Showing papers on "Norepinephrine (medication) published in 1986"
TL;DR: There is marked regional variation, inapparent from measurements of plasma norepinephrine concentration, in sympathetic nerve activity in patients with congestive heart failure.
Abstract: The analysis of plasma kinetics of the sympathetic neurotransmitter norepinephrine can be used to estimate sympathetic nervous "activity" (integrated nerve firing rate) for the body as a whole and for individual organs. In 12 patients with cardiac failure (left ventricular ejection fraction 10% to 39%), the mean arterial plasma norepinephrine concentration was 557 +/- 68 pg/ml (mean +/- SE) compared with 211 +/- 21 pg/ml in 15 subjects without heart failure (p less than .002). The difference was due to both increased release of norepinephrine to plasma (indicating increased "total" sympathetic activity) and reduced clearance of norepinephrine from plasma. The increase in sympathetic activity did not involve all organs equally. Cardiac (32 +/- 9 vs 5 +/- 1 ng/min; p less than .002) and renal (202 +/- 45 vs 66 +/- 9 ng/min; p = .002) norepinephrine spillover were increased by 540% and 206%, respectively, but norepinephrine spillover from the lungs was normal. Adrenomedullary activity was also increased in the patients with heart failure, whose mean arterial plasma epinephrine concentration was 181 +/- 38 pg/ml compared with 71 +/- 12 pg/ml in control subjects (p less than .02). There is marked regional variation, inapparent from measurements of plasma norepinephrine concentration, in sympathetic nerve activity in patients with congestive heart failure. The finding of increased cardiorenal norepinephrine spillover has important pathophysiologic and therapeutic implications.
1,076 citations
TL;DR: Whether sympathetic nerve activity is increased in patients with heart failure and whether plasma norepinephrine levels correlate with levels of mSNA in heart failure are determined and microneurography is used to directly record sympathetic nerve action to muscle.
Abstract: Patients with heart failure have increased vascular resistance and evidence for increased neurohumoral drive. High levels of circulating norepinephrine are found in patients with heart failure, but it is not known whether they reflect increased sympathetic neural activity or result from altered synthesis, release, or metabolism of norepinephrine. We used microneurography (peroneal nerve) to directly record sympathetic nerve activity to muscle (mSNA) and also measured plasma norepinephrine levels in patients with heart failure and in normal control subjects. Our goal was to determine whether sympathetic nerve activity is increased in patients with heart failure and whether plasma norepinephrine levels correlate with levels of mSNA in heart failure. Resting muscle sympathetic nerve activity in 16 patients with moderate to severe heart failure (54 +/- 5 bursts/min, mean +/- SE) was significantly higher (p less than .01) than the levels of activity in either nine age-matched normal control subjects (25 +/- 4 bursts/min) or 19 "young" normal control subjects (24 +/- 2 bursts/min). We found a significant correlation between plasma norepinephrine levels and mSNA (r = .73, p less than .05). Neither mSNA nor plasma norepinephrine levels correlated with total systemic vascular resistance, cardiac index, left ventricular ejection fraction, or heart rate. However, both mSNA and plasma norepinephrine levels showed significant positive correlations (p less than .05) with left ventricular filling pressures (r = .80, mSNA vs filling pressures; r = .82, norepinephrine levels vs filling pressures) and mean right atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
822 citations
282 citations
TL;DR: Cardiorenal sympathetic nervous system tone appears to be increased in essential hypertension, particularly in younger patients, which contributes substantially to the higher plasma noradrenaline values found.
