications by authors named "Feuerstein G"

Catecholamine and vasopressin content were studied in discrete brain nuclei of the Sabra strain of hypertension prone (SBH) and resistant (SBN) rats. Higher concentrations of dopamine, norepinephrine and epinephrine were observed in the median eminence of SBN compared to SBH or controls (SB) rats. Dopamine and epinephrine levels were higher in the lateral septal nucleus of SBH rats as compared to SBN or SB.

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Following spinal injury, the opiate antagonist naloxone selectively elevates plasma dopamine levels, with the dopamine changes significantly correlated with improved cardiovascular function. Moreover, the cardiovascular effects of naloxone are significantly attenuated by pretreatment with the dopamine antagonist domperidone. From these data, it is concluded that the cardiovascular effects of naloxone after spinal injury are in part dopamine mediated.

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Severe endotoxemia, a condition where microembolization and intravascular coagulation are thought to play important roles, was treated experimentally with prostacyclin (PGI(2)). In a study of 24 dogs, 8 control animals injected with 1.75 mg.

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Injection of prostaglandin F2 alpha (1 nmol/rat) into the paraventricular, dorsomedial and posterior hypothalamic nuclei of halothane anesthetized rats elicited rapid increases of heart rate and blood pressure. The injection of this same dose of prostaglandin F2 alpha into the cerebroventricular system or intravenously had no effect on these parameters. The cardiovascular responses observed following prostaglandin F2 alpha injection into these hypothalamic nuclei were accompanied by increases in plasma levels of norepinephrine and epinephrine, with peak levels at the maximal cardiovascular response.

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The effects of prostaglandins (PGE2 and 16,16-dimethyl-PGE1) on epinephrine (E) and norepinephrine (NE) release, in response to a hypotensive stimulus (bleeding 5 ml/300 g), were studied in relation to blood pressure and heart rate responses in the rat. PGE2 (10 micrograms/kg-1 . min-1) and 16,16-dimethyl-PGE1 (1 microgram .

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The following experiments were designed in order to examine the inter-relationships of various prostaglandins (PG's) and the adrenergic nervous system, in conjunction with blood pressure and heart rate responses, in vivo. Stimulation of the entire spinal cord (50v, 0.3-3 Hz, 1.

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The effect of amiloride on lithium-induced polydipsia and polyuria and on the lithium concentration in the plasma, brain, kidney, thyroid and red blood cells was investigated in rats, chronically treated with LiCl. Amiloride reduced the drinking and urine volume of rats in an acute (6 or 12 h) and a subacute (3 days) experiment. 6 h after the administration of amiloride, a reduction was observed in the lithium content of the renal medulla but not in the other organs studied.

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Injection of muscimol (4 mg/kg, i.a.) to unanesthetized SHR rats reduced the arterial blood pressure and heart rate more than in WKY rats.

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Isoproterenol infusion (0.1 microgram/kg per min) into the renal artery of the cat induced an increase in plasma renin concentration (PRC) from 14.3 +/- 5.

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Treatment of rats with indomethacin, 1.5 mg/kg per day, for one week, significantly reduced the number of beta-adrenoceptors in the heart without altering their affinity for the specific beta-adrenergic ligand. In indomethacin-treated rats there was a reduction in the cardiac response to epinephrine in vivo as indicated by a shift to the right of the epinephrine dose-heart rate response curve.

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Hemorrhage, 15 ml/kg induced a rapid fall of blood pressure in intact and anephric cats, but only intact cats demonstrated significant blood pressure recovery following bleeding. Naloxone, 0.1 mg/kg x min, i.

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1 The mechanism involved in catecholamine (CA) release from the cat adrenal gland in response to insulin hypoglycaemia was studied. In intact cats, hypoglycaemia induced an 11 fold increase in adrenomedullary CA secretion. 2 Acute bilateral nephrectomy nearly abolished the increased CA release from the adrenal gland during hypoglycaemia.

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In vivo isoprenaline infusion (0.1 micrograms/kg.min)) into the renal artery of unilaterally nephrectomized cats elicited a 5-fold increase in plasma renin concentration (PRC).

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Angiotensin II (AII) induced an increase of adrenaline (A) release from rat adrenal glands in vitro. The response of the adrenal glands was completely abolished 22--24 h after bilateral nephrectomy. Adrenal glands from DOCA-salt-treated rats did not respond to AII as well, whereas adrenal glands from rats treated with furosemide and a low salt diet retained this response.

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Adrenal catecholamine secretion induced by haemorrhage in the cat was increased by administration of indomethacin to intact or to bilaterally nephrectomized animals. Infusion of PGE2 (but not of PGF2 alpha) suppressed the increased catecholamine secretion caused by indomethacin.

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