Abstract 1753: Augmented Adrenergic Activation Induced by Transient Stress is Sustained in Both Heart and Kidney of Conscious Hypertensive Rats
Transient hypoxic and hypercapnic stress in patients with sleep apnea syndrome results in increased plasma catecholamine levels in the day-time, suggesting that transient stress might cause the sustained elevation of sympathetic drive. However, it remains unclear whether it is also true for hypertension, and whether cardiac adrenergic response to transient stress is similar to that of kidney. Accordingly, we investigated cardiac and renal interstitial norepinephrine (iNE) and the response of iNE to transient hypercapnic stress in conscious hypertensive rats. Salt-sensitive (DS) and -resistant (DR) Dahl rats were fed 8% NaCl diet started from the age of 6 weeks (wk). iNE was determined using the microdialysis method. Microdialysis probes (0.2mm ID, 7mm length) were inserted into left ventricle (LV) along the left coronary artery and into the inner cortex of kidney. After the recovery from the probe implantation (48 hours), iNE was determined before, during, and after 3 times exposure of 10% CO2 for 5 minutes in the conscious rats of 12wk. In DS rats, systolic blood pressure increased markedly and the ratio of LV to body weight increased significantly, as compared to those of DR rats. However, dP/dtmax normalized to the systolic LV pressure, dP/dt/P, remained unchanged in DS rats, indicating preserved LV systolic function. In DS rats, plasma levels of NE did not increase but cardiac NE contents were reduced, as compared to DR rats (262 ± 85 vs 597 ± 72 ng/g, p < 0.05), whereas renal NE contents were unchanged. Before the stress, both cardiac and renal iNEs were significantly higher in DS (n = 5, 228 ± 89, 274 ± 240 pg/ml) than in DR (n = 5, 87 ± 64, 71 ± 93 pg/ml). After the cessation of stress, increased iNEs of DS was markedly sustained in both LV (542 ± 267 vs 55 ± 48 pg/ml) and kidney (618 ± 428 vs 48 ± 57 pg/ml), although iNEs during the stress were also significantly greater in DS rats of both LV (678 ± 248 vs 158 ± 128 pg/ml) and kidney (658 ± 395 vs 180 ± 191 pg/ml). Despite reduced tissue contents of NE in hypertensive hearts, augmented response of cardiac iNEs to transient stress was similar to that of kidney. Sustained increases in cardiac and renal iNEs after transient stress may contribute to developing target organ damage in hypertensive rats.