Abstract: Increased sympathetic nervous system tone may be the initiating pathophysiologic event in some patients with essential hypertension. We estimated sympathetic nervous activity from radiotracer-derived measurements of noradrenaline release to plasma in 34 patients with essential hypertension and 23 subjects with normal blood pressure. The plasma concentration of noradrenaline (32% increased) and the rate of release of noradrenaline to plasma (38% increased) were elevated overall in patients with essential hypertension, largely due to higher noradrenaline release in hypertensive patients aged less than 40 years. Noradrenaline release from the kidneys and heart was elevated; renal noradrenaline spillover was 2.4 times normal in patients aged less than 40 years. Increased renal noradrenaline spillover accounted for 42% and increased cardiac noradrenaline spillover for 4% of the excess total noradrenaline spillover in essential hypertension, leaving 54% unexplained. Total noradrenaline spillover to plasma was normal in hypertensive patients aged 60 years and over. The plasma noradrenaline concentration was similar in younger and older hypertensive patients, despite lower noradrenaline release in the latter due to an age-dependent fall in noradrenaline plasma clearance in essential hypertension. Cardiorenal sympathetic nervous system tone appears to be increased in essential hypertension, particularly in younger patients. This contributes substantially to the higher plasma noradrenaline values found.
203 citations
197 citations
TL;DR: Sudden, short-lived psychological stimuli causing marked cardiovascular responses and moderate elevations in plasma concentrations of catecholamines and cortisol are unlikely to disturb metabolic control in patients with Type I diabetes.
Abstract: Acute psychological stress is believed to cause disturbances of metabolic control in patients with Type I diabetes. To examine the validity of this assumption, we subjected nine healthy persons (mean [±SEM] blood glucose level, 74±2 mg per deciliter), nine patients with Type I diabetes who had normoglycemia (130±10 mg per deciliter), and nine diabetic patients with hyperglycemia (444±17 mg per deciliter) to two acute psychological stresses: mental arithmetic and public speaking. Subjects in the three groups were matched for age, weight, sex, and socioeconomic status. For all subjects, the mean increase in heart rate was 20 beats per minute while they were doing mental arithmetic and 25 beats per minute while they were speaking publicly (P<0.001). In all three groups, systolic and diastolic pressure rose markedly, the plasma epinephrine level increased by 50 to 150 pg per milliliter, and the norepinephrine level by 100 to 200 pg per milliliter under both stress conditions (P<0.001). The plasma cor...
142 citations
TL;DR: It is suggested that the mechanisms responsible for the amine release in acutely stressed animals, as well as those mechanisms subserving the increased amine levels evident after chronic stressor application, may be subject to conditioning or sensitization processes.
111 citations
TL;DR: It is concluded that atriopeptin secretion by the atrial myocyte is stimulated by activation of the α-1 adrenergic receptor, which suggests an involvement of the sympathetic nervous system in the physiologic regulation of the secretion of this hormone.
110 citations
TL;DR: Attenuated systemic pressor responses to infused angiotensin II characterize normal human and ovine pregnancy; moreover, uterine vascular refractoriness is greater than that of the systemic vasculature overall.
106 citations
TL;DR: The data support the view that chronic diabetes in rats is associated with increased sympathetic activity and indicate that the cardiac norepinephrine concentration in diabetic rats may be maintained at a higher than normal level by an increased synthesis and uptake of norpinephrine in the adrenergic nerve terminals.
Abstract: Cardiac norepinephrine turnover and metabolism were examined in rats 8 weeks after the induction of chronic diabetes by an intravenous injection of streptozotocin (65 mg/kg). Cardiac norepinephrine concentration, norepinephrine turnover, and norepinephrine uptake were markedly increased in chronic diabetes in comparison with control values; these changes were reversible by 28-day insulin therapy. When the animals were exposed to cold for 6 hours, norepinephrine turnover rate constant increased in control and decreased in diabetic animals; cold exposure also increased norepinephrine concentration in diabetic hearts. Both cardiac norepinephrine concentration and turnover rate in diabetic rats were restored toward control values by ganglionic blockade with pentolinium. The conversion of [3H]tyrosine to [3H]catecholamine was enhanced and tyrosine hydroxylase as well as dopa decarboxylase activities were increased in diabetic hearts. The higher concentrations of [3H]normetanephrine and deaminated catechols indicated a faster metabolic rate of norepinephrine metabolism in hearts from diabetic rats; both monoamine oxidase and catechol-O-methyltransferase activities were also increased. The increased activities of the enzymes for the synthesis and metabolism of norepinephrine were not evident on treating the diabetic animals with insulin. These data not only support the view that chronic diabetes in rats is associated with increased sympathetic activity but also indicate that the cardiac norepinephrine concentration in diabetic rats may be maintained at a higher than normal level by an increased synthesis and uptake of norepinephrine in the adrenergic nerve terminals.
