Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether sympathetic hyperactivity of hypothalamic origin contributes to keep blood pressures high in spontaneous hypertension, aortic pressures and sympathetic nerve spike potentials were recorded during electrical stimulation of the posterior hypothalamus in urethane-anesthetized normotensive or hypertensive rats. Basal sympathetic nerve activity was higher in spontaneously hypertensive rats than in either normotensive or deoxycorticosterone acetate-salt hypertensive ones even before stimulation began. Blood pressure elevations produced by hypothalamic stimulation were always preceded by substantial increases in amplitude and rate of neural firing. Changes in amplitude could not be quantified, but rates of neural firing accelerated much more in spontaneous hypertensives than in normotensives during stimulation with 50- and 100-muA currents. Similar differences between deoxycorticosterone acetate-salt hypertensives and either normotensives or spontaneous hypertensives were not statistically significant. Nerve activity invariably became quiescent immediately after hypothalamic stimulation was discontinued, and recovery from this poststimulatory inhibition was faster in spontaneously hypertensive than in normotensive rats. Although spontaneous hypertensives generally also had stronger pressor responses to various sympathomimetic stimuli, responses to hypothalamic stimulation were enhanced to a greater extent than those to either norepinephrine or sympathetic nerve stimulation. Because this selectivity indicates participation of mechanisms other than augmented cardiovascular reactivity, further enhancement of responsiveness to hypothalamic stimuli was attributed to the associated increase in sympathetic nerve firing. These results are in accord with the hypothesis that the blood pressure elevation in rats with established spontaneous hypertension is a result, at least in part, of sympathetic hyperactivity emanating from the posterior hypothalamus.
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PMID:Sympathetic hyperactivity during hypothalamic stimulation in spontaneously hypertensive rats. 69 Jan 89

Increased vascular reactivity to noradrenaline was revealed in patients with Stages I and II hypertensive disease; the reaction to the sympathomimetic agent of indirect action ephedrine remained at the control level. A salt load increased the discrepancy between the level of the reactions to these two agents. It is suggested that processes of catecholamine storage and excretion in the tissues are disturbed in hypertensive disease and that sodium ions probably take part in this process. The daily excretion of noradrenaline was in negative relation with the reactivity to noradrenaline and correlated positively with the reactivity to angiotensin.
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PMID:[Vascular reactivity and catecholamine excretion in hypertension]. 72 41

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10

Antihypertensive drugs have differing effects on renal hemodynamics, tubular function, plasma electrolytes, and hormonal responses. Nonselective beta-blockers without intrinsic sympathomimetic activities, such as propranolol, have been reported to reduce renal blood flow and to cause a modest decrease in glomerular filtration rate. Carvedilol is a new multiple action agent displaying nonselective beta-blockade without intrinsic sympathicomimetic activity, alpha 1-adrenoceptor blockade (probably responsible for its vasodilator activity), and possibly also calcium antagonist properties. The presence of these different pharmacodynamic properties results in a different effect on the kidney as compared with, e.g., propranolol. In the dog, intrarenal infusion of carvedilol resulted in a renal vasodilator response with preservation of renal blood flow and without inducing sodium retention; in contrast, propranolol induced a renal vasoconstrictor response and sodium retention in this model. A renal vasodilator response to carvedilol was also reported in spontaneously hypertensive rats (SHR) and in DOCA-salt SHR. In contrast to labetalol, i.v. infusion of hypotensive doses of carvedilol in conscious SHR did not cause sodium retention. Carvedilol was effective in controlling hypertension and preserving renal function in a rat model of progressive hypertensive renal disease. In patients with essential hypertension, carvedilol was reported to reduce renal vascular resistance in the presence of reduced perfusion pressure, allowing for normal renal autoregulation of renal blood flow. Although a small reduction in glomerular filtration rate was seen after acute administration, renal function was preserved during chronic treatment. It is concluded from these studies that renal perfusion and renal function are well maintained during acute and chronic treatment with carvedilol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carvedilol and the kidney. 135 Apr 79

