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Endothelial derived hyperpolarization in vivo in hypertensive rats
Author(s) -
Brasen J. Christian,
Stannov Søs Urup,
Salomonsson Max,
Sorensen Charlotte Mehlin
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.739.12
Subject(s) - prazosin , in vivo , renal blood flow , endocrinology , medicine , mean arterial pressure , hyperpolarization (physics) , vasodilation , blood pressure , kidney , vascular resistance , chemistry , mesenteric arteries , renal circulation , antagonist , receptor , heart rate , artery , biology , microbiology and biotechnology , organic chemistry , nuclear magnetic resonance spectroscopy
Endothelial derived hyperpolarization (EDH) plays a role in regulation of vascular tone, but little is known about its role in renal arteries in vivo. Whether EDH is affected by hypertension or vice versa is also unknown. We have investigated if the magnitude of EDH in renal arteries in vivo is different between normotensive and hypertensive rats and what the difference could be due to. In this study we quantify renal EDH in vivo in normotensive Sprague Dawley (SpD) rats and spontaneous hypertensive rats (SHR). Renal blood flow is measured in sevoflurane anesthetized rats. The ACh‐induced increase in renal blood flow (RBF) is measured before and after inhibition of the nitric oxide synthase and cyclooxygenase with L‐NAME and indomethacin, respectively. Mean arterial pressure (MAP) is significantly higher in SHR (139 mmHg) compared to SpD (97 mmHg). Infusion of L‐NAME and indomethacin decreased RBF and increased MAP in both strains. We therefore used renal vascular resistance (RVR) to quantify EDH. Following infusion of L‐NAME and indomethacin RVR increased from 14 to 25 mmHg × min/ml in the SpD, whereas RVR increased from 27 to 72 mmHg × min/ml in the SHR. When L‐NAME and indomethacin were infused the decrease in RVR following infusion of ACh was greater in the SHR (from 73 to 67 mmHg × min/ml) compared to the SpD (from 21 to 18 mmHg × min/ml). In the SpD inhibition of the alpha‐1 adrenergic receptor with prazosin had no significant effect on RVR in the presence of L‐NAME and indomethacin. The magnitude of the EDH response was also not significantly different with or without prazosin. In the SHR RVR was not significantly different after prazosin infusion in the presence of L‐NAME and indomethacin. However, the effect of EDH measured as a decrease in RVR was greater in the prazosin treated animals. The vasodilator papaverine did not change EDH in SpD, but in the SHR it was reduced. Infusion of NE or AngII did not change the EDH response the SpD or SHR. These results suggest that alpha adrenoceptor activity might be responsible for the reduced EDH in SHR.