105 citations
TL;DR: It is demonstrated that a percentage of animals subjected to middle cerebral artery occlusion have myocardial damage and an increase in plasma concentration of norepinephrine and epinephrine, which suggests that a rise in plasma catecholamine levels, due to increased sympathetic activity aftermiddle cerebral artery Occlusion, may cause myocardIAL damage.
Abstract: Focal cerebral ischemia in humans increases the incidence of cardiac arrhythmias, and serum cardiac enzyme and plasma norepinephrine levels. In addition, systemic administration of catecholamines causes myocardial damage. This suggests that cerebral ischemia may cause myocardial damage as a consequence of elevated plasma norepinephrine levels. Therefore, experiments were done in 23 chloralosed, paralyzed and artificially ventilated cats to investigate the effects of occluding (n = 17) or sham-occluding (n = 6) the left middle cerebral artery on the myocardium and on circulating levels of plasma catecholamines. After occlusion of the middle cerebral artery for 12-22 hr, 41% (7/17) of the hearts had either acute myocardial necrosis (3/7), focal hemorrhage (3/7), or both (1/7). In animals with acute myocardial damage the levels of plasma norepinephrine and epinephrine were significantly increased compared to pre- middle cerebral artery occlusion values (+46 +/- 18% and +142 +/- 45%, respectively). As well, in cats with acute myocardial damage, changes from initial levels of plasma norepinephrine and epinephrine were significantly increased over those of experimental cats without acute myocardial damage. In animals which did not have acute myocardial damage (10/17) the circulating plasma levels of catecholamines were not significantly different from pre-occlusion values. Similarly, sham occlusion did not alter plasma catecholamine levels. These data demonstrate that a percentage of animals subjected to middle cerebral artery occlusion have myocardial damage and an increase in plasma concentration of norepinephrine and epinephrine. This suggests that a rise in plasma catecholamine levels, due to increased sympathetic activity after middle cerebral artery occlusion, may cause myocardial damage.
TL;DR: It is concluded that central noradrenergic pathways may play an important role in the control of vasopressin release and that this control may involve alpha-1, alpha-2 and beta adrenoreceptors.
Abstract: The role of central adrenergic receptors in the control of vasopressin release was studied in the conscious rat. Norepinephrine (10 micrograms) and the alpha-1 agonist, phenylephrine (50 micrograms), administered intracerebroventricularly resulted in significant increases in the plasma vasopressin concentration and blood pressure. The alpha-2 agonist, BHT 933 (50 micrograms) and the beta agonist, isoproterenol (10 micrograms) both caused a significant decrease in the plasma vasopressin concentration with only small changes in blood pressure. The central administration of the alpha-1 antagonist corynanthine (20 micrograms) had no effect on the plasma vasopressin concentration; however, increases in plasma vasopressin levels were observed when either the alpha-2 antagonist yohimbine (20 micrograms) or the beta antagonist propranolol (20 micrograms) were given. It is concluded that central noradrenergic pathways may play an important role in the control of vasopressin release and that this control may involve alpha-1, alpha-2 and beta adrenoreceptors.
TL;DR: The data suggest that in diabetic patients, subnormal baseline plasma norepinephrine levels may signify profound, possibly structural defects of sympathetic pathways, and that normal resting levels of respiratory sinus arrhythmia may have different implications, however, since vagal, unlike sympathetic reflex abnormalities, can be reversed partly by arterial pressure elevations.
