Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of central angiotensin II (AII) in the shaking stress-induced adrenocorticotropic hormone (ACTH), plasma catecholamine secretion and pressor response were investigated using conscious rats. We also studied whether or not vasopressin (VP) is involved in the shaking stress-induced pressor response. The shaking stress caused significant elevations in plasma ACTH, catecholamine, and systolic blood pressure. Intra-third ventricular administration of the AII antagonist, Sar1, Ile8-angiotensin II (saralasin) significantly attenuated pressor response and plasma noradrenaline elevation but not plasma ACTH elevation. Pretreatment with the vascular-type VP receptor (V1) antagonist, d(CH2)5Tyr(Me)AVP, did not attenuate pressor response nor plasma catecholamine elevation. These results indicate that the central angiotensinergic pathway at least partly mediates the shaking stress-induced activation of the sympathetic nervous system without VP involvement, and that central AII does not mediate the ACTH secretion evoked by shaking stress.
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PMID:Role of central angiotensinergic mechanism in shaking stress-induced ACTH and catecholamine secretion. 196 26

The influence of angiotensin II (ANG II) on the synthesis of glomerular prostanoids is controversial, possibly because of the different methodologies employed. In order to assess this inter-relationship isolated rat glomeruli were incubated with and without shaking. The use of shaking during incubation significantly increased the amounts of prostanoid synthesized, most probably because of continuous non-specific activation of phospholipase (PLA2) activity. After preincubation in a non-shaking bath, ANG II was added for a second incubation period. A marked increase of prostaglandin (PG) E2, and, to lesser degree, of thromboxane (TX) B2 was noted, with no change on PGF2 alpha synthesis. These results show (a) that preincubation without shaking, by lowering the non-specific activation of the PLA2 activity, may unmask, in vitro, specific peptide stimulation, and (b) that ANG II, stimulating principally PGE2 synthesis, may modify the vasoactive status of the glomerular vasculature.
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PMID:Effect of angiotensin II on prostanoid synthesis in isolated rat glomeruli. 345 71

Dispersed rat anterior pituitary cells were allowed to reassociate into spherical aggregates by gyrotory shaking in serum-free chemically defined culture medium. When aggregates were superfused after being cultured for 5 days in this medium, stimulation of PRL release by TRH, VIP, angiotensin II and the beta-adrenergic agonist isoproterenol was comparable to that of aggregates cultured in serum-supplemented culture medium. Addition to the serum-free medium of 80 nM dexamethasone (Dex) resulted in a significant enhancement of the stimulation of PRL release by TRH, VIP and angiotensin II but not of the stimulation of PRL release by isoproterenol. Dex also failed to influence the inhibition of PRL release by 10 min exposure to 10 nM dopamine (DA). However, Dex significantly enhanced the post-DA rebound secretion of PRL. After 3 weeks in culture Dex provoked a similar potentiation of the response to angiotensin as at 5 days in culture but it abolished almost completely the stimulatory effect of isoproterenol. It is concluded that pituitary cell aggregates cultured in defined serum-free medium are a reliable system to study the multifactorial control of PRL release. The data show that peptidergic, dopaminergic and beta-adrenergic control at the pituitary level is differentially modulated by corticosteroids.
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PMID:Influence of corticosteroids on prolactin release from anterior pituitary cell aggregates cultured in serum-free medium. Differential effects on dopamine-induced inhibition, post-dopamine rebound and stimulation by TRH, vasoactive intestinal peptide (VIP), angiotensin II and isoproterenol. 642 98

