115 research outputs found
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Effect of PPARĪ³ Inhibition during Pregnancy on Posterior Cerebral Artery Function and Structure
Peroxisome proliferator-activated receptor-Ī³ (PPARĪ³), a ligand-activated transcription factor, has protective roles in the cerebral circulation and is highly activated during pregnancy. Thus, we hypothesized that PPARĪ³ is involved in the adaptation of cerebral vasculature to pregnancy. Non-pregnant (NP) and late-pregnant (LP) rats were treated with a specific PPARĪ³ inhibitor GW9662 (10ā]mg/kg/day, in food) or vehicle for 10ādays and vascular function and structural remodeling were determined in isolated and pressurized posterior cerebral arteries (PCA). Expression of PPARĪ³ and angiotensin type 1 receptor (AT1R) in cerebral (pial) vessels was determined by real-time RT-PCR. PPARĪ³ inhibition decreased blood pressure and increased blood glucose in NP rats, but not in LP rats. PPARĪ³ inhibition reduced dilation to acetylcholine and sodium nitroprusside in PCA from NP (pā<ā0.05 vs. LP-GW), but not LP rats. PPARĪ³ inhibition tended to increase basal tone and myogenic activity in PCA from NP rats, but not LP rats. Structurally, PPARĪ³ inhibition increased wall thickness in PCA from both NP and LP rats (pā<ā0.05), but increased distensibility only in PCA from NP rats. Pregnancy decreased expression of PPARĪ³ and AT1R (pā<ā0.05) in cerebral arteries that was not affected by GW9662 treatment. These results suggest that PPARĪ³ inhibition had significant effects on the function and structure of PCA in the NP state, but appeared to have less influence during pregnancy. Down-regulation of PPARĪ³ and AT1R in cerebral arteries may be responsible for the lack of effect of PPARĪ³ in cerebral vasculature and may be part of the vascular adaptation to pregnancy
placental protein 13 pp13 induced vasodilation of resistance arteries from pregnant and nonpregnant rats occurs via endothelial signaling pathways
ABSTRACTPlacental protein 13 (PP13) induces hypotension in rats. This study aims to evaluate PP13 effects on isolated uterine arteries from nonpregnant and mid-pregnant rats. Vessels were isolated, cannulated, and pressurized to 50 mmHg within an arteriograph, preconstricted and exposed to increasing PP13 concentrations (10ā13ā10ā8 M). PP13 elicited 38ā50% arterial vasodilation with half-maximum response (EC50) = 1 pM. The relaxation was mediated by activating the endothelial-signaling pathways of prostaglandin and nitric oxide (NO). Accordingly, these results encourage evaluation of PP13 as a possible therapy for gestational diseases characterized by insufficient uteroplacental blood flow and/or maternal hypertension
Effects of pH on Vascular Tone in Rabbit Basilar Arteries
Effects of pH on vascular tone and L-type Ca2+ channels were investigated using Mulvany myograph and voltage-clamp technique in rabbit basilar arteries. In rabbitbasilar arteries, high K+ produced tonic contractions by 11Ā±0.6 mN (meanĀ±S.E., n=19). When extracellular pH (pHo) was changed from control 7.4 to 7.9 ([alkalosis]o), K+-induced contraction was increased to 128Ā±2.1% of the control (n=13). However, K+-induced contraction was decreased to 73Ā±1.3% of the control at pHo 6.8 ([acidosis]o, n=4). Histamine (10 ĀµM) also produced tonic contraction by 11Ā±0.6 mN (n=17), which was blocked by post-application of nicardipine (1 ĀµM). [alkalosis]o and [acidosis]o increased or decreased histamine-induced contraction to 134Ā±5.7% and 27Ā±7.6% of the control (n=4, 6). Since high K+- and histamine-induced tonic contractions were affected by nicardipine and pHo, the effect of pHo on voltage-dependent L-type Ca2+ channel (VDCCL) was studied. VDCCL was modulated by pHo: the peak value of Ca2+ channel current (IBa) at a holding of 0 mV decreased in [acidosis]o by 41Ā±8.8%, whereas that increased in [alkalosis]o by 35Ā±2.1% (n=3). These results suggested that the external pH regulates vascular tone partly via the modulation of VDCC in rabbit basilar arteries
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Evidence both L-type and non-L-type voltage-dependent calcium channels contribute to cerebral artery vasospasm following loss of NO in the rat
We recently found block of NO synthase in rat middle cerebral artery caused spasm, associated with depolarizing oscillations in membrane potential (Em) similar in form but faster in frequency (circa 1 Hz) to vasomotion. T-type voltage-gated Ca2+ channels contribute to cerebral myogenic tone and vasomotion, so we investigated the significance of T-type and other ion channels for membrane potential oscillations underlying arterial spasm. Smooth muscle cell membrane potential (Em) and tension were measured simultaneously in rat middle cerebral artery. NO synthase blockade caused temporally coupled depolarizing oscillations in cerebrovascular Em with associated vasoconstriction. Both events were accentuated by block of smooth muscle BKCa. Block of T-type channels or inhibition of Na+/K+-ATPase abolished the oscillations in Em and reduced vasoconstriction. Oscillations in Em were either attenuated or accentuated by reducing [Ca2+]o or block of KV, respectively. TRAM-34 attenuated oscillations in both Em and tone, apparently independent of effects against KCa3.1. Thus, rapid depolarizing oscillations in Em and tone observed after endothelial function has been disrupted reflect input from T-type calcium channels in addition to L-type channels, while other depolarizing currents appear to be unimportant. These data suggest that combined block of T and L-type channels may represent an effective approach to reverse cerebral vasospasm
Is Vasomotion in Cerebral Arteries Impaired in Alzheimerās Disease?
A substantial body of evidence supports the hypothesis of a vascular component in the pathogenesis of Alzheimerās disease (AD). Cerebral hypoperfusion and blood-brain barrier dysfunction have been indicated as key elements of this pathway. Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder, frequent in AD, characterized by the accumulation of amyloid-Ī² (AĪ²) peptide in cerebral blood vessel walls. CAA is associated with loss of vascular integrity, resulting in impaired regulation of cerebral circulation, and increased susceptibility to cerebral ischemia, microhemorrhages, and white matter damage. Vasomotionā the spontaneous rhythmic modulation of arterial diameter, typically observed in arteries/arterioles in various vascular beds including the brainā is thought to participate in tissue perfusion and oxygen delivery regulation. Vasomotion is impaired in adverse conditions such as hypoperfusion and hypoxia. The perivascular and glymphatic pathways of AĪ² clearance are thought to be driven by the systolic pulse. Vasomotion produces diameter changes of comparable amplitude, however at lower rates, and could contribute to these mechanisms of AĪ² clearance. In spite of potential clinical interest, studies addressing cerebral vasomotion in the context of AD/CAA are limited. This study reviews the current literature on vasomotion, and hypothesizes potential paths implicating impaired cerebral vasomotion in AD/CAA. AĪ² and oxidative stress cause vascular tone dysregulation through direct effects on vascular cells, and indirect effects mediated by impaired neurovascular coupling. Vascular tone dysregulation is further aggravated by cholinergic deficit and results in depressed cerebrovascular reactivity and (possibly) impaired vasomotion, aggravating regional hypoperfusion and promoting further AĪ² and oxidative stress accumulation
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