| This dissertation investigates the mechanisms of cardio-respiratory integration during sleep in: spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto (WKY), Zucker lean and Zucker obese, and Sprague Dawley rats.;One of the goals of this study was to demonstrate that, in rats, chronic hypertension is associated with increased apnea expression. For that reason, SHR rats were compared to their normotensive WKY group before and after hydralazine-induced hypotension. The rate of apneas was elevated significantly during NREM sleep in SHR versus WKY rats. Acute normalization of blood pressure in SHR rats reduced the number of sleep apneas to equivalence with WKY rats.;In similar fashion, acute lowering of BP in Zucker lean and Zucker obese rats was also accompanied by a decrease in the number of apneas. This observation was repeated in Sprague-Dawley rats which were implanted with radio transmitters, allowing continuous and much more precise measurement of blood pressure.;In an attempt to pharmacologically stimulate apnea expression by increasing baroreceptor afferent firing, protoveratrines were used. These alkaloids are known to stimulate the baroreflexes. In Sprague-Dawley rats, protoveratrine administration increased the number of apneas dramatically, suggesting an important role of baroreflex afferent firing in apnea genesis.;Each animal was surgically implanted with EEG and EMG electrodes for measurement of sleep states and was put in a plethysmographic chamber for measurement of respiration. Some animals were also implanted with radio-transmitters for telemetry measurement of blood pressure. Recordings were done from 10 AM to 4 PM.;The final step was based on the agent losartan, an angiotensin II receptor antagonist. When chronically infused to SHR rats, losartan elicited a sustained reduction in blood pressure with a delayed increase in baroreflex activity, allowing the opposing effects of decreasing and increasing baroreceptor firing on apnea expression to be identified.;Together these observations demonstrated that blood pressure changes have influence on sleep apnea genesis in rats, with the most likely mechanism for this effect being alteration of baroreceptor firing. |
