Recent studies indicate that renal sympathetic nerve activity is chronically suppressed during ANG II hypertension. To determine whether cardiopulmonary reflexes and/or arterial baroreflexes mediate this chronic renal sympathoinhibition, experiments were conducted in conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated (Den) and innervated (Inn) kidneys. Dogs were studied 1) intact, 2) after thoracic vagal stripping to eliminate afferents from cardiopulmonary and aortic receptors [cardiopulmonary denervation (CPD)], and 3) after subsequent denervation of the carotid sinuses to achieve CPD plus complete sinoaortic denervation (CPD + SAD). After control measurements, ANG II was infused for 5 days at a rate of 5 ng. kg(-1). min(-1). In the intact state, 24-h control values for mean arterial pressure (MAP) and the ratio for urinary sodium excretion from Den and Inn kidneys (Den/Inn) were 98 +/- 4 mmHg and 1.04 +/- 0.04, respectively. ANG II caused sodium retention and a sustained increase in MAP of 30-35 mmHg. Throughout ANG II infusion, there was a greater rate of sodium excretion from Inn vs. Den kidneys (day 5 Den/Inn sodium = 0.51 +/- 0.05), indicating chronic suppression of renal sympathetic nerve activity. CPD and CPD + SAD had little or no influence on baseline values for either MAP or the Den/Inn sodium, nor did they alter the severity of ANG II hypertension. However, CPD totally abolished the fall in the Den/Inn sodium in response to ANG II. Furthermore, after CPD + SAD, there was a lower, rather than a higher, rate of sodium excretion from Inn vs. Den kidneys during ANG II infusion (day 5 Den/Inn sodium = 2.02 +/- 0.14). These data suggest that cardiac and/or arterial baroreflexes chronically inhibit renal sympathetic nerve activity during ANG II hypertension and that in the absence of these reflexes, ANG II has sustained renal sympathoexcitatory effects.

14 Recent studies indicate that renal sympathetic nerve activity is chronically supressed during angiotensin (ANG II) hypertension. To determine whether cardiopulmonary reflexes and/or arterial baroreflexes mediate this chronic renal sympathoinhibition, experiments were conducted in 5 conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated (DEN) and innervated (INN) kidneys. Dogs were studied before and after deafferentation of cardiopulmonary receptors and arterial baroreceptors (CPD + SAD). After control measurements, ANG II was infused for 5 days at a rate of 5 ng/kg/min; this was followed by a 5-day recovery period. In the intact state, 24-h control values for mean arterial pressure (MAP) and the ratio for urinary sodium excretion from DEN and INN kidneys (DEN/INN) were 98±4 mm Hg and 1.04±0.04 respectively. As expected, sodium retention occurred for several days during ANG II infusion before sodium balance was achieved at an increase in MAP of 30-35 mm Hg. Throughout ANG II infusion, there was a substantially greater rate of sodium excretion from INN versus DEN kidneys (day 5 DEN/INN-sodium = 0.51±0.05), indicating chronic suppression of renal sympathetic nerve activity. CPD + SAD did not influence baseline values for either MAP or the DEN/INN-sodium, nor did it alter the severity of ANG II hypertension. However, after CPD + SAD there was an appreciably lower, rather than a greater, rate of sodium excretion from INN versus DEN kidneys during ANG II hypertension (day 5 DEN/INN-sodium = 2.02±0.14). These data indicate that cardiac and/or arterial baroreflexes chronically inhibit renal sympathetic nerve activity during ANG II hypertension and that in the absence of these reflexes, ANG II has sustained renal sympathoexcitatory effects that promote sodium retention.