We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 gg ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of 25 of the 27 patients. The injection of 20 to 100 gg ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm. Circulation 74, No. 5, 955-963, 1986. IT IS NOW widely accepted that spasm of an epicardial coronary artery (coronary spasm) plays an important role in the pathogenesis, not only of variant angina, but also of other forms of resting angina, some types of exertional angina, and types of acute myocardial infarction. quently Endo et al.'0 confirmed our results. On the basis of this fact and the fact that the activity of the parasympathetic nervous system is enhanced at rest and is suppressed by physical activity," we postulated that the activity of parasympathetic nervous system might be related to the pathogenesis of variant angina or coronary spasm.7 It has been shown that stimulation of the parasympathetic (vagus) nerve or intracoronary injection of ACh causes coronary vasodilatation, as demonstrated by an increase in coronary blood flow in dogs,'2-'5 and that ACh dilates isolated epicardial coronary arteries in dogs'6 and monkeys. 17 In humans subcutaneous injection of methacholine causes profound dilatation of systemic vasculature, resulting in a transient fall in blood pressure and compensatory tachycardia due to reflex sympathetic discharge.7 We therefore speculated that coronary spasm might be induced by sympathetic discharge by way of a-adrenergic stimulation.7 Recently, however, reports have appeared that show that ACh contracts strips of human coronary arteries obtained from hearts of transplant recipients'8 or cadav-955
The role was studied of ephrin-B3, a ligand of the Eph family of tyrosine kinase receptors, in the formation of cortical connectivity. In situ hybridization and immunohistochemistry showed that EphA4, a receptor of ephrin-B3, was expressed in the lateral thalamus (visual and somaotosensory thalamus) of the developing rat brain, but not in the medial thalamic nuclei which project to the limbic cortex. Correspondingly, ephrin-B3 was expressed strongly in the developing limbic cortex including amygdala, entorhinal cortex and hippocampus. To examine the action of ephrin-B3 on thalamic axons, either lateral or medial thalamic explants were cultured on membranes obtained from ephrin-B3-expressing COS cells. Axonal growth was inhibited for cells from the lateral thalamus but not from the medial thalamus. These results suggest that ephrin-B3 contributes to regional specificity by suppressing axonal growth of lateral thalamic neurons.
We examined the effect of the dihydropyridine calcium channel blocker (CCB) benidipine, the angiotensin II type 1 receptor blocker (ARB) candesartan, and the combination of these drugs on blood pressure and kidney and vascular function in rats with salt-induced hypertension. Dahl salt-sensitive (DS) rats were fed with a high-salt (8% NaCl) diet from 7 weeks of age. Benidipine (1, 3 mg/kg), candesartan (1, 3 mg/kg), benidipine
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