TY - JOUR
T1 - Interactions between renal vascular resistance and endothelium-derived hyperpolarization in hypertensive rats in vivo
T2 - Renal endothelial hyperpolarization in hypertension
AU - Stannov, Søs U
AU - Brasen, Jens Christian
AU - Salomonsson, Max
AU - Holstein-Rathlou, Niels-Henrik
AU - Sorensen, Charlotte M
N1 - © 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
PY - 2019/8
Y1 - 2019/8
N2 - Endothelium derived signaling mechanisms play an important role in regulating vascular tone and endothelial dysfunction is often found in hypertension. Endothelium-derived hyperpolarization (EDH) plays a significant role in smaller renal arteries and arterioles, but its significance in vivo in hypertension is unresolved. The aim of this study was to characterize the EDH-induced renal vasodilation in normotensive and hypertensive rats during acute intrarenal infusion of ACh. Our hypothesis was that the increased renal vascular resistance (RVR) found early in hypertension would significantly correlate with reduced EDH-induced vasodilation. In isoflurane-anesthetized 12-week-old normo- and hypertensive rats blood pressure and renal blood flow (RBF) was measured continuously. RBF responses to acute intrarenal ACh infusions were measured before and after inhibition of NO and prostacyclin. Additionally, RVR was decreased or increased using inhibition or activation of adrenergic receptors or by use of papaverine and angiotensin II. Intrarenal infusion of ACh elicited a larger increase in RBF in hypertensive rats compared to normotensive rats suggesting that endothelial dysfunction is not present in 12-week-old hypertensive rats. The EDH-induced renal vasodilation (after inhibition of NO and prostacyclin) was similar between normo- and hypertensive rats. Reducing RVR by inhibition of α1 -adrenergic receptors significantly increased the renal EDH response in hypertensive rats, but a similar increase was found after activating α-adrenergic receptors using norepinephrine. The results show that renal EDH is present and functional in 12-week-old normo- and hypertensive rats. Interestingly, both activation and inactivation of α1 -adrenergic receptors elicited an increase in the renal EDH-induced vasodilation.
AB - Endothelium derived signaling mechanisms play an important role in regulating vascular tone and endothelial dysfunction is often found in hypertension. Endothelium-derived hyperpolarization (EDH) plays a significant role in smaller renal arteries and arterioles, but its significance in vivo in hypertension is unresolved. The aim of this study was to characterize the EDH-induced renal vasodilation in normotensive and hypertensive rats during acute intrarenal infusion of ACh. Our hypothesis was that the increased renal vascular resistance (RVR) found early in hypertension would significantly correlate with reduced EDH-induced vasodilation. In isoflurane-anesthetized 12-week-old normo- and hypertensive rats blood pressure and renal blood flow (RBF) was measured continuously. RBF responses to acute intrarenal ACh infusions were measured before and after inhibition of NO and prostacyclin. Additionally, RVR was decreased or increased using inhibition or activation of adrenergic receptors or by use of papaverine and angiotensin II. Intrarenal infusion of ACh elicited a larger increase in RBF in hypertensive rats compared to normotensive rats suggesting that endothelial dysfunction is not present in 12-week-old hypertensive rats. The EDH-induced renal vasodilation (after inhibition of NO and prostacyclin) was similar between normo- and hypertensive rats. Reducing RVR by inhibition of α1 -adrenergic receptors significantly increased the renal EDH response in hypertensive rats, but a similar increase was found after activating α-adrenergic receptors using norepinephrine. The results show that renal EDH is present and functional in 12-week-old normo- and hypertensive rats. Interestingly, both activation and inactivation of α1 -adrenergic receptors elicited an increase in the renal EDH-induced vasodilation.
U2 - 10.14814/phy2.14168
DO - 10.14814/phy2.14168
M3 - Journal article
C2 - 31368238
SN - 2051-817X
VL - 7
JO - Physiological Reports
JF - Physiological Reports
IS - 15
M1 - e14168
ER -