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You are here: Home Research Groups Renal Hemodynamics Recent Activities Dynamics of endothelium-dependent vasodilation
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Dynamics of endothelium-dependent vasodilation

Am J Physiol Regu 305(9): R987-98, 2013

Nov 20, 2013

Dynamics of endothelium-dependent vasodilation

Am J Physiol Regulatory, November 2013

Dautzenberg M., Just A.
Temporal characteristics of nitric oxide-, prostaglandin-, and EDHF-mediated components of endothelium-dependent vasodilation in the kidney.
Am J Physiol Regul Integr Comp Physiol 2013 Nov, 305(9): R987-R998



We studied the temporal characteristics of nitric oxide (NO), prostaglandins (PG), and endothelium-derived hyperpolarizing factor (EDHF) in endothelium-dependent vasodilation. NO, PG, and EDHF were found to contribute >50%, 20-40%, and <20% to the dilator responses of acetylcholine and bradykinin. EDHF acts faster and more transiently (max after 16 s) than NO and PG (max after 30 s). Attenuation by NO and PG of constrictor responses to norepinephrine and angiotensin II is varying over time, reaching maximum attenuation later than peak constriction. Thereby, the constrictions are not only mitigated but also rendered more transient.



Endothelium-dependent vasodilation is mediated by nitric oxide (NO), prostaglandins (PG), and endothelium-derived hyperpolarizing factor (EDHF). We studied the contributions and temporal characteristics of these components in the renal vasodilator responses to acetylcholine (ACh) and bradykinin (BK) and in the buffering of vasoconstrictor responses to norepinephrine (NE) and angiotensin II (ANG II). Renal blood flow (RBF) and vascular conductance (RVC) were studied in anesthetized rats in response to renal arterial bolus injections before and after inhibition of NO-synthase (N(G)-nitro-l-arginine methyl ester, l-NAME), cyclooxygenase (indomethacin, INDO), or both. ACh increased RVC peaking at maximal time (tmax) = 29 s. l-NAME (n = 8) diminished the integrated response and made it substantially faster (tmax = 18 s). The point-by-point difference caused by l-NAME (= NO component) integrated to 74% of control and was much slower (tmax = 38 s). INDO (n = 9) reduced the response without affecting tmax (36 vs. 30 s). The difference (= PG) reached 21% of the control with tmax = 25 s. l-NAME+INDO (n = 17) reduced the response to 18% and markedly accelerated tmax to 16s (= EDHF). Results were similar for BK with slightly more PG and less NO contribution than for ACh. Constrictor responses to NE and ANG II were augmented and decelerated by l-NAME and l-NAME+INDO. The calculated difference (= buffering by NO or NO+PG) was slower than the constriction. It is concluded that NO, PG, and EDHF contribute >50%, 20-40%, and <20% to the renal vasodilator effect of ACh and BK, respectively. EDHF acts substantially faster and less sustained (tmax = 16 s) than NO and PG (tmax = 30 s). Constrictor buffering by NO and PG is not constant over time, but renders the constriction less sustained.






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