Bidimensional passive and active mechanical behavior of rat tail artery segments in vitro

1989 ◽  
Vol 84 (4) ◽  
pp. 442-448 ◽  
Author(s):  
K. Pascale
Keyword(s):  
Mechanical Behavior ◽  
Rat Tail Artery ◽  
Tail Artery ◽  
Rat Tail

Persistent release of noradrenaline caused by anticancer drug 4′-epidoxorubicin in rat tail artery in vitro

1998 ◽  
Vol 356 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Toyohiko Sakai ◽  
Rika Inagaki ◽  
Takanobu Taniguchi ◽  
Kazumasa Shinozuka ◽  
Masaru Kunitomo ◽  
...  
Keyword(s):  
Anticancer Drug ◽  
Rat Tail Artery ◽  
Release Of Noradrenaline ◽  
Tail Artery ◽  
Rat Tail

Slow and incomplete sympathetic reinnervation of rat tail artery restores the amplitude of nerve-evoked contractions provided a perivascular plexus is present

2011 ◽  
Vol 300 (2) ◽  
pp. H541-H554 ◽  
Author(s):  
Diana Tripovic ◽  
Svetlana Pianova ◽  
Elspeth M. McLachlan ◽  
James A. Brock
Keyword(s):  
Rat Tail Artery ◽  
Adult Rats ◽  
Tail Artery ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Perivascular Plexus ◽  
Evoked Contractions ◽  
Comparable Amplitude ◽  
Rat Tail

We have investigated the recovery of sympathetic control following reinnervation of denervated rat tail arteries by relating the reappearance of noradrenergic terminals to the amplitude of nerve-evoked contractions of isometrically mounted artery segments in vitro. We have also assessed reactivity to vasoconstrictor agonists. Freezing the collector nerves near the base of the tail in adult rats denervated the artery from ∼40 mm along the tail. Restoration of the perivascular plexus declined along the length of the tail, remaining incomplete for >6 mo. After 4 mo, nerve-evoked contractions were prolonged but of comparable amplitude to control at ∼60 mm along the tail; they were smaller at ∼110 mm. At ∼60 mm, facilitation of contractions to short trains of stimuli by the norepinephrine transporter blocker, desmethylimipramine, and by the α2-adrenoceptor antagonist, idazoxan, was reduced in reinnervated arteries. Blockade of nerve-evoked contractions by the α1-adrenoceptor antagonist, prazosin, was less and by idazoxan greater than control after 8 wk but similar to control after 16 wk. Sensitivity of reinnervated arteries to the α1-adrenoceptor agonist, phenylephrine, was raised in the absence but not in the presence of desmethylimipramine. Sensitivity to the α2-adrenoceptor agonist, clonidine, was maintained in 16-wk reinnervated arteries when it had declined in controls. Thus regenerating sympathetic axons have a limited capacity to reinnervate the rat tail artery, but nerve-evoked contractions match control once a relatively sparse perivascular plexus is reestablished. Functional recovery involves prolongation of contractions and deficits in both clearance of released norepinephrine and autoinhibition of norepinephrine release.

Hydrallazine: Mode of Action at the Neuroarterial Junction

1980 ◽  
Vol 59 (s6) ◽  
pp. 445s-447s ◽  
Author(s):  
C. Chevillard ◽  
B. Saiag ◽  
M. Worcel
Keyword(s):  
Wistar Rats ◽  
Direct Action ◽  
Nerve Terminals ◽  
Rat Tail Artery ◽  
Experimental Conditions ◽  
Tail Artery ◽  
Marked Inhibition ◽  
6 Hydroxydopamine ◽  
Rat Tail

1. Hydrallazine relaxes the rat tail artery by a direct action on vascular smooth muscle cells, which appears to be modulated by the action of sympathetic nerve terminals. 2. There is a gradient of response to hydrallazine in arteries from normotensive Wistar rats, the proximal segments being poorly responsive. This gradient disappears after denervation with 6-hydroxydopamine in vitro. 3. Exogenously added purines inhibit noncompetitively the vasodilator response to hydrallazine in denervated segments from normotensive Wistar rats. Their order of potency is 2-Cl-adenosine > adenosine > ATP > inosine. 4. The effect of hydrallazine in innervated, poorly responsive segments is greatly potentiated by theophylline (50 μmol/l) and propranolol (5 μmol/l). These results, together with the effect of denervation, suggest that there are endogenous purines leaking from the nerve terminals under our experimental conditions. 5. Hydrallazine produces a marked inhibition of stimulus-induced contraction and 3H release after [3H]noradrenaline loading. The mechanism of this prejunctional action appears to be different from the mechanism of the postjunctional effect.

Cyclic AMP and the vascular action of parathyroid hormone

1986 ◽  
Vol 64 (12) ◽  
pp. 1543-1547 ◽  
Author(s):  
Peter K. T. Pang ◽  
May C. M. Yang ◽  
Thomas E. Tenner Jr. ◽  
Alexander D. Kenny ◽  
Cary W. Cooper
Keyword(s):  
Parathyroid Hormone ◽  
Phosphodiesterase Inhibitor ◽  
Rat Tail Artery ◽  
Hypotensive Action ◽  
Camp Content ◽  
Tail Artery ◽  
Anesthetized Dogs ◽  
Active Fragment ◽  
Rat Tail

The involvement of tissue cAMP in the vasodilating action of parathyroid hormone (PTH) was investigated. The bovine active fragment bPTH-(1–34) was used in all studies. In anesthetized dogs, theophylline, a phosphodiesterase inhibitor, potentiated the hypotensive action of bPTH-(1–34) at the dose of 1 μg/kg. The potentiation was related to the dose of theophylline infused. In an in vitro rat tail artery helical strip assay, dibutyryl cAMP produced dose-related relaxation in arginine vasopressin (AVP) constricted blood vessels. bPTH-(1–34) also produced dose-related relaxation in the tail artery constricted by AVP. In the presence of isobutylmethylxanthine, another phosphodiesterase inhibitor, the bPTH-(1–34) dose-response curve was shifted to the left, indicating potentiation. Imidazole, which has phosphodiesterase stimulating activity, significantly decreased the in vitro vasorelaxing effect of bPTH-(1–34). In addition, bPTH-(1–34) increased significantly the rat tail artery cAMP content. b-PTH-(1–34) oxidized with hydrogen peroxide lost its vasorelaxing activity and was also ineffective in increasing the tail artery cAMP content. All these data strongly suggest that cAMP may be involved in eliciting the vasorelaxing action of bPTH-(1–34).

scholarly journals Melatonin potentiates NE-induced vasoconstriction without augmenting cytosolic calcium concentration

2001 ◽  
Vol 280 (1) ◽  
pp. H420-H425 ◽  
Author(s):  
C. Vandeputte ◽  
P. Giummelly ◽  
J. Atkinson ◽  
P. Delagrange ◽  
E. Scalbert ◽  
...  
Keyword(s):  
Calcium Concentration ◽  
Perfusion Pressure ◽  
Cytosolic Calcium ◽  
Rat Tail Artery ◽  
Tail Artery ◽  
Vasoconstrictor Effect ◽  
Intracellular Ca ◽  
In Vitro Effects ◽  
Rat Tail

Because little is known of the intracellular mechanisms involved in the vasoconstrictor effect of melatonin (Mel), we examined the in vitro effects of Mel by using perfused cylindrical segments of the rat tail artery loaded with the intracellular Ca2+ concentration ([Ca2+]i)-sensitive fluorescent dye, fura 2. Mel (10−14 to 10−4 M) had no effect on baseline perfusion pressure or [Ca2+]i but increased, at submicromolar concentrations, the vasoconstrictor effect of norepinephrine (NE) ( P = 0.0029). Mel did not modify NE-induced [Ca2+]i mobilization, and thus the [Ca2+]i sensitivity of NE-induced contraction increased in the presence of Mel. Mel consistently increased KCl-induced vasoconstriction and [Ca2+]isensitivity of contraction, but differences were not statistically significant. In conclusion, Mel increases the [Ca2+]i sensitivity of vasoconstriction evoked by NE suggesting that Mel may amplify endogenous vasoconstrictor responses to sympathetic outflow.

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