Abstract: Resting diabetic patients may have excessively rapid heart rates, reduced heart rate variability, and subnormal plasma catecholamine levels. Although all of these abnormalities may relate in some way to baroreceptor reflex function, there have been surprisingly few attempts to evaluate systematically baroreflex mechanisms in diabetic patients. Accordingly, we studied autonomic responses over a range of pharmacologically induced arterial pressure changes in 10 unselected young adult insulin-dependent diabetic patients who had no symptoms of autonomic neuropathy, and 12 age-matched nondiabetic subjects. Sympathetic responses were estimated from antecubital vein plasma norepinephrine levels, and parasympathetic responses were estimated from electrocardiographic R-R intervals and their variability (standard deviation). Both were correlated with other noninvasive indexes of peripheral and central nervous system function. Multiple derangements of baroreflex function were found in the diabetic patients studied. Sympathetic abnormalities included subnormal baseline norepinephrine levels, virtual absence of changes of norepinephrine levels during changes of arterial pressure, and supranormal pressor responses to phenylephrine infusions. Parasympathetic abnormalities included subnormal baseline standard deviations of R-R intervals, and R-R interval prolongations during elevations of arterial pressure which were unmistakably present, but subnormal. Our data suggest that in diabetic patients, subnormal baseline plasma norepinephrine levels may signify profound, possibly structural defects of sympathetic pathways. Subnormal resting levels of respiratory sinus arrhythmia may have different implications, however, since vagal, unlike sympathetic reflex abnormalities, can be reversed partly by arterial pressure elevations.
TL;DR: It is proposed that one of norepinephrine's actions on supraoptic neurons involves K+ channels, perhaps by modulation of a transient K+ current known as A current.
Abstract: Intracellular data were obtained from 35 supraoptic nucleus neurosecretory neurons maintained in vitro in intra-arterially perfused explants of rat hypothalamus. Addition of norepinephrine, phenylephrine, or methoxamine, but not isoproterenol (30-200 microM), consistently induced membrane depolarization, bursting activity, and an associated prolongation in action potential duration, effects that were reversibly antagonized by the alpha 1-antagonist prazosin. Norepinephrine-evoked depolarizations demonstrated no consistent change in membrane resistance and were reduced both by membrane hyperpolarization and by raising extracellular K+. Norepinephrine shortened the time course of spike hyperpolarizing afterpotentials and increased the magnitude of late depolarizing afterpotentials. It is proposed that one of norepinephrine's actions on supraoptic neurons involves K+ channels, perhaps by modulation of a transient K+ current known as A current.
TL;DR: The present result indicates that ANF inhibits noradrenergic neurotransmission in the rat mesenteric arteries through a prejunctional mechanism, which may in part contribute to its vasodilation action.
TL;DR: This CRF antagonist administered to Sprague-Dawley rats neither prevented the rise of MAP or HR following electrical stimulation of the central nucleus of the amygdala, nor did it affect nitroprusside-induced hypotension and tachycardia.
TL;DR: It is concluded that the NE-antagonistic effect of ANF and the consecutive amelioration of GFR may play an important role in the recovery of impaired renal function.
Abstract: The effect of the atrial natriuretic factor (ANF) on early norepinephrine-induced acute renal failure (ARF) was investigated. In anaesthetized female Sprague-Dawley rats, weighing 247 ± 36 g, ARF of t
TL;DR: To determine whether venous plasma norepinephrine concentrations consistently reflect changes in sympathetic nervous activity, the influence of mental arithmetic, static handgrip, and submaximal bicycle exercise on intra-arterial blood pressure, heart rate, and plasma norpinephrine was studied in 51 subjects with untreated essential hypertension.
