AIR-JET NOISE EXPOSURE RAPIDLY INCREASES BLOOD-PRESSURE IN YOUNG BORDERLINE HYPERTENSIVE RATS

The present study tested the hypothesis that air jet noise exposure elicits sympathetically-mediated increases in the blood pressure of weaning-aged borderline hypertensive rats (BHR). BHR were the F1 offspring of spontaneously hypertensive female rats and male Wistar-Kyoto rats. Beginning at weaning (4 weeks of age), restrained BHR were exposed to air jet noise (30-120 s pulses of 120 dB) for 2 h/day, 5 days per week. Controls were restrained but did not receive air jet noise exposure. After only 1 week of air jet exposure, the systolic blood pressure (SBP) levels of the noise-exposed rats were increased significantly above those of restrained controls. Measures of mean arterial pressure (MAP) made in the home age after 2 weeks of noise exposure confirmed the increased SBP. Ten weeks of air jet noise exposure increased MAP compared with restrained controls (144 +/- 4 versus 128 +/- 4 mmHg), with both SBP and diastolic blood pressure (DBP) being significantly increased. Baroreceptor sensitivity, assessed by bradycardic responses to graded doses of phenylephrine (0.5, 1, 2 and 4-mu-g/kg, intravenously), did not differ from restrained controls after 10 weeks of noise exposure. Autonomic (largely sympathetic) influence on home-cage blood pressure, inferred from ganglion blockade with chlorisondamine, also did not differ between groups after 10 weeks of stress. After maximal vasodilation with hydralazine, the DBP of air jet noise-exposed rats was somewhat higher than restrained controls (62 +/- 5 versus 49 +/- 3 mmHg; P = 0.08), suggesting that structural changes may have contributed to the increased MAP in air jet noise-exposed rats. In summary, exposure of weanling BHR rats to chronic air jet noise increased blood pressure within 1 week and pressure remained elevated during 10 weeks of stress. While autonomic mechanisms were not found to mediate the higher home-cage blood pressure observed in air jet noise-exposed BHR, structural changes in the vasculature may have contributed.