title: Spontaneous oscillatory contractions in aortas of rats with arterial pressure lability caused by sinoaortic denervation.
abstract: 1. The spontaneous variation of blood pressure is defined as arterial pressure lability. Sinoaortic denervation (SAD) is characterized by arterial pressure lability without sustained hypertension. 2. The phenomenon of spontaneous oscillatory contractions (SOCs) occurs more frequently in the vascular beds of hypertensive animals. In large arteries, such as the aorta, SOCs occur only occasionally or they can be initiated by application of chemical stimuli. 3. In the present study, we investigated whether the arterial pressure lability evoked by SAD could be related to the emergence of SOCs in the aorta of rats submitted to SAD compared with sham-operated rats (SO). Three days after surgery (SAD or SO), aortic rings were placed in an organ chamber and the incidence (percentage of rats presenting SOCs), frequency (number of SOCs in 10 min) and amplitude (mN) of SOCs were measured. The participation of external Ca(2+) and K(+) channels in the maintenance of SOCs was also verified. 4. The incidence and frequency of SOCs were higher in endothelium-denuded aortas from SAD rats (82% and 38 +/- 4 SOCs/10 min, respectively) than in aortas from SO rats (40% and 14 +/- 2 SOCs/10 min, respectively). In aortas from SAD rats, verapamil (0.2 micromol/L), pinacidil (0.3 micromol/L) and tetraethylammonium (TEA; 5 mmol/L) totally inhibited SOCs, whereas increasing the CaCl(2) concentration to 2.0 and 2.5 mmol/L increased the frequency of SOCs. Interestingly, increasing the concentration of CaCl(2) to 3.5 mmol/L inhibited these contractions in aortas from SAD rats. 5. These results show that although SAD rats did not become hypertensive, their aortas were capable of initiating SOCs without the application of any chemical stimuli. The SOCs seem to be dependent on Ca(2+) influx sensitive to verapamil and also involve K(+) channels sensitive to pinacidil and TEA.
authors.affiliation: Department of Physics and Chemistry, Faculty of Pharmaceutical Sciences of Ribeirão Preto, University of Sao Paulo, Ribeirão Preto, Brazil.
authors.forename: Matheus L
authors.initials: ML
authors.lastname: Rocha
authors.forename: Lusiane M
authors.initials: LM
authors.lastname: Bendhack
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000294:innervation / Q000378:metabolism*; D017763:Autonomic Denervation; D001794:Blood Pressure; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D002122:Calcium Chloride / Q000494:pharmacology; D008297:Male; D009991:Oscillometry; D020110:Pinacidil / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D019789:Tetraethylammonium / Q000494:pharmacology; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014665:Vasodilator Agents; D019789:Tetraethylammonium; D020110:Pinacidil; D014700:Verapamil; D002122:Calcium Chloride; D011188:Potassium; D002118:Calcium