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Alterations of autonomic tone can induce cardiac dysrhythmias. In the present experiments intravenous administration of epinephrine (15 micrograms/kg) caused dysrhythmias in rat hearts. Bilateral vagotomy or yohimbine treatment did not suppress the dysrhythmic effects of epinephrine. Atropine, glycopyrrolate, and pertussis toxin reduced the number of premature ventricular contractions and eliminated missed beats caused by epinephrine. Neostigmine increased the number of missed beats but did not change the number of premature ventricular contractions. These results indicate that epinephrine induces cardiac dysrhythmias in part by local release of acetylcholine. Muscarinic receptors and pertussis toxin sensitive G proteins are involved in epinephrine-induced arrhythmogenesis.

S. Pljesa, G. Golubović, L. Ignjatovic, M. Stajić, L. Lambic, G. Perunicić, A. Cavala, N. Žakula

J. Huskic, Husein Kulenovic, Filip Čulo

Serum angiotensin-converting enzyme was measured in 60 patients with endemic nephropathy and in 30 healthy individuals. According to the arterial blood pressure, the patients with endemic nephropathy were further divided into groups with arterial hypertension (n = 30) and without arterial hypertension (n = 30). The activity of angiotensin-converting enzyme was determined by a spectrophotometric method using hippuryl-l-histidyl-l-leucine as a substrate. The serum activity of angiotensin-converting enzyme was significantly increased in the patients with endemic nephropathy (28.51 +/- 1.64 U/l) as compared with healthy individuals (20.83 +/- 1.33 U/l). The level of the enzyme was further increased if the endemic nephropathy was accompanied by arterial hypertension (37.09 +/- 1.45 U/l). The possible mechanisms of the increase in the angiotensin-converting enzyme activity are discussed.

M. Budalica, S. Guska, A. Hadžismailović, M. Kacila, Z. Cerimagić, E. Hajdarević

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