The influence of blood gases on α₁‐ and α₂‐adrenoceptor‐mediated pressor responses in the pithed rat

Abstract

1The influence of blood gases on a-and a2-adrenoceptor-mediated pressor responses was studied in the pithed rat by varying the inspired gas mixture or the ventilation stroke volume. 2 Acidosis favoured the peak responses to the m2-adrenoceptor agonist, xylazine, while alkalosis favoured the peak responses to the a,-adrenoceptor agonist, phenylephrine. A combination of hypoxia and hypercapnia greatly depressed the ml response to phenylephrine whereas the M2 response to xylazine remained relatively unaffected. 3 When Pao2 was varied in either acidotic or alkalotic conditions the response to the phenylephrine increased as Pao2 increased. 4 To prevent hypoxia in air ventilated rats, large stroke volumes were required. This caused alkalosis and hence decreased responsiveness to xylazine. Consequently, air ventilated pithed rats gave poorer responses to xylazine than did those ventilated on 100% 02. 5 The results show that ml-and a2-adrenoceptor-mediated pressor responses can be differentially affected by blood gases. The relative contribution of al-and M2-adrenoceptors to vascular tone may be either under-or over-estimated depending on the arterial blood gases.

Effect of artificial respiratory volume on the cardiovascular responses to an α1‐ and an α2‐adrenoceptor agonist in the air‐ventilated pithed rat

“…Our results show that there was no effect of moderate changes in blood gases and pH, induced by the changes in respiratory volume, on the net pressor effect of phenylephrine. This is in contrast to studies in which a greater range of blood gas and pH values have been investigated (McGrath et al, 1982;Grant et al, 1985;Korstanje et al, 1985). Nevertheless, the present work does show that even these relatively small blood gas and pH changes differentially affect the responses of individual vascular beds to phenylephrine.…”

“…The response to phenylephrine was biphasic, as observed by other workers (e.g. Grant et al, 1985), and the microsphere injection was made as soon as the second phase had ceased to rise. For both agonists this was less than 90 s from the start of the bolus injection.…”

“…Grant et al (1985) showed that the peak pressor responses to the ax-adrenoceptor agonist phenylephrine and the a2-adrenoceptor agonist xylazine were potentiated by alkalosis and acidosis respectively. They also found that hypoxia combined with hypercapnia selectively depressed the pressor responses to phenylephrine although these responses were enhanced as Pao2 increased.…”

Cardiovascular responses to verapamil and nifedipine in hypoventilated and hyperventilated rats

“…Hyperventilation or hypoventilation was found to cause significant increases or decreases, respectively, in the blood pressure and pulse rate. This phenomenon is not at variance with the effects of blood gases, pH or ventilator stroke volumes on cardiovascular parameters found by others (Nahas & Cavert, 1957, Grant et al, 1985Phillips et al, 1985;MacLean & Hiley, 1988). The changes in pulse rate may result from a reflex increase or decrease in activities of the vagus nerve, the pulmonary stretch mechanoreceptors or cardio-inhibitory centre, or a combination of several of these factors (Daly & Scott, 1958;Evans & Evans, 1968).…”

“…Detar & Bohr (1968) showed that oxygen tension was an important determinant of the contractile force developed by the isolated helical strips of the rabbit aorta in response to adrenaline. Grant et al (1985) showed that the al-and c2-adrenoceptormediated pressor responses of pithed rats were differentially affected by changes in blood gases. Dai & Wong (1985) found that in urethane-anaesthetized rats, the effects of adrenaline on blood pressure, and of adrenaline or acetylcholine on pulse rate, were significantly reduced during hypoventilation which induced hypoxaemia, hypercapnia and acidosis.…”