Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes various old and new positive inotropic drugs with respect to their mechanisms of action. Drugs with established cardiotonic effects include cardiac glycosides, beta 1-adrenergic agents, glucagon, histamine and the methylxanthines. New agents discussed are prenalterol, beta 2- and alpha-adrenergic drugs, amrinone and sulmazole. Prenalterol is a beta 1-adrenergic agent. Beta 2-adrenergic drugs, amrinone and sulmazole, combine a positive inotropic and a vasodilator effect. The latter resemble theophylline and other methylxanthines in that they appear to act mainly as phosphodiesterase inhibitors with a subsequent increase in cyclic adenosine monophosphate (cAMP). The mechanism of the positive inotropic effect of alpha-adrenergic stimulating agents (for example, phenylephrine) is unknown. It is independent of the cAMP system and is not accompanied by changes in frequency.
 ...
PMID:Inotropic drugs and their mechanisms of action. 633 Jan 95

A case of massive metoprolol poisoning (50 g) is described. Clinical signs included coma, seizures, hypoventilation, unmeasurable blood pressure, nodal bradycardia, and metabolic acidosis. Treatment comprised intubation, assisted ventilation, gastric lavage, atropine, bicarbonate, glucagon and repeated doses of prenalterol (a total of 160 mg over 15 hours). Prenalterol dosage was simple and could be guided by blood pressure response. Pacemaker treatment was not required. Ethanol concentration was 50 mmol/l (2.4%) on admission. Plasma metoprolol was 68 mumol/l (18 000 ng/ml) 2 hours after admission. The patient was awake after 15 hours.
 ...
PMID:Massive metoprolol poisoning treated with prenalterol. 666 32

The hemodynamic, hormonal and electrolyte effects of prenalterol, a synthetic selective beta 1 agonist, were studied in six patients with New York Heart Association functional class II and III heart failure. Prenalterol was infused incrementally at 60, 120 and 240 nmol/min, each rate for 24 hours, producing steady-state plasma prenalterol levels of 52 +/- 3, 121 +/- 6 and 194 +/- 9 nmol/1, respectively (mean +/- SEM). Hemodynamic and hormonal measurements were performed before, during and after prenalterol administration under conditions of constant body posture and a regulated intake of dietary sodium and potassium. Prenalterol induced a statistically significant increase in cardiac index (from 2.6 +/- 0.2 to 3.1 +/- 0.3 1/min/m2), with parallel increases in stroke index (from 28 +/- 2 to 34 +/- 2 ml/beat/m2). Forearm blood flow measurements increased (from 2.9 +/- 0.5 to 4.1 +/- 0.6 ml/min/100 g), while calculated systemic vascular resistance fell, as did pulmonary capillary wedge pressure (from 13.7 +/- 1.6 to 10.5 +/- 1.7 mm Hg). The drug did not alter heart rate, arterial pressure, right heart pressures or the frequency of ventricular premature beats. Prenalterol increased plasma renin activity (from 2.9 +/- 0.8 to 6.6 +/- 1.8 nmol/1/hour), angiotensin II (from 59 +/- 12 to 89 +/- 22 pmol/1), urinary aldosterone excretion (from 41 +/- 10 to 78 +/- 34 nmol/day) and plasma insulin (from 10.6 +/- 2.2 to 19.8 +/- 3.9 mU/1). Circulating catecholamines, cortisol, glucose, glucagon or pancreatic polypeptide did not change. Dose-response studies in five patients showed dose-dependent increments in hemodynamic variables, while hormonal changes plateaued at the second dose level. We conclude that prenalterol infusion augments myocardial contractility, reduces systemic vascular resistance, and stimulates insulin release and the renin-angiotensin-aldosterone system.
 ...
PMID:Hemodynamic, hormonal and electrolyte responses to prenalterol infusion in heart failure. 682 3