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)

Studies in normal volunteers documented the positive inotropic effects of Etilefrin-HCL, a direct sympathomimetic drug, with increases of systolic blood pressure, renal blood flow and glomerular filtration rate. Sodium and potassium excretion as well as serum potassium decreased. After an additional injection of Metoprolol, a beta 1-sympatholytic drug, blood pressure, renal blood flow and glomerular filtration rate normalized, whereas electrolyte excretion decreased further. Renin release was decreased during administration of Etilefrin as well as during combined Etilefrin and Metoprolol application. Reziprocal to changes of blood pressure, plasma norepinephrine concentration decreased during Etilefrin and increased during combined administration of Etilefrin and Metoprolol. The results lead to the following interpretation: Changes of blood pressure and renal hemodynamics are mediated by beta 1-adrenergic effects of Etilefrin, whereas the electrolyte excretion is influenced by beta 2-adrenergic effects. Renin release seems to be influenced by beta 1 as well as beta 2-adrenergic receptors.
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PMID:[Hemodynamic and humoral changes during administration of a sympathomimetic and a sympatholytic drug with special notes on the regulation of renin release (author's transl)]. 3 50

Beta adrenoceptor blocking drugs are all competitive inhibitors of the beta receptor although they may or may not possess, beta 1-(cardio)selectivity, intrinsic sympathomimetic activity (ISA) or partial agonist activity, alpha-blocking properties, while membrane stabilizing activity is now thought not to be important. Drugs with ISA give less of a reduction in resting and maximal exercising heart rate and consequently in cardiac output, than those without ISA. The possession of alpha-blocking activity also leads to less fall in cardiac output. Overall evidence suggests that peripheral resistance and peripheral blood flow is less reduced by ISA drugs. Post-beta blockade hypersensitivity which may be important in patients with ischemic heart disease if beta blocking drugs are suddenly stopped, is absent after beta-blocking drugs with ISA as they result in down regulation of beta receptors. Beta 1-selective drugs may result in less of a rise in blood pressure in response to isometric exercise, insulin hypoglycemia or smoking. There do not appear to be important differences in the effect on coronary flow. While presently available drugs can produce asthma in susceptible subjects there seems little doubt that beta 1 selective agents have less effect than other beta-blocking drugs, and give less inhibition of sympathomimetic bronchodilators. Nonselective, non ISA, beta-blocking drugs elevate triglycerides, cardioselective drugs possibly less so. Those with ISA may elevate HDL unlike those beta-blocking agents without this property. Beta adrenergic blocking drugs without ISA do not lower resting plasma noradrenaline, evidence suggests an increase; whereas those agents with marked ISA, suggests an increase; whereas those agents with marked ISA, e.g., pindolol, reduce it. Renin levels are lowered, but less so with ISA possessing agents. Some agents, e.g. atenolol, nadolol, sotalol, are hydrophilic, show poor brain penetration, are long-acting, are not liver metabolized, but are excreted by the kidneys unchanged. Others are lipophilic, e.g., metoprolol, propranolol, penetrate the brain, and are liver metabolized. Pindolol is metabolized about 50% by each route. Similarities between beta blocking drugs are dominant but differences are often clinically relevant.
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PMID:The additional properties of beta adrenoceptor blocking drugs. 242 33

The cause and mechanism of post-carotid endarterectomy hypertension remains unknown. To determine the influence of the sympathetic and renin-angiotensin system, we measured cranial and peripheral plasma levels of catecholamine and renin in patients undergoing carotid endarterectomy. Baseline samples were drawn just before carotid clamping (sample I) and compared with study samples drawn immediately after clamp release (sample II), 2 to 6 hours after surgery (sample III), and then 18 to 24 hours after surgery (sample IV). The patients with post-carotid endarterectomy hypertension had an associated increase of cranial and peripheral norepinephrine levels in the postoperative hypertensive period whereas the patients without post-carotid endarterectomy hypertension did not. This association was most pronounced and statistically significant in cranial samples II (p = 0.032) and III (p = 0.005). Epinephrine and dopamine values did not correlate with post-carotid endarterectomy hypertension. Renin values were higher in cranial than in peripheral samples at time period 2 (p = 0.011), suggestive of a central nervous system Goldblatt phenomenon. However, the renin values did not correlate with post-carotid endarterectomy hypertension. We conclude that post-carotid endarterectomy hypertension is associated with elevated cranial norepinephrine levels, suggestive of a central nervous system sympathomimetic mechanism. Optimal prevention and treatment of this brief but frequently occurring hypertension should include a central-acting sympatholytic agent.
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PMID:Post-carotid endarterectomy hypertension: association with elevated cranial norepinephrine. 264 44

The rest and exercise hemodynamic-inotropic response to administration of the beta-blocker pindolol was evaluated in 10 patients with congestive cardiomyopathy to determine whether the intrinsic sympathomimetic activity (ISA) of this agent may preserve ventricular function in the setting of beta-blockade. A significant (p less than .05) rise in systemic and pulmonary vascular resistance and a decline in stroke volume and cardiac index was observed after a single 10 mg dose. The change in cardiac index was negatively correlated with free drug concentration (r = -.59, p less than .01); the change in pulmonary and systemic vascular resistance showed a positive correlation with plasma concentration (r = .67, r = .57, respectively; all p less than .05). The response to exercise reflected a predominant beta-blocking effect, with a significant decrease in peak heart rate and cardiac index and an increase in pulmonary vascular resistance. There were no significant changes in variables of right or left ventricular inotropy after administration of the drug. The mean baseline plasma norepinephrine concentration for the population was 609 +/- 172 pg/ml (normal = 196 +/- 7 pg/ml) and was markedly elevated in two patients (931 and 2053 pg/ml) who developed severe pindolol-induced hypotension. Renin increased markedly in these two patients, but decreased in each of the remaining eight patients. These data indicate that although inotropy is not adversely affected by pindolol, increased afterload, which appears to be mediated by peripheral beta-blockade, results in a reduction in ventricular performance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic-inotropic response to beta-blocker with intrinsic sympathomimetic activity in patients with congestive cardiomyopathy. 353 53

To investigate the possible effects of newly synthesized beta-adrenergic blockers on plasma renin activity, an assay was developed using unanesthetized mice and radioimmunoassay. Renin activity was significantly increased by the administration of hydralazine (1 mg/kg, i.p.), furosemide (20 mg/kg, i.v.), and isoproterenol (0.1 mg/kg, s.c.). Unlike isoproterenol, norepinephrine (1 mg/kg, s.c.) and epinephrine (1 mg/kg, s.c.) were active but considerably less effective stimulants. The increase caused by isoproterenol was blocked by clonidine, pindolol, bunolol, atenolol, and l-propranolol, but not d-propranolol. The beta-blockers with intrinsic sympathomimetic activity such as pindolol were found to increase renin activity when given alone, but blocked an increase in renin activity when given prior to isoproterenol. In general, nonselective beta-blocking drugs possessing both beta 1- and beta 2-(vascular) blocking activity were found to be most effective in blocking plasma renin activity on oral administration.
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PMID:Drug effects on plasma renin activity in the mouse. 617 84