Characteristics and possible mechanisms of low - Na+ induced contractions in rat aorta

Toma, Catalin; Şerban, Dragomir Nicolae; Branisteanu, Victor Costache Dimitrie D.

doi:10.1007/bf00169194

Cited by 3 publications

(1 citation statement)

References 18 publications

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“…The adrenergic neuron blocker guanethidine (3 μ M ), which was present for 30 min before testing, showed no effect on low Na + ‐induced constriction in these endothelium‐denuded aortic rings (Figure 1a), indicating that sympathetic nerves were not involved. Guanethidine was found to be an effective adrenergic neuron transmission blocker in rat aorta at a concentration of 3 μ M ( Berry et al ., 1992 ; Toma et al ., 1995 ). The NCX inhibitor KB‐R7943 (1 μ M ) significantly attenuated this effect of lowering [Na + ] o (Figure 2a).…”

Section: Resultsmentioning

confidence: 99%

Endothelial nitric oxide attenuates Na⁺/Ca²⁺ exchanger‐mediated vasoconstriction in rat aorta

Zhao

Majewski

2008

British J Pharmacology

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Background and purpose: The Na þ /Ca 2 þ exchanger (NCX) may be an important modulator of Ca 2 þ entry and exit. The present study investigated whether NCX was affected by prostacyclin and nitric oxide (NO) released from the vascular endothelium, as NCX contains phosphorylation sites for PKA and PKG. Experimental approach: Rat aortic rings were set up in organ baths. Tension was measured across the ring with a force transducer. Key results: Lowering extracellular [Na þ ] ([Na þ ] o ) to 1.18 mM induced vasoconstriction in rat endothelium-denuded aortic rings. This effect was blocked by the NCX inhibitor KB-R7943 (2-2-[4-(4-nitrobenzyloxy)phenyl] ethyl isothiourea methanesulphonate; 1 mM). In endothelium-intact aortic rings, decreasing [Na þ ] o did not constrict the aortic rings significantly, but after treatment with the guanylate cyclase inhibitor ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; 1 mM) or the NOS inhibitor L-NAME (N o -nitro-L-arginine methyl ester; 50 mM), a vasoconstriction that was similar in size to that in endothelium-denuded preparations was evident. The vasorelaxation induced by the NO donor sodium nitroprusside sodium nitroprusside dihydrate (30 nM) was the same in the endothelium-denuded aortic rings preconstricted with either low Na þ (1.18 mM), the thromboxane A2 agonist U46619 (9,11-dideoxy-9a, 11a-methanoepoxy prostaglandin F 2a ; 0.1 mM) or high K þ (80 mM). Conclusions and implications:The results suggest that the endothelium inhibits NCX operation via guanylate cyclase/NO. This is stronger than for other constrictors such as phenylephrine and may relate to concomitant NCX-stimulated NO release from the endothelium. This finding may be important where NCX operates in reverse mode, such as during ischaemia, and highlights a new mechanism whereby the endothelium modulates Ca 2 þ homoeostasis in vascular smooth muscle.

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Section: Resultsmentioning

confidence: 99%

Endothelial nitric oxide attenuates Na⁺/Ca²⁺ exchanger‐mediated vasoconstriction in rat aorta

Zhao

Majewski

2008

British J Pharmacology

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KATP channel opening does not contribute significantly to the vasodilatory effect of SH-group-containing ACE inhibitors

et al. 1996

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Angiotensin-converting enzyme (ACE) inhibitors are widely used in the management of hypertension, heart failure, and nephropathy. It has been suggested that ACE inhibitors containing the sulfhydryl group (SH) have an additional effect on KATP channels. To prove this hypothesis, we studied the effects of the SH-containing ACE inhibitors, captopril and zofenopril, on KATP channel opening of bovine coronary arteries and guinea pig thoracic aortas. Bovine coronary arteries were precontracted with the thromboxane A2 analogue, U46619, and guinea pig thoracic aortas were precontracted with phenylephrine and then relaxed with either captopril or zofenopril (n = 8). Inhibition of KATP channel opening with glibenclamide moderately attenuated the zofenopril-induced relaxation of guinea pig thoracic aorta. However, in the bovine coronary arteries, the relaxing effect of both captopril and zofenopril remained uneffected by glibenclamide. In experiments with enalapril (a non SH-containing ACE inhibitor; n = 6) on guinea pig thoracic aortas, no effect on KATP channels could be seen. From our experiments, we conclude that the postulated opening of KATP channels by SH-group-containing ACE inhibitors contributes little to the vasodilation of guinea pig thoracic aortas caused by ACE inhibitors, and that SH groups have no influence upon KATP channels of bovine coronary arteries.

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Differential Regulation of Norepinephrine- and Prostaglandin F2α-Induced Contraction by Extracellular Na+ in Rat Aorta

Rapoport

Campbell²,

Chang³

2000

Journal of Cardiovascular Pharmacology

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The purpose of this study was to test whether extracellular Na+ differentially regulates agonist-induced contraction in vascular smooth muscle. Exposure of rat aorta to 20 nM extracellular Na+ by substitution of 123 mM Na+ with N-methyl-D-glucamine or choline, inhibited norepinephrine-induced contraction to a greater magnitude than contraction to prostaglandin F2alpha. In the absence of extracellular Ca2+ and in 20 mM Na+ solution containing 123 mM N-methyl-D-glucamine, the norepinephrine and prostaglandin F2alpha contraction remained unaltered. In contrast, in the absence of extracellular Ca2+ and in 20 mM Na+ solution containing 123 mM choline, the norepinephrine and prostaglandin F2alpha contraction were decreased and increased, respectively. Contraction to the phorbol ester, phorbol dibutyrate, was inhibited in 20 mM extracellular Na+ solution containing N-methyl-D-glucamine. Removal of extracellular Ca2+ inhibited the phorbol dibutyrate contraction, and 20 mM extracellular Na+ solution containing N-methyl-D-glucamine did not inhibit the phorbol dibutyrate contraction elicited in the absence of extracellular Ca2+. Complete replacement of extracellular Na+ with choline, and concomitant treatment with nifedipine to reduce the elevated basal tone after Na+ replacement, also resulted in greater inhibition of norepinephrine- as compared with prostaglandin F2alpha-induced contraction. Ethylisopropylamiloride, a Na+/H+ exchange inhibitor, did not alter norepinephrine contraction, as determined in the presence of nifedipine to reduce the elevated basal tone due to ethylisopropylamiloride. Acidification, which may result from decreased Na+/H+ exchange, inhibited the prostaglandin F2alpha-induced contraction to a greater magnitude than contraction to norepinephrine. These results demonstrate that extracellular Na+ selectively regulates agonist-induced contraction. The study further suggests that the selectivity may be related to an extracellular Na+-dependent process that is activated by protein kinase C, such as Na+/Ca2+ exchange, and is unrelated to the release of intracellular Ca2+ and Na+/H+ exchange.

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Characteristics and possible mechanisms of low - Na+ induced contractions in rat aorta

Cited by 3 publications

References 18 publications

Endothelial nitric oxide attenuates Na⁺/Ca²⁺ exchanger‐mediated vasoconstriction in rat aorta

Endothelial nitric oxide attenuates Na⁺/Ca²⁺ exchanger‐mediated vasoconstriction in rat aorta

KATP channel opening does not contribute significantly to the vasodilatory effect of SH-group-containing ACE inhibitors

Differential Regulation of Norepinephrine- and Prostaglandin F2α-Induced Contraction by Extracellular Na+ in Rat Aorta

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Characteristics and possible mechanisms of low - Na+ induced contractions in rat aorta

Cited by 3 publications

References 18 publications

Endothelial nitric oxide attenuates Na+/Ca2+ exchanger‐mediated vasoconstriction in rat aorta

Endothelial nitric oxide attenuates Na+/Ca2+ exchanger‐mediated vasoconstriction in rat aorta

KATP channel opening does not contribute significantly to the vasodilatory effect of SH-group-containing ACE inhibitors

Differential Regulation of Norepinephrine- and Prostaglandin F2α-Induced Contraction by Extracellular Na+ in Rat Aorta

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Endothelial nitric oxide attenuates Na⁺/Ca²⁺ exchanger‐mediated vasoconstriction in rat aorta

Endothelial nitric oxide attenuates Na⁺/Ca²⁺ exchanger‐mediated vasoconstriction in rat aorta