A simple and rapid stability-indicating liquid chromatographic method is described for quantitative determination of 6 sympathomimetic drugs in various liquid and solid formulations. Analyses were carried out on a C18 reverse phase column using 0.01M 1-octanesulfonic acid, sodium salt in 0.2% acetic acid-methanol (70 + 30) as the mobile phase with photometric detection at 220 nm. Coefficients of variation for 5 consecutive injections of a mixed standards solution ranged from 0.62% for metaraminol to 1.40% for epinephrine. Standard recoveries ranged from 98.8% for metaraminol to 100.8% for epinephrine. The method was linear between 0.2 and 10 micrograms of drug injected and was used successfully to analyze 17 commercial products in a variety of dosage forms.
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PMID:Liquid chromatographic determination of six sympathomimetic drugs in dosage forms. 205 Jun 10

Experiments were designed to determine the effects of cooling on alpha-1 and alpha-2 adrenergic responses in a cutaneous vein of the rabbit. Rings of saphenous vein were suspended in physiological salt solution for the recording of isometric force. Cooling (from 37-24 degrees C) caused no significant increase in force in quiescent rings. Similarly, the same degree of cooling had no significant effect on the response to exogenous norepinephrine (10(-9)-10(-5) M), whether under control conditions or in the presence of either the alpha-1 adrenergic antagonist prazosin (3 X 10(-7) M) or the alpha-2 adrenergic antagonist rauwolscine (10(-7) M). Contractions evoked by the alpha-1 adrenergic agonist phenylephrine were reduced, but those induced by the alpha-2 adrenergic agonist UK 14,304 (10(-9)-10(-5) M) were unaffected by the same degree of cooling. Cooling augmented the response elicited by electrical field stimulation of the sympathetic nerves, although only under conditions of alpha-1 or combined alpha-1 and alpha-2 adrenergic blockade. Data obtained with the sympathomimetic tyramine suggest that both alpha-1 and alpha-2 adrenoceptors are innervated in this blood vessel. Together, the present data suggest that the effects of acute cooling on the saphenous vein of the rabbit, unlike that of the dog, are not mediated by changes in the affinity of postjunctional alpha-2 adrenoceptors.
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PMID:Cooling and alpha adrenergic responses in the saphenous vein of the rabbit. 254 Mar 21

In general, rises in systolic blood pressure to over 200 mm Hg during exercise with a workload of 100W are regarded as pathological. Excessive exercise blood pressure values are to be expected in principle in all hypertensives. However, there are so far no generally accepted criteria for diagnosis of isolated systolic exercise hypertension (with normal values of resting blood pressure). The incidence of isolated systolic exercise hypertension is estimated to be about 10% of a selected population. In patients with excessive rises in blood pressure during exercise who want to engage actively in sport, general measures (reduction of obesity, restriction of alcohol and salt intake) and endurance training should be recommended initially. For endurance training, sporting activities that involve dynamic exercise are to be recommended (walking, running, mountain hiking, cycling, swimming, cross-country skiing). Activities involving isometric exercise (rowing, diving, tennis) and sport of a competitive nature are not suitable. In moderately severe and severe hypertension (diastolic blood pressure values in excess of 105 mm Hg), sporting activities and endurance training are contraindicated. If the exercise blood pressure values cannot be lowered below 220 mm Hg with the general measures mentioned, pharmacotherapy is to be considered. The drugs of choice for suppressing excessive rises in blood pressure during exercise are beta-blockers. In this group, beta 1-blockers are to be preferred to non-selective beta-blockers because of the metabolic neutrality of the former. beta-Blockers without intrinsic sympathomimetic activity (ISA) lower the blood pressure-pulse rate product more effectively than beta-blockers with ISA. Alternatively, calcium antagonists of the verapamil type and ACE inhibitors can be employed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of hypertension in actively exercising patients. Implications for drug selection. 264 57

