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. Author manuscript; available in PMC: 2023 Oct 1.
Published in final edited form as: Hypertension. 2022 Aug 22;79(10):2250–2261. doi: 10.1161/HYPERTENSIONAHA.122.19862

Figure 2. Role of NO in S1P-induced dilation of the human microvasculature.

Figure 2.

A) S1P-induced dilation in arterioles from nonCAD patients is reduced in the presence of the nitric oxide synthase (NOS) inhibitor L-NAME (100μM, n=5, ‡p<0.01) L-NAME versus S1P alone, as well as during exposure to the NO scavenger cPTIO (100μM, n=5, ‡p<0.01) (B). C) NO increases from baseline following exposure to increasing doses of S1P (n=4) which is quenched in the presence of L-NAME (100μM, n=3). D) NO formation in response to maximal flow (20μL/min, n=8) which is significantly reduced with L-NAME (100μM, n=3, *p<0.05). E) Representative images of NO production in vessels exposed to S1P +/− L-NAME (100μM). F) Representative images of NO formation in arterioles exposed to maximal flow (20μL/min) +/− L-NAME (100μM). Data are expressed as the mean±SEM.