Clinical and Experimental Hypertension, 32(8): 555–559, (2010) Copyright © Informa Healthcare USA, Inc. ISSN 1064-1963 print/1525-6006 online DOI: 10.3109/10641963.2010.503296 555 LCEH Acute Obstructive Apnea Produces Natriuresis in Spontaneously Hypertensive Rats (SHR) by a Renal Nerve-Dependent Acute Obstructive Apnea in Hypertensive Rat Tadeu U. Andrade, 1 João V. M. Franquini, 1 Antônio M. Cabral, 3 Elisardo C. Vasquez, 2 Maria T. Araújo, 2 Margareth R. Moysés, 2 Gláucia R. Abreu, 2 Nazare S. Bissoli 3 1 Department of Pharmacy, University Center of Vila Velha, Vila Velha, Brazil, 2 Department of Physiology, Federal University of Espirito Santo, Vitoria, Brazil, 3 Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, Brazil Abstract The role of renal nerve in excretion was investigated during acute obstructive apnea (OA) episodes in SHR. The animals (SHR and control, C) were presented for renal denervation (D; CD; SHRD) or undenervation (U; CU; SHRU). Tracheal catheterization was performed to induce OA via its total occlusion. Urine samples were collected every 2 min after 20 s of OA. Obstructive apnea resulted in bradycardia, hypotension, and induced elevations in the urinary measurements in SHRU, but not in CU. Conversely, the denervation increased in CD, but not in the SHRD. Urinary excretion was dependent of renal nerve in SHR during OA Keywords: obstructive apnea, renal nerve, SHR, sodium excretion, hypertension INTRODUCTION Obstructive sleep apnea (OSA) affects middle-aged adults and is associated with adverse health outcomes. Cardiovascular disturbances are the most serious com- plications of OSA (1). A growing body of evidence supports the premise that a chemoreflex-mediated elevation of basal sympathetic activity may play an important role in the pathogenesis of hypertension among OSA patients (1–5). A chronic elevation of sympathetic activity would logically lead to vascular remodeling and sustained changes in the vascu- lar reactivity and tone, which are the hallmark manifesta- tions of essential hypertension. Therefore, it is well established that there is a link between obstructive apnea (OA) and cardiovascular abnormalities (1–3). However, the physiological mechanism(s) linking OA and alter- ations in the cardiovascular system remain unclear, and differences could exist depending on the manifestation of acute or chronic hypoxia in experimental animals. Studies in animals have helped to elucidate the mechanisms underlying the cardiorespiratory and other changes elicited by OSA. Two models of OSA are often used— repeated occlusions (6) and chronic intermit- tent hypoxia (5). Exposure to chronic intermittent hypoxia, such as OSA, elicits a sustained elevation in sympathetic activity and mean arterial pressure (MAP) in experimental animals (4,5,7). Bao et al. (7) demon- strate that adrenal demedullation or renal artery dener- vation eliminated the diurnal mean BP response to chronic episodic hypoxia, whereas sham-operated controls continued to show persistent elevation of sys- temic arterial pressure. Nevertheless, acute hypoxia results in hypotension and bradycardia. These results were demonstrated by Franquini et al. (8) and Guilleminault et al. (9) and Yalkut et al. (10). We demonstrated that acute OA events resulted in an increase in diuresis and natriuresis in denervated normotensive rats and the basal values of sodium content excretion and volume of urine were not affected by OA episodes in undenervated animals, but these episodes were capable of eliciting reductions in heart rate (HR) and MAP values in both denerveted and undernevated rats (8). Then, denervation seems to change the renal response elicited by OA in normoten- sive rats, but we are not aware of any study evaluating the effect of renal denervation in hypertensive animals using our model of OA. Therefore, the goal of this study was to investigate the influence of hypertension on sodium and water excretion, and hemodynamic changes during severe, acute OA episodes in rats with innervated and dener- vated kidneys. Address correspondence to Nazare Bissoli, Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, 29040090 Brazil. E-mail: naza@npd.ufes.br Received 12 November 2009; revised 23 March 2010; accepted 29 March 2010.