Endoplasmic reticulum contribution to the relaxant effect of cGMP- and cAMP-elevating agents in feline aorta

Mundiña‐Weilenmann, Cecilia; Vittone, Leticia; Rinaldi, Gustavo; Said, Matilde; Cingolani, Gladys Chiappe de; Mattiazzi, Alicia

doi:10.1152/ajpheart.2000.278.6.h1856

Cited by 20 publications

(15 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…uptake into the SR via phospholamban phosphorylation and activation of SR Ca 2? -ATPase, with the resultant relaxant effect may be mediated by cGMP-and cAMP-elevating agents, such as sodium nitroprusside and forskolin, as revealed in feline aorta, where this mechanism represents approximately one-third of the total relaxant effect of both compounds, which is consistent with the multiple mechanisms responsible for relaxation in smooth muscle [77].…”

Section: Increased Sequestration In the Srsupporting

confidence: 62%

Cyclic nucleotide-dependent relaxation pathways in vascular smooth muscle

Morgado

Cairrão

Santos-Silva

et al. 2011

Cell. Mol. Life Sci.

169

131

View full text Add to dashboard Cite

Vascular smooth muscle tone is controlled by a balance between the cellular signaling pathways that mediate the generation of force (vasoconstriction) and release of force (vasodilation). The initiation of force is associated with increases in intracellular calcium concentrations, activation of myosin light-chain kinase, increases in the phosphorylation of the regulatory myosin light chains, and actin-myosin crossbridge cycling. There are, however, several signaling pathways modulating Ca(2+) mobilization and Ca(2+) sensitivity of the contractile machinery that secondarily regulate the contractile response of vascular smooth muscle to receptor agonists. Among these regulatory mechanisms involved in the physiological regulation of vascular tone are the cyclic nucleotides (cAMP and cGMP), which are considered the main messengers that mediate vasodilation under physiological conditions. At least four distinct mechanisms are currently thought to be involved in the vasodilator effect of cyclic nucleotides and their dependent protein kinases: (1) the decrease in cytosolic calcium concentration ([Ca(2+)]c), (2) the hyperpolarization of the smooth muscle cell membrane potential, (3) the reduction in the sensitivity of the contractile machinery by decreasing the [Ca(2+)]c sensitivity of myosin light-chain phosphorylation, and (4) the reduction in the sensitivity of the contractile machinery by uncoupling contraction from myosin light-chain phosphorylation. This review focuses on each of these mechanisms involved in cyclic nucleotide-dependent relaxation of vascular smooth muscle under physiological conditions.

show abstract

Section: Increased Sequestration In the Srsupporting

confidence: 62%

Cyclic nucleotide-dependent relaxation pathways in vascular smooth muscle

Morgado

Cairrão

Santos-Silva

et al. 2011

Cell. Mol. Life Sci.

169

131

View full text Add to dashboard Cite

show abstract

“…The greater relaxation induced by SNP and 8-BrcGMP, as well as their lower EC 50 in the denuded HS rings, favors a higher sensitivity of the vascular smooth muscle cells of HS rats to NO-related compounds and suggests that events occurring after cGMP formation are involved. In addition to SERCA activation (15) and actin-myosin complex dissociation (13,27) by cGMP, the enhanced relaxation to 8-BrcGMP observed in the current HS rings may be also related to changes in repolarization through the large-conductance, voltage-dependent, and BK Ca . Highly expressed in the vascular smooth muscle cell (26), BK Ca is involved in the relaxation to ACh and NO donor (4,5,6,19), and cGMP has a role in its modulation (2,20,21).…”

Section: Discussionmentioning

confidence: 87%

“…The stable cGMP analog, 8-bromoadenosine 3Ј5Ј cGMP (8-BrcGMP) was reported to activate the myosin light chain phosphatase of smooth muscle strips isolated from the rabbit femoral artery (13,27). In feline aorta strips, the relaxant effect of nitroprusside and 8-BrcGMP partly occurred via calcium uptake by the endoplasmic reticulum and involves sarcoplasmic reticulum calcium-ATPase (SERCA) (15). cGMP relaxes vascular smooth muscle cells also via hyperpolarization, resulting from activation of cGMP-dependent protein kinase (PKG) and the large-conductance voltage-gated, calcium-sensitive potassium channel (BK Ca ) (2).…”

