Answers are grounded in this paper and cite their sources.
The central nitrergic system modulates angiotensin-II-induced neuroendocrine secretion, fluid balance, and blood pressure in rats, with nitric oxide exerting an inhibitory effect.
BACKGROUND: Nitric oxide (NO) synthesis has been described in several circumventricular and hypothalamic structures in the central nervous system that are implicated in mediating central angiotensin-II (ANG-II) actions during water deprivation and hypovolemia. Neuroendocrine and cardiovascular responses, drinking behavior, and urinary excretions were examined following central angiotensinergic stimulation in awake freely-moving rats pretreated with intracerebroventricular injections of Nω-nitro-L-arginine methyl ester (L-NAME, 40 μg), an inhibitor of NO synthase, and L-arginine (20 ug), a precursor of NO. RESULTS: Injections of L-NAME or ANG-II produced an increase in plasma vasopressin (VP), oxytocin (OT) and atrial natriuretic peptide (ANP) levels, an increase in water and sodium intake, mean arterial blood pressure and sodium excretion, and a reduction of urinary volume. L-NAME pretreatment enhanced the ANG-II response, while L-arginine attenuated VP and OT release, thirst, appetite for sodium, antidiuresis, and natriuresis, as well as pressor responses induced by ANG-II. DISCUSSION AND CONCLUSION: Thus, the central nitrergic system participates in the angiotensinergic responses evoked by water deprivation and hypovolemia to refrain neurohypophysial secretion, hydromineral balance, and blood pressure homeostasis.
No takes yet. Share an insight, caveat, or question.
Reis et al. (2010) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: