Effects of pertussis and cholera toxins on α-adrenoceptor function in rat tail artery: differences in hypertension

1993 ◽  
Vol 71 (10-11) ◽  
pp. 791-799 ◽  
Author(s):  
Xiao-Fang Li ◽  
Christopher R. Triggle
Keyword(s):  
Cholera Toxin ◽  
Pertussis Toxin ◽  
Rat Tail Artery ◽  
Response Curves ◽  
Contractile Responses ◽  
Tail Artery ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
The Right ◽  
Rat Tail

The α1- and α2-adrenoceptor-stimulated contractile responses of rat tail artery rings were compared in Sprague–Dawley (SD), spontaneously hypertensive (SHR), and Wistar–Kyoto (WKY) rats that were untreated, treated with pertussis toxin, or treated with cholera toxin. The maximal responses, expressed as milligrams of tension, induced by clