Heterogeneous control of blood flow amongst different vascular beds

Hill, Caryl E.; Phillips, Jacqueline; Sandow, Shaun L.

doi:10.1002/1098-1128(200101)21:1<1::aid-med1>3.3.co;2-y

Cited by 50 publications

(87 citation statements)

References 171 publications

(222 reference statements)

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“…These findings, the specific distribution of Cx43 between smooth muscle cells and selected ECs of vessels, and the regulation of Cx43 levels in both vascular endothelial and smooth muscle cells exposed to shear stress and other mechanical challenges (33)(34)(35)(36)(37) provide evidence that the cellto-cell communication mediated by Cx43 channels contributes to…”

Section: Discussionmentioning

confidence: 78%

Connexin43-dependent mechanism modulates renin secretion and hypertension

Haefliger¹

2006

Journal of Clinical Investigation

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To investigate the function of Cx43 during hypertension, we studied the mouse line Cx43KI32 (KI32), in which the coding region of Cx32 replaces that of Cx43. Within the kidneys of homozygous KI32 mice, Cx32 was expressed in cortical and medullary tubules, as well as in some extra-and intraglomerular vessels, i.e., at sites where Cx32 and Cx43 are found in WT mice. Under such conditions, renin expression was much reduced compared with that observed in the kidneys of WT and heterozygous KI32 littermates. After exposure to a high-salt diet, all mice retained a normal blood pressure. However, whereas the levels of renin were significantly reduced in the kidneys of WT and heterozygous KI32 mice, reaching levels comparable to those observed in homozygous littermates, they were not further affected in the latter animals. Four weeks after the clipping of a renal artery (the 2-kidney, 1-clip [2K1C] model), 2K1C WT and heterozygous mice showed an increase in blood pressure and in the circulating levels of renin, whereas 2K1C homozygous littermates remained normotensive and showed unchanged plasma renin activity. Hypertensive, but not normotensive, mice also developed cardiac hypertrophy. The data indicate that replacement of Cx43 by Cx32 is associated with decreased expression and secretion of renin, thus preventing the renin-dependent hypertension that is normally induced in the 2K1C model.

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Section: Discussionmentioning

confidence: 78%

Connexin43-dependent mechanism modulates renin secretion and hypertension

Haefliger¹

2006

Journal of Clinical Investigation

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“…[2][3][4][5][6] In contrast to the reduced NO-mediated relaxation, ACh-induced, EDHF-like relaxation was upregulated in mesenteric arteries of DS rats fed a high-salt diet in this study. As the overall endotheliumdependent vasodilation to ACh was preserved in the mesenteric arteries of DS rats fed a high-salt diet, it appears that upregulation of EDHF compensates for the loss of NO.…”

Section: Discussionmentioning

confidence: 93%

“…[1][2][3][4][5][6] In disease states, such as hypertension, this balance is disrupted that leads to endothelial dysfunction. 7,8 Although the mechanisms for endothelial dysfunction during hypertension may vary depending on the animal models studied, many previous studies have described diminished NO-mediated vasodilation as a principal factor for endothelial dysfunction during hypertension.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of endothelium-derived hyperpolarizing factor compensates for the loss of nitric oxide in mesenteric arteries of dahl salt-sensitive hypertensive rats

et al. 2012

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This study was designed to determine whether a high-salt diet would alter endothelial function and, if so, the relative contributions of endothelium-derived hyperpolarizing factor (EDHF) and nitric oxide (NO) to any changes in vasomotor responses. Male Dahl salt-sensitive (DS) rats were given either a high-salt diet (8% NaCl, DS-H) or a low-salt diet (0.4% NaCl, DS-L) for 6 weeks. Membrane potentials and contractile responses were recorded from the isolated superior mesenteric arteries. After salt loading, DS-H developed hypertension, while DS-L remained normotensive. No difference was found in acetylcholine (ACh)-induced, endothelium-dependent relaxation between the groups. However, after treatment with indomethacin and NO synthase inhibitor, EDHF-like relaxation was significantly greater in DS-H than in DS-L. In contrast, NO-mediated relaxation was significantly smaller in DS-Hthan in DS-L. Iberiotoxin (IbTx), a specific blocker of large-conductance calcium-dependent potassium (BKCa) channels, attenuated EDHF-like relaxation in DS-H but not in DS-L. IbTx marginally inhibited EDHFmediated hyperpolarization only in DS-H. Endothelium-independent relaxation in response to sodium nitroprusside or levcromakalim was similar in both groups. In conclusion, EDHF-like relaxation is upregulated through the activation of BKCa channels in the mesenteric arteries of DS-H. As the overall relaxation in response to ACh did not differ between the groups, the upregulation of EDHF appears to compensate for the loss of NO in the mesenteric arteries of DS-H.

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“…In contrast, Karamsetty et al (34) observed that thapsigargin-induced relaxation of isolated rat intralobar pulmonary arteries was blocked by NOS inhibition, suggesting the response did not involve EDHF. A likely explanation for this difference is that whereas endothelium-dependent relaxation of conduit arteries is mediated largely by NO, EDHF activity is generally more important in peripheral resistance arteries (29,30,46,49), which would have been responsible for the changes in perfusion pressure in the perfused lungs.…”

Section: Discussionmentioning

confidence: 99%

EDHF-mediated vasodilation involves different mechanisms in normotensive and hypertensive rat lungs

Morio

Carter

Oka

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. EDHF-mediated vasodilation involves different mechanisms in normotensive and hypertensive rat lungs. Am J Physiol Heart Circ Physiol 284: H1762-H1770, 2003. First published January 9, 2003 10.1152/ajpheart.00831.2002The role of endothelium-derived hyperpolarizing factor (EDHF) in regulating the pulmonary circulation and the participation of cytochrome P-450 (CYP450) activity and gap junction intercellular communication in EDHF-mediated pulmonary vasodilation are unclear. We tested whether tonic EDHF activity regulated pulmonary vascular tone and examined the mechanism of EDHF-mediated pulmonary vasodilation induced by thapsigargin in salt solution-perfused normotensive and hypoxia-induced hypertensive rat lungs. After blockade of both cyclooxygenase and nitric oxide synthase, inhibition of EDHF with charybdotoxin plus apamin did not affect either normotensive or hypertensive vascular tone or acute hypoxic vasoconstriction but abolished thapsigargin vasodilation in both groups of lungs. The CYP450 inhibitors 7-ethoxyresorufin and sulfaphenazole and the gap junction inhibitor palmitoleic acid, but not 18␣-glycyrrhetinic acid, inhibited thapsigargin vasodilation in normotensive lungs. None of these agents inhibited the vasodilation in hypertensive lungs. Thus tonic EDHF activity does not regulate either normotensive or hypertensive pulmonary vascular tone or acute hypoxic vasoconstriction. Whereas thapsigargin-induced EDHF-mediated vasodilation in normotensive rat lungs involves CYP450 activity and might act through gap junctions, the mechanism of vasodilation is apparently different in hypertensive lungs. pulmonary vasoregulation; pulmonary hypertension; endothelium-derived hyperpolarizing factor; cytochrome P-

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Heterogeneous control of blood flow amongst different vascular beds

Cited by 50 publications

References 171 publications

Connexin43-dependent mechanism modulates renin secretion and hypertension

Connexin43-dependent mechanism modulates renin secretion and hypertension

Upregulation of endothelium-derived hyperpolarizing factor compensates for the loss of nitric oxide in mesenteric arteries of dahl salt-sensitive hypertensive rats

EDHF-mediated vasodilation involves different mechanisms in normotensive and hypertensive rat lungs

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