Abstract: To determine whether venous plasma norepinephrine concentrations consistently reflect changes in sympathetic nervous activity, the influence of mental arithmetic, static handgrip, and submaximal bicycle exercise on intra-arterial blood pressure, heart rate, and plasma norepinephrine was studied in 51 subjects with untreated essential hypertension (mean age, 46 years; range, 16-69 years). At rest, plasma norepinephrine was unrelated to age or blood pressure. Mental arithmetic increased mean arterial pressure from 108 +/- 18 to 127 +/- 18 mm Hg (mean +/- S.D.; p less than 0.001) and heart rate from 69 +/- 7 to 93 +/- 13 beats/min (p less than 0.001) but not plasma norepinephrine (547 +/- 297 to 518 +/- 250 pg/ml). Isometric exercise raised mean arterial pressure from 115 +/- 18 to 148 +/- 21 mm Hg (p less than 0.001) and heart rate from 76 +/- 9 to 95 +/- 13 beats/min (p less than 0.001) but not plasma norepinephrine (683 +/- 253 to 741 +/- 253 pg/ml). Bicycle exercise increased mean arterial pressure from 114 +/- 20 to 146 +/- 26 mm Hg (p less than 0.001), heart rate from 77 +/- 9 to 128 +/- 19 beats/min (p less than 0.001), and plasma norepinephrine from 645 +/- 228 to 1151 +/- 462 pg/ml (p less than 0.001). Both the maximum mean arterial pressure and the peak heart rate attained during bicycle exercise were related to the exercise plasma norepinephrine level (r = 0.33, p less than 0.02 and r = 0.28, p less than 0.03, respectively). Increases in plasma norepinephrine with exercise were not greater in older or more hypertensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The modulation of the delayed rectifier potassium channel in calf cardiac Purkinje fibers by the neurohormone norepinephrine is investigated and it is found that 0.5 microM norpinephrine increases this K channel current by a factor of 2.7.
TL;DR: The cerebrovascular response to catecholamine infusion was critically dependent on the agent administered, the level of hypertension achieved, and the brain region examined.
Abstract: The effects of hypertension induced by norepinephrine and dopamine infusion on the relationship between local cerebral blood flow (CBF) and local glucose use (GU) were examined in rats with the use of quantitative autoradiographic techniques. After rats recovered from anesthesia, dopamine or norepinephrine was infused at a rate that ensured moderate hypertension [mean arterial blood pressure (MABP) approximately 150 mmHg]. During dopamine infusion (approximately 200 micrograms X kg-1 X min-1), overall CBF-to-GU ratio throughout the brain was elevated (P less than 0.0001) when compared with saline controls. In contrast, during norepinephrine infusion (approximately 10 micrograms X kg-1 X min-1), the overall CBF-to-GU relationship was not altered significantly. The differential effect of the catecholamines was a consequence of the marked increases in local CBF and moderate decreases in GU observed during dopamine infusion, whereas during norepinephrine administration CBF and GU were not significantly altered in most brain regions. Blood-brain barrier (BBB) permeability was increased during moderate hypertension induced by dopamine and not when induced by norepinephrine. During extreme hypertension (MABP greater than 165 mmHg), heterogeneous increases in CBF and BBB permeability occurred (e.g., in the cerebellum and thalamus). Thus the cerebrovascular response to catecholamine infusion was critically dependent on the agent administered, the level of hypertension achieved, and the brain region examined.
TL;DR: The results suggest that norepinephrine increases cyclic AMP accumulation in rat cerebral cortex through α 1 -adrenoceptors similar to those increasing phosphatidylinositol metabolism in the same tissue.
TL;DR: It is concluded that the adrenergic inhibition of N-acetyltransferase activity in chicken pineal gland probably occurs via stimulation of postsynaptic α 2 -adrenergic receptors.
TL;DR: The results suggest a homeostasis for control of glucose in a hypothalamic feeding system and injection of norepinephrine into the medial hypothalamic sites that normally elicit feeding behavior elevated serum glucose.
TL;DR: Results indicate that opiate antagonists stimulate and agonists suppress the release of iβ‐END, possibly by affecting the patient's perceived level of pain and anxiety, and suggests that endogenous opioid peptides inhibit the perception of intraoperative pain even in the presence of concurrent local anesthesia.