1. The alpha-adrenoceptor antagonist, beta 1-adrenoceptor antagonist and beta 2-partial agonist activity of dilevalol, a beta-adrenoceptor antagonist with vasodilating properties and labetalol were investigated in two studies. 2. In the first study, six healthy male subjects received serially increasing concentrations phenylephrine after single oral doses of dilevalol 200 mg, labetalol 400 mg and placebo at weekly intervals in a randomised double-blind manner. An exercise step test was performed at the end of the infusions. 3. The doses of phenylephrine required to increase systolic and diastolic blood pressures by 20 mmHg (PS20 and PD20 respectively) were increased by labetalol 400 mg (P < 0.05) but unchanged by dilevalol 200 mg. The dose ratios for PS20 (means +/- s.d.) were: dilevalol 200 mg 1.1 +/- 0.1, labetalol 400 mg 2.2 +/- 0.1. There was no difference in the percentage reduction in exercise tachycardia between dilevalol and labetalol. 4. In the second study, 10 healthy male subjects received infusions with serially increasing concentrations of phenylephrine and angiotensin II before and after single oral doses of dilevalol 200, 400 and 800 mg, labetalol 200 mg and placebo at weekly intervals in a double-blind randomised manner. Finger tremor was measured (piezoelectric accelerometer) with each infusion. An exercise step test was performed at the end of the infusions. 5. The PS20 and PD20 of phenylephrine were increased by labetalol 200 mg and unchanged by dilevalol. The dose ratios for PS20 were: dilevalol 200 mg 1.1 +/- 0.2. dilevalol 400 mg 1.1 +/- 0.4, dilevalol 800 mg 1.4 +/- 0.4 and labetalol 200 mg 2.5 +/- 0.7. The dose ratios for PD20 were: dilevalol 200 mg 1.1 +/- 0.4, dilevalol 400 mg 0.9 +/- 0.3. dilevalol 800 mg 1.3 +/- 0.4 and labetalol 200 mg 2.3 +/- 0.9. 6. The PS20 and PD20 of angiotensin II were unchanged by any of the drugs. 7. Exercise heart rate was reduced by dilevalol 200 mg (130 +/- 13 beats min-1), 400 mg (123 +/- 12 beats min-1), 800 mg (125 +/- 9 beats min) and labetalol 200 mg (143 +/- 12 beats min-1) vs placebo (161 +/- 17 beats min-1). 8. Finger tremor was significantly increased by dilevalol 800 mg (13.17 +/- 10.51 vs 6.62 +/- 4.51 centivolts for placebo: P < 0.01). Neither phenylephrine nor angiotensin II had an effect on finger tremor. 9. In conclusion, dilevalol 200, 400 and 800 mg demonstrated beta 1-adrenoceptor antagonist activity with no evidence of alpha 1-adrenoceptor antagonist activity. Labetalol 200 and 400 mg showed both beta 1- and alpha 1-antagonist activity. Dilevalol 800 mg demonstrated significant partial beta 2-adrenoceptor agonist activity by increasing finger tremor.
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PMID:The dose dependency of the alpha-adrenoceptor antagonist and beta-adrenoceptor partial agonist activity of dilevalol and labetalol in man. 911 12

The postural orthostatic tachycardia syndrome is a disease characterized by excessively increased heart rate during orthostatic challenge associated with symptoms of orthostatic intolerance including dizziness, exercise intolerance, headache, fatigue, memory problems, nausea, blurred vision, pallor, and sweating, which improve with recumbence. Postural orthostatic tachycardia syndrome patients may present with a multitude of additional symptoms that are attributable to vascular vasoconstriction. Observed signs and symptoms in a patient with postural orthostatic tachycardia syndrome include tachycardia at rest, exaggerated heart rate increase with upright position and exercise, crushing chest pain, tremor, syncope, loss of vision, confusion, migraines, fatigue, heat intolerance, parasthesia, dysesthesia, allodynia, altered traditional senses, and thermoregulatory abnormalities. There are a number of possible dermatological manifestations of postural orthostatic tachycardia syndrome easily explained by its recently discovered pathophysiology. The author reports the case of a 22-year-old woman with moderate-to-severe postural orthostatic tachycardia syndrome with numerous dermatological manifestations attributable to the disease process. The cutaneous manifestations observed in this patient are diverse and most noticeable during postural orthostatic tachycardia syndrome flares. The most distinct are evanescent, hyperemic, sharply demarcated, irregular patches on the chest and neck area that resolve upon diascopy. This distinct "evanescent hyperemia" disappears spontaneously after seconds to minutes and reappears unexpectedly. Other observed dermatological manifestations of this systemic disease include Raynaud's phenomenon, koilonychia, onychodystrophy, madarosis, dysesthesia, allodynia, telogen effluvium, increased capillary refill time, and livedo reticularis. The treatment of this disease poses a great challenge. The author reports the unprecedented use of an oral angiotensin II type 1 receptor antagonist resulting in remarkable improvement.
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PMID:Postural orthostatic tachycardia syndrome: a dermatologic perspective and successful treatment with losartan. 2516 60