mentioning

confidence: 99%

Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet

Cordaillat¹,

Fort²,

Virsolvy³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Cordaillat M, Fort A, Virsolvy A, Elghozi J-L, Richard S, Jover B. Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet. Am J Physiol Regul Integr Comp Physiol 292: R1557-R1562, 2007. First published December 21, 2006; doi:10.1152/ajpregu.00624.2006.-Vascular smooth muscle cell contraction and endothelium-dependent relaxation was evaluated in aortic rings isolated from weaned, 5-moold Sprague-Dawley rats fed a normal (NS; 0.8% NaCl) or high (HS; 8% NaCl) sodium diet. Arterial pressure was 140 Ϯ 6 (NS) and 145 Ϯ 6 mmHg (HS). In endothelium-denuded rings, the response to phenylephrine (PE) was not modified by the sodium diet, while that of depolarizing agent KCl and intracellular calcium releasing agent caffeine increased in the HS group. When endothelium was preserved, PE-evoked contraction was reduced in both NS and HS groups, the contraction being yet lower in the HS group. This effect was partially obliterated by addition of N G -nitro-L-arginine methyl ester (L-NAME), independently of the sodium diet. Relaxation to ACh in intact rings and to sodium nitroprusside (SNP) and 8-bromoadenosine 3Ј5Ј cyclic guanosine monophosphate (8-BrcGMP) in the absence of endothelium was enhanced in rings isolated from HS rats. In addition, the dose-response curve to 8-BrcGMP was shifted to the right in the presence of iberiotoxin, an inhibitor of large conductance, voltagedependent, and calcium-sensitive potassium channel (BKCa). However, shift was more marked in rings from HS rats. Present results provide evidence that response of vascular smooth muscle cell to nitric oxide/cGMP-related compounds is increased in HS rings and is associated with a greater activation of the repolarizing BKCa channels. Such changes might counterbalance enhanced contractile response to membrane depolarization and thus participate in maintenance of arterial pressure in the present model of early and long-term HS feeding in rats. vascular smooth muscle cell; endothelial cell; sodium nitroprusside; iberiotoxin.EXCESSIVE CONSUMPTION OF SODIUM is reported to induce cardiac, vascular, and renal alterations in normotensive and hypertensive humans and animals (9, 30). In various strains of rat, a high salt (HS) diet is associated with changes in the reactivity of aortic rings. Many studies conducted in salt-loaded models have shown an increased contraction of vascular smooth muscle cells in response to agonists (1,14). In addition, relaxation evoked by acetylcholine (ACh) or sodium nitroprusside (SNP) was obliterated in aortic rings isolated from adult spontaneously hypertensive and Dalh-sensitive rats fed a 8% NaCl diet for 4 -8 wk (12,14,16). These results suggest that concomitant increase in vascular smooth muscle cell contraction and impaired endothelium-dependent relaxation both participate in the development of hypertension in the salt-sensitive strains. In contrast, an enhanced influence of nitric oxide (NO) may have a major role in the lack of rise in blood pressure of sodiumr...

show abstract

“…In addition, and depending on vascular beds, the endothelial NO pathway has been found to be involved in the relaxation elicited by activation of ␤ARs (8, 28). The final transduction mechanisms of these pathways involve several processes, including membrane hyperpolarization due to opening of K ϩ channels, (34), enhanced Ca 2ϩ sequestration by the endoplasmic reticulum (33), or reduction in Ca 2ϩ sensitization (35). When the femoral arteries were stimulated by high K ϩ (62.5 mM), opening of K ϩ channels could not cause further hyperpolarization and thus could not exert any further relaxation effect (40).…”

Section: Discussionmentioning

confidence: 99%

Hypotension in the chronically hypoxic chicken embryo is related to the β-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia

Lindgren

Crossley

Villamor

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Lindgren I, Crossley II D, Villamor E, Altimiras J. Hypotension in the chronically hypoxic chicken embryo is related to the ␤-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia. Am J Physiol Regul Integr Comp Physiol 301: R1161-R1168, 2011. First published July 27, 2011; doi:10.1152/ajpregu.00458.2010.-Prolonged fetal hypoxia leads to growth restriction and can cause detrimental prenatal and postnatal alterations. The embryonic chicken is a valuable model to study the effects of prenatal hypoxia, but little is known about its long-term effects on cardiovascular regulation. We hypothesized that chicken embryos incubated under chronic hypoxia would be hypotensive due to bradycardia and ␤AR-mediated relaxation of the systemic and/or the chorioallantoic (CA) arteries. We investigated heart rate, blood pressure, and plasma catecholamine levels in 19-day chicken embryos (total incubation 21 days) incubated from day 0 in normoxia or hypoxia (14 -15% O2). Additionally, we studied ␣-adrenoceptor (␣AR)-mediated contraction, relaxation to the ␤-adrenoceptor (␤AR) agonist isoproterenol, and relaxation to the adenylate cyclase activator forskolin in systemic (femoral) and CA arteries (by wire myography). Arterial pressure showed a trend toward hypotension in embryos incubated under chronic hypoxic conditions compared with the controls (mean arterial pressure 3.19 Ϯ 0.18 vs. 2.59 Ϯ 0.13 kPa, normoxia vs. hypoxia, respectively. P ϭ 0.056), without an accompanied bradycardia and elevation in plasma norepinephrine and lactate levels. All vessels relaxed in response to ␤AR stimulation with isoproterenol, but the CA arteries completely lacked an ␣AR response. Furthermore, hypoxia increased the sensitivity of femoral arteries (but not CA arteries) to isoproterenol. Hypoxia also increased the responsiveness of femoral arteries to forskolin. In conclusion, we suggest that hypotension in chronic hypoxic chicken embryos is the consequence of elevated levels of circulating catecholamines acting in vascular beds with exclusive (CA arteries) or exacerbated (femoral arteries) ␤AR-mediated relaxation, and not a consequence of bradycardia. prenatal hypoxia; hypoxic hypotension; chorioallantoic membrane; ␤-adrenoceptors; ␣-adrenoceptors

show abstract

Endoplasmic reticulum contribution to the relaxant effect of cGMP- and cAMP-elevating agents in feline aorta

Cited by 20 publications

References 40 publications

Cyclic nucleotide-dependent relaxation pathways in vascular smooth muscle

Cyclic nucleotide-dependent relaxation pathways in vascular smooth muscle

Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet

Hypotension in the chronically hypoxic chicken embryo is related to the β-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia

Contact Info

Product

Resources

About