Abstract: Forty-eight patients received either naloxone (10 mg), fentanyl (0.1 mg), diazepam (0.3 mg/kg), or saline solution placebo, and then underwent surgical removal of impacted third molars under local anesthesia. Placebo resulted in significantly elevated levels of immunoreactive β-endorphin (iβ-END), norepinephrine, and anxiety during surgery. Patients receiving naloxone had significantly greater intraoperative iβ-END and pain as compared with those receiving placebo. The naloxone effect on intraoperative pain was a result of a difference in perceived unpleasantness. Both the fentanyl and diazepam groups had significantly lower intraoperative iβ-END and anxiety levels as compared with the placebo group. Norepinephrine levels increased significantly in response to surgical stress in all groups except the diazepam group. Postoperative circulating levels of iβ-END and norepinephrine and pain increased significantly from the 1 to 3—hour postoperative period for all groups, with the exception of stable norepinephrine levels observed in patients receiving diazepam. Results indicate that opiate antagonists stimulate and agonists suppress the release of iβ-END, possibly by affecting the patient's perceived level of pain and anxiety. In addition, the association of intraoperative hyperalgesia with naloxone predosing suggests that endogenous opioid peptides inhibit the perception of intraoperative pain even in the presence of concurrent local anesthesia.
Clinical Pharmacology and Therapeutics (1986) 40, 165–171; doi:10.1038/clpt.1986.159
Journal Article•
TL;DR: It is suggested that ATP released from sympathetic neurons in the vessel wall contributes to the cooling-induced augmentation of contractile responses to sympathetic nerve stimulation in canine cutaneous veins, which may explain the increased prominence of purinergic mechanisms in cutaneous blood vessels.
Abstract: In canine cutaneous veins, cooling augments the contractile responses evoked by sympathetic nerve stimulation despite a cooling-induced reduction in the release of norepinephrine. With exogenous norepinephrine, the increased responsiveness observed during cooling results from enhanced sensitivity of the postjunctional alpha-2 adrenoceptors. The present experiments were performed to analyze the mechanism of the increased neurogenic response during cooling. Rings of canine saphenous vein were suspended for isometric tension recording in organ chambers filled with modified Krebs-Ringer bicarbonate solution, gassed with 95% O2-5% CO2. Cooling (from 37-24 degrees C) increased the contractile response evoked by nerve stimulation under control conditions, after alpha-1 adrenergic blockade with prazosin, alpha-2 adrenergic blockade with rauwolscine or the combination of both antagonists. The influence of cooling to enhance the neurogenic response was inhibited only by combined alpha adrenergic and purinergic-receptor blockade (alpha,beta-methylene ATP). Electrical stimulation failed to evoke a contractile response (either at 37 or 24 degrees C) in the presence of tetrodotoxin or after acute sympathetic denervation with 6-hydroxydopamine. alpha,beta-Methylene ATP abolished the contractile response evoked by ATP but did not affect the concentration-effect curves to alpha-1 (phenylephrine) or alpha-2 (UK 14,304) adrenergic stimulation. Cooling augmented the contractile responses evoked by ATP. The results suggest that ATP released from sympathetic neurons in the vessel wall contributes to the cooling-induced augmentation of contractile responses to sympathetic nerve stimulation in canine cutaneous veins. This may explain the increased prominence of purinergic mechanisms in cutaneous blood vessels.
TL;DR: If plasma norepinephrine levels following yohimbine administration are monitored, the biochemical and hemodynamic response to the drug may provide a sensitive indication of the capacity of the sympathetic nervous system to be activated in patients with autonomic dysfunction.
Abstract: We studied the effects of clonidine, an alpha 2-adrenoreceptor agonist, and yohimbine, an alpha 2-adrenoreceptor antagonist, on blood pressure, heart rate, and plasma catecholamines in 12 patients with autonomic dysfunction. Clonidine (0.1 mg, orally) lowered blood pressure 18 +/- 3 torr in six subjects and raised it 5 +/- 1 torr in six. The change in blood pressure in response to this dose of clonidine was inversely proportional to the supine level of norepinephrine (P less than 0.05). Yohimbine (4-64 micrograms/kg) raised plasma norepinephrine and blood pressure in six patients with degenerative autonomic dysfunction. Yohimbine also attenuated by 50% (P less than 0.05) the hypotensive response to head-up tilt of patients with degenerative autonomic dysfunction. Clonidine depends upon postjunctional hypersensitivity and the degree of autonomic insufficiency to elicit its pressor response. In contrast, the pressor response to yohimbine is related to the capacity of the sympathetic nervous system to be activated and release norepinephrine. If plasma norepinephrine levels following yohimbine administration are monitored, the biochemical and hemodynamic response to the drug may provide a sensitive indication of the capacity of the sympathetic nervous system to be activated in patients with autonomic dysfunction.
TL;DR: The results show that noradrenergic neurotransmission in the portal vein nervous plexus is controlled presynaptically by a strong local alpha 2- adrenergic autoinhibition.
Abstract: A technique is described in which a silicon catheter is utilized for permanent catheterization of the portal vein, and curved platinum stimulation electrodes around this vein are used for the stimulation of the local nervous plexus. The method has a success ratio of over 70% during a period of more than 2 mo. Five animals were used in experiments over a period longer than 5 mo. Using this technique, we investigated the influence of variation of current density, pulse duration, and frequency of stimulation on the electrically evoked release of norepinephrine in portal blood. Enhancement of all stimulation parameters proportionally increased the evoked norepinephrine release. The alpha 2-adrenoceptor antagonist yohimbine was found to increase basal norepinephrine levels 4.43-fold and facilitated the evoked release additionally with a factor of 4.70. The results show that noradrenergic neurotransmission in the portal vein nervous plexus is controlled presynaptically by a strong local alpha 2-adrenergic autoinhibition. The method offers the means to explore locally the presynaptic modulation of endogenous neurotransmitter release in unrestrained unanesthetized animals.
TL;DR: Results cast doubts on the possibility of linking the development of human low renin hypertension to an endogenous Na+, K+-ATPase inhibitor.
Abstract: A circulating Na+, K+-ATPase inhibitor may cause arterial hypertension in patients with suppressed plasma renin activity, either directly or by sensitizing peripheral vessels to alpha-adrenergic stimulation. This hypothesis was tested by evaluating forearm arteriolar (plethysmographic technique) response to exogenous alpha-adrenergic stimulation by a 2-minute intra-arterial infusion of norepinephrine (0.1 microgram/dl tissue per minute) and to Na+, K+-ATPase inhibition by sequential 20-minute intra-arterial infusions of ouabain (0.36 and 0.72 microgram/dl tissue per minute). Two groups of hypertensive subjects with suppressed plasma renin activity, either essential or secondary to aldosterone excess, were compared with age-matched and sex-matched hypertensive subjects with normal plasma renin activity (n = 7 per group). No significant differences in forearm vascular response to norepinephrine were found among the three groups. Ouabain caused a highly significant, dose-related increment in forearm vascular resistance that was not accompanied by changes in the contralateral limb or systemic blood pressure. No significant interindividual differences in vascular responsiveness to ouabain were found. The individual increments in forearm vascular resistance during ouabain administration were unrelated to basal values or to plasma aldosterone, norepinephrine, or potassium concentrations. These data are not consistent with the hypothesis that suppressed basal Na+, K+-ATPase activity is primarily a characteristic of hypertensive patients with unresponsive plasma renin activity. Overall, these results cast doubts on the possibility of linking the development of human low renin hypertension to an endogenous Na+, K+-ATPase inhibitor.
TL;DR: It is concluded that surges of catecholamines from a pheochromocytoma may provoke pulmonary edema in a manner similar to that by which neurogenic pulmonaryEdema related to cerebral disorders occurs.
Abstract: A 40-year-old man was admitted to the hospital with pulmonary edema without signs of left ventricular failure. Noncardiogenic pulmonary edema was diagnosed, and a subsequent workup identified a pheochromocytoma as the cause of this condition. The clinical picture could be mimicked by infusion of exogenous norepinephrine. It is concluded that surges of catecholamines from a pheochromocytoma may provoke pulmonary edema in a manner similar to that by which neurogenic pulmonary edema related to cerebral disorders occurs.