1. Intravenous infusion of a physiological dose of fowl angiotensin II (ANG II) in salt-loaded ducks raised systemic arterial blood pressure, inhibited nasal salt gland fluid and solute secretion, and stimulated renal-cloacal urine production. 2. Beta-adrenergic receptor blockade by propranolol lowered arterial pressure but did not prevent the effects of ANG II on salt and water excretion. 3. Alpha-adrenergic receptor blockade by prazosin decreased both arterial pressure and plasma glucose levels, but it did not impair the osmoregulatory actions of ANG II. 4. These observations indicate that redistribution by ANG II of salt and water excretion is independent of adrenergic receptor mechanisms and therefore does not depend on the sympathomimetic activity of the hormone.
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PMID:Osmoregulatory actions of angiotensin II are independent of adrenergic receptor mechanisms in the duck, Anas platyrhynchos. 289 Apr 89

Treatment of heart failure comprises the use of diuretics, vasodilators and inotropic substances. Unloading of the heart and the circulation in hydropic states is classically achieved with diuretics. The retention of salt and water in chronic heart failure requires chronic treatment with diuretics. This mode of treatment is basic to all forms of hydropic heart failure. Inotropic substances such as digitalis glycosides, sympathomimetic amines or phosphodiesterase inhibitors have certain disadvantages: Inotropic stimulation increases energy demand of the working heart muscle. Most of the substances used today increase energy consumption inordinately, thereby decreasing economy of myocardial contraction. This aspect calls for caution in the application of these substances in chronic heart failure, although they seem indispensable (sympathomimetic amines) in acute hypotensive failure and shock. Digitalis glycosides, basically suited for longterm treatment, exert only mild inotropic effects. In addition inotropic stimulation brings with it arrhythmogenic effects. All inotropic substances can induce ventricular arrhythmias already at therapeutic levels. Vasodilating substances have found increasing acceptance as a particularly useful and safe group of drugs for the treatment of heart failure. Nitrates: With the different nitrate compounds and nitrate preparations an effective venodilation with preload reduction can safely be achieved. At higher doses, arteriolar also dilatation can be induced. Although tolerance may be a problem with chronic application, this can be avoided with prudent dosing. The strong venodilating property makes these drugs together with their rapid onset of action ideally suited for the treatment of acute heart failure with pulmonary congestion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of heart failure: status of therapy with vasodilator agents]. 343 15

1. Rats and guinea-pigs were injected with 1-thyroxine or thyroidectomized. Sensitivity of isolated tissues and of the intact cardiovascular system to drugs was investigated.2. Thyroxine increased the sensitivity of the isolated perfused heart to noradrenaline, adrenaline, isoprenaline, acetylcholine and histamine.3. Thyroxine increased the sensitivity of the rat isolated uterus to noradrenaline, adrenaline, isoprenaline, acetylcholine, histamine and 5-hydroxytryptamine.4. In contrast, thyroxine decreased the sensitivity of the isolated ileum to acetylcholine, histamine and 5-hydroxytryptamine, but not to adrenaline.5. Thyroxine also decreased the sensitivity of the isolated aorta to noradrenaline, adrenaline, histamine and 5-hydroxytryptamine.6. In pithed rats, thyroxine potentiated pressor responses to (+)-amphetamine but not to noradrenaline or synephrine.7. In anaesthetized thyroxine-treated rats, blood pressure responses to (+)-amphetamine were potentiated while those to noradrenaline were unaltered. Responses to acetylcholine were increased, and the response to isoprenaline became purely pressor.8. Thyroxine-induced changes in the sensitivity of the isolated uterus and ileum to modification of the concentration of calcium in the physiological salt solution paralleled the changes in drug sensitivity of these tissues.9. In general, thyroidectomy produced the opposite effects to those of thyroxine.10. It is concluded that there is no specific interaction between thyroxine and sympathomimetic amines, the effect of thyroxine on drug sensitivity being non-specific.
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PMID:Influence of thyroid hormones on the sensitivity of cardiac and smooth muscle to biogenic amines and other drugs. 542 Jan 45


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