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Hypothesis:   A lack of contraction of cerebral microarterioles to Ang II (“resilience”) depends on cyclooxygenase (COX) and lipocalin type prostaglandin D sythase L-PGDS producing PGD 2  that activates prostaglandin D type 1 receptors (DP1Rs) and nitric oxide synthase (NOS).Materials &amp; Methods:   Contractions were assessed in isolated, perfused vessels and NO by fluorescence microscopy.Results:   The mRNAs of penetrating intraparenchymal cerebral microarterioles versus renal afferent arterioles were &gt;3000-fold greater for L-PGDS and DP1R and 5-fold for NOS III and COX 2. Larger cerebral arteries contracted with Ang II. However, cerebral microarterioles were entirely unresponsive but contracted with endothelin 1 and perfusion pressure. Ang II contractions were evoked in cerebral microarterioles from COX1 –/– mice or after blockade of COX2, L-PGDS or NOS and in deendothelialized vessels but effects of deendothelialization were lost during COX blockade. NO generation with Ang II depended on COX and also was increased by DP1R activation.Conclusion:   The resilience of cerebral arterioles to Ang II contractions is specific for intraparenchymal microarterioles and depends on endothelial COX1 and two products that are metabolized by L-PGDS to generate PGD 2  that signals via DP1Rs and NO.

Endothelial prostaglandin D2 opposes angiotensin II contractions in mouse isolated perfused intracerebral microarterioles

Endothelial prostaglandin D₂ opposes angiotensin II contractions in mouse isolated perfused intracerebral microarterioles