Systemic inhibition of AT1 receptors does not alter respiratory-sympathetic synchronization in anesthetized rats (1130.13)

Sympathetic nerve discharge contains a respiratory‐related rhythm. Arterial chemoreceptors possess angiotensin AT1 receptors which have been reported to increase chemoreceptor afferent discharge. To determine if angiotensin might modulate respiratory‐sympathetic interactions, we tested if synchronization between phrenic nerve activity (PNA) and renal sympathetic nerve activity (RSNA) would be altered by systemic blockade of AT 1 receptors. Spectral analysis and cross correlation were used to examine the synchronization in anesthetized, vagotomized and mechanically ventilated Sprague‐Dawley rats (300‐400g, n=5). Intravenous injections of losartan (a selective angiotensin II type‐1 receptor (AT 1 )antagonist, 1 mg/ml/kg body weight) inhibited the increase in blood pressure following iv. angiotensin II injection (50 ng/0.1 ml) from 40±7 mmHg to ‐6±8 mmHg (n=5, P<0.05). Following losartan, we estimated coherence between spectral power of PNA and RSNA at central respiratory drive frequency, defined as frequency of the main peak in PNA before and after losartan injection. Losartan did not alter the spectral power of either PNA or RSNA (P>.05). Coherence did not differ before (0.78 ± 0.21) compared to after (0.72 ± 0.34) losartan. Phase difference also did not change before (0.21 ± 0.25) and after (0.20 ± 0.24) losartan. These results suggest that systemic inhibition of AT1 receptors does not alter respiratory‐sympathetic synchronization. Grant Funding Source : HL088052; CAPES (18890‐12‐1); FAPESP; CNPq