Central and renal I1 @entity947 preferring receptors: two unique sites mediating natriuresis in the XXXX .

@entity3159 @entity23703 @entity1372 @entity9006 @entity35 @entity947
Based on previous studies we postulated that, whereas the natriuresis observed following intracerebroventricular (i.c.v.) @entity23703 was mediated by a decrease in renal sympathetic nerve activity, the natriuresis observed following intrarenal (i.r.) infusion of @entity23703 was mediated by a direct stimulation of renal I1- @entity947 preferring receptors. @entity35 were unilaterally nephrectomized and i.c.v. cannulated 7 to 10 days and 3 days prior to the day of the experiment, respectively. On the day of the experiment, @entity35 were anesthetized (pentobarbital) and the renal function was isolated. Administration of i.c.v. as well as i.r. @entity23703 produced an increase in @entity1372 excretion and urine flow fate. Pretreatment with intravenous @entity3159 (0.15 mg/kg) completely attenuated the response to i.c.v. @entity23703 (1 nmol/5 microliters) but only slightly altered the response to i.r. @entity23703 (3 nmol/kg/min). Conversely, intravenous pretreatment with the @entity947 preferring receptor antagonist @entity9006 (0.3 mg/kg) completely blocked the response to i.r. @entity23703 (3 nmol/kg/min) without altering the response to i.c.v. @entity23703 (0.3 nmol/kg). These results would be consistent with the natriuresis observed following i.c.v. @entity23703 as being mediated by @entity947 preferring receptors located centrally, whereas that following i.r. @entity23703 was mediated directly by renal @entity947 -preferring receptors, with a small component of this response conceivably due to activation of central @entity947 preferring receptors. In summary, the antihypertensive effect of @entity947 preferring receptor agonists may be associated with a natriuresis that is due to stimulation of these receptors, found both peripherally (renal) and centrally.
