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  • Title: Baroreflex control of heart rate during hypoxia and hypercapnia in chronically hypertensive rabbits.
    Author: Groom AS, Malpas SC.
    Journal: Clin Exp Pharmacol Physiol; 1997; 24(3-4):229-34. PubMed ID: 9131290.
    Abstract:
    1. It has been proposed that hypertension alters the respiratory and cardiovascular responses to chemoreceptor stimulation. However, in studies of human hypertension or in genetic animal models of hypertension it has been difficult to unequivocally attribute the changes to hypertension per se, rather than to a genetic predisposition towards an altered chemoreflex response independent of hypertension. 2. In the present study a group of seven rabbits were made hypertensive via a continuous 7 week infusion of angiotensin II (AngII; 50 ng/kg per min, i.v.). Animals were studied twice before AngII treatment commenced, twice during infusion and 48 h after stopping infusion. At each of these times the relationship between heart rate (HR) and mean arterial pressure (MAP) was determined under normoxic, acute hypoxic (10% O2 + 3% CO2) and acute hypercapnic (18% O2 +, 6.5% CO2) conditions for 20 min. A group of six animals also served as time controls. 3. Angiotensin II infusion increased arterial pressure from control levels of 80 +/- 2 to 114 +/- 8 mmHg and maintained it at this level throughout the 7 week period. After 1 week of AngII infusion there was a rightward shift in the heart rate-baroreflex curve, indicating that the baroreflex was now operating at an increased level of pressure. These changes were associated with reductions in the gain from -7.6 +/- 1.6 to -3.0 +/- 0.2 b.p.m./ mmHg, HR range and curvature of the baroreflex. These effects were maintained throughout the 7 weeks of hypertension and were reversed within 2 days of ceasing AngII infusion. Acute hypoxia and hypercapnia in normotensive animals caused a reduction in the HR range of 19 +/- 7 and 15 +/- 7 b.p.m., respectively, but caused no change in the gain (sensitivity) of the baroreflex. Despite the marked changes in the baroreflex produced by the hypertension, the effect of hypoxia or hypercapnia on the HR baroreflex was not different in the hypertensive group. 4. It is concluded that chronic experimental AngII-based hypertension does not alter the HR baroreflex response to hypoxia or hypercapnia and suggests that the altered responses seen in other studies is due to a genetic predisposition as opposed to the effect of raised arterial pressure.
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