Effect of clonidine on the contractile responsiveness of aortic smooth muscle to norepinephrine.
A length-tension relationship was established for aortic smooth muscle of rats by means of membrane depolarization with KCl. Maximal tension was developed by aortic rings when the preload initial tension was 8--9 g. Two aortic rings (4 mm thick) were removed from segments of the aorta cut 1.5 (upper) and 2.4 cm (lower) below the aortic arch. Upper rings appeared to develop a greater tension than lower rings during depolarization with KCl. However, in spite of this quantitative difference between rings from upper and lower segments of the aorta, there were no qualitative differences observed. Clonidine, an antihypertensive agent, induced a contraction in aortic smooth muscle, apparently by way of alpha-adrenoreceptor stimulation. Clonidine also attenuated significantly the development of active tension by norepinephrine but did not inhibit significantly the development of active tension following membrane depolarization with KCl. This suggests that there is a partial antagonism between norepinephrine and clonidine, presumably at the site of the receptors on smooth muscle, and that clonidine does not interfere with the contractile mechanism, per se.
D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000294:innervation; D003000:Clonidine / Q000494:pharmacology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects* / Q000294:innervation; D009638:Norepinephrine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011189:Potassium Chloride / Q000037:antagonists & inhibitors / Q000494:pharmacology; D051381:Rats; D011984:Sensory Receptor Cells / Q000187:drug effects
D011189:Potassium Chloride; D003000:Clonidine; D009638:Norepinephrine