The aim of the present study was to examine the effect of prolonged passive smoking (lasting 3 weeks) on plasma catecholamine levels and reactivity of isolated rabbit arteries. Plasma noradrenaline, adrenaline and dopamine levels were determined radioenzymatically. Isolated rings of the thoracic aorta and carotid artery were suspended in organ chambers and connected to a force transducer for the recording of isometric tension. Plasma noradrenaline levels were found to be significantly elevated in rabbits subjected to passive smoking for 3 weeks. Plasma adrenaline and dopamine levels were not changed. Transmural nerve stimulation of arterial rings evoked frequency-dependent contractions. Prolonged passive smoking did not affect neurogenic contractions of the arteries tested. On the other hand, endothelium-dependent relaxations of phenylephrine-precontracted arteries were significantly impaired. Furthermore, hypertrophy of the left ventricle was observed. In conclusion, passive smoking impairs endothelium-dependent relaxations but not neurogenic contractions of systemic arteries. The impaired relaxations of arteries may be, at least in part, mediated through the degradation of released nitric oxide by superoxide anions derived from cigarette smoke., J. Török, A. Gvozdjáková, J. Kucharská, I. Balažovjech, S. Kyselá, F. Šimko, J. Gvozdják., and Obsahuje bibliografii
The responsiveness of isolated high-pressure (aorta, renal artery) and low-pressure vessels (pulmonary artery) was compared during systemic hypertension induced by chronic inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME) in rats. L-NAME (40 mg/kg/day) was given to animals in their drinking water. After 4 weeks of L-NAME treatment, systolic blood pressure increased by 37 % as compared with that in the control group. Chronic L-NAME treatment resulted in significant reduction of endothelium-dependent relaxation to acetylcholine (10-8 to 3xl0-6 mol/1) in both types of vessels. The reduced relaxation was not influenced by acute pretreatment with indomethacin (10"5 mol/1), however, it was further reduced by acute pretreatment with additional L-NAME (10-4 mol/1). L-arginine (10-4 mol/1) improved the reduced relaxation. Endothelium- independent relaxation to sodium nitroprusside (10-9 to 10-6 mol/1) was unaffected by L-NAME treatment. /3-adrenoceptor-mediated relaxation to isoprénaline (10“8 to 3xl0-6 mol/1) was also not influenced by chronic L-NAME treatment Similar alterations in the responsiveness of high- and low- pressure vessels indicate rather the decisive role of nitric oxide restriction than that of elevated blood pressure in their development
The effect of long-term inhibition of nitric oxide synthase on the relaxation and contraction ability of the thoracic aorta, carotid and pulmonary arteries was studied in the early postnatal period. Starting from the fifth day after birth, puppies were administered NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day subcutaneously) for 6 weeks. After this period, mean blood pressure increased from the control value of 94±14 mm Hg to 168±5 mm Hg (P<0.01) and the heart/body weight ratio from 6.22±0.25 to 8.23±0.45 (PcO.Ol). In control arterial rings precontracted by phenylephrine (10“5 mol/1), acetylcholine caused dose-dependent relaxations; the maximal values were reached in the range of 10 "8 to 10"* mol/1. In arteries from L-NAME treated puppies, acetylcholine also induced dose-dependent relaxations, the maximum values in the thoracic aorta (81.0±2.9 %) and carotid artery (87.2±6.9 %) were significantly reduced, not, however, in the pulmonary artery (76.4±7.8 %). Dose-response curves to acetylcholine in all the examined arteries from L-NAME-treated animals were shifted to the right indicating a decrease in sensitivity to acetylcholine. Neurogenic contractions, induced by electrical stimulation of adrenergic nerves, were not significantly altered in the thoracic aorta and carotid artery. However, in the pulmonary artery the contractions were greater at high frequency of stimulation. The findings that (i) submaximal doses of L-NAME attenuate acetylcholine-induced relaxation only slightly, and (ii) that it does not appreciably influence adrenergic contractions justify the hypothesis that the endothelium of vessels in newborn dogs is very probably endowed with a high content of nitric oxide synthase.