The renal vasodilation from β-adrenergic activation in vivo in rats is not driven by KV7 and BKCa channels

Aim: The underlying mechanisms behind β-adrenergic renal vasodilation is not clarified. Several classes of K + channels are potentially activated, so we tested the hypothesis that voltage-sensitive K V 7 and Ca 2+ -activated BK Ca channels contribute to the decrease in renal vascular tone in vivo and in vitro. Methods: Changes in renal blood flow (RBF) during β-adrenergic stimulation was measured in isoflurane-anesthetized rats using an ultrasonic flow probe. The isometric tension of segmental arteries from normo- and hypertensive rats and segmental arteries from wild-type mice and mice lacking functional K V 7.1 channels was examined in a wire-myograph. Results: The β-adrenergic agonist isoprenaline increased RBF significantly in vivo. Neither activation nor inhibition of K V 7 or BK Ca channels reduced the β-adrenergic RBF response. In segmental arteries from normo- and hypertensive rats, inhibition of K V 7 channels significantly decreased the β-adrenergic vasorelaxation. However, inhibiting the BK Ca channel was equally effective. The β-adrenergic vasorelaxation was not different between segmental arteries from wild-type mice and mice lacking a functional K V 7.1 channel. As opposed to rats, inhibition of K V 7 channels did not affect the murine β-adrenergic vasorelaxation. Conclusion: Although inhibition and activation of K V 7 and BK Ca channels significantly changed baseline RBF in vivo, none of the treatments affected the β-adrenergic vasodilation. In segmental arteries however, inhibition of K V 7 and BK Ca channels significantly reduced the β-adrenergic vasorelaxation indicating that the regulation of RBF in vivo is driven by several actors in order to maintain an adequate RBF. Our data stresses the importance of verifying data in intact animals. None. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.