Abstract
Angiotensin (Ang) II plays an important role in the brain as a neurotransmitter and is involved in psychological stress reactions, for example through activation of the sympatho-adrenomedullary system. We investigated the effects of centrally administered Ang II on the micturition reflex, which is potentially affected by the sympatho-adrenomedullary system, and brain Ang II receptors in urethane-anesthetized (1.0 g/kg, intraperitoneally) male rats. Central administration of Ang II (0.01, 0.02, and 0.07 nmol per rat, intracerebroventricularly, icv) but not vehicle rapidly and dose-dependently decreased the urinary bladder intercontraction interval, without altering the bladder detrusor pressure. Central administration of antagonists of Ang II type 1 but not type 2 receptors inhibited the Ang II-induced shortening of intercontraction intervals. Administration of the highest dose of Ang II (0.07 nmol per rat, icv) but not lower doses (0.01 and 0.02 nmol per rat, icv) elevated the plasma concentration of adrenaline. Bilateral adrenalectomy reduced Ang II-induced elevation in adrenaline, but had no effect on the Ang II-induced shortening of the intercontraction interval. These data suggest that central administration of Ang II increases urinary frequency by acting on brain Ang II type 1 receptors, independent of activation of the sympatho-adrenomedullary system.
Highlights
Psychological stress increases Ang II as a stress hormone in order to modulate the neuroendocrine system and influence behaviour[11]
We have previously shown that central Ang II is involved in activation of the SA system via brain AT1 receptors (AT1R)[7]
Centrally administered vehicle or Ang II had no effect on the maximum voiding pressure (MVP)
Summary
Psychological stress increases Ang II as a stress hormone in order to modulate the neuroendocrine system and influence behaviour[11]. Val icv + Ang II iv + Ang II iv + Ang II ADX + Ang II values in each rat before the first Ang II administration were set as 100%. Activation of the sympathetic nervous system by stressors increases the release of catecholamines, such as noradrenaline (NA) and adrenaline (Ad)[13]. A previous report demonstrated that intraperitoneally administered NA and alpha 1 or alpha 2 adrenoceptor agonists increases the frequency of voiding contraction in a dose-dependent manner[16]. We have previously shown that central Ang II is involved in activation of the SA system via brain AT1 receptors (AT1R)[7]. The aim of the current study was to investigate the relationship between central Ang II as a neurotransmitter and the micturition reflex
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