1 Electrically driven chicken and guinea-pig atria were used to investigate the negative inotropic effects of the muscarinic agonists methacholine and acetylcholine (ACh). The release of ACh from isolated hearts into the perfusate in response to (preganglionic) vagal or (pre-and postganglionic) field stimulation was bioassayed on the guinea-pig ileum or determined by labelling with ['H]-choline. (Pz) and atropine were 40 and 5.4 nmol -'in chicken atria and 330 and 3.5 nmol '-', respectively, in guineapig atria. Thus, the respective potency ratios (IC0pJIC5j,trope) were 7.4 and 94.3 in the two species.3 Pirenzepine in low concentrations increased the release of unlabelled and 'H-labelled ACh from isolated hearts evoked by vagal and field stimulation only in chicken, but not in guinea-pigs. The halfmaximally-effective concentration of pirenzepine was about 30 nmol I' in the chicken heart, whereas, in the guinea-pig heart, an increased release was observed at 300 nmol I-'. (+ )-Tubocurarine [(+ )-Tc; 100 pmol I-'] reduced the release of ACh evoked by (preganglionic)vagal stimulation to a (+ )-Tc-resistant release of about 30%. The time-course of the neuronal release of['H]-ACh was markedly altered: the onset was delayed and the termination was extended beyond the period of stimulation ( min or 5 s) by several seconds. The (+)-Tc-resistant release was nearly abolished by 30 nmol I' pirenzepine. 5 In conclusion, the pre-and post-synaptic muscarinic receptors of the parasympathetic neuroeffector junction of the heart both belong to the M,-subtype in the chicken and to an M2-subtype in the guinea-pig. Block of the nicotinic ganglionic transmission in the chicken heart by (+ )-Tc unmasked a muscarinic transmission, which presumably was mediated through M,-receptors stimulating a low and prolonged postganglionic release of ACh.

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Twenty-three patients with blood urea nitrogen (BUN) over 70 and thought clinically to be in renal failure were examined by ultrasound. A correct diagnosis of kidney size and the presence or absence of hydronephrosis or polycystic kidney was made in all but one instance. One kidney in a patient with end-stage renal failure was not seen ultrasonically but was subsequently demonstrated on a retrograde pyelogram. In 10 patients, excretory urography (on 4 occasions with tomography) failed to demonstrate the kidneys adequately. It is suggested that ultrasound should either be the first or second imaging technique in the investigation of patients who present in renal failure of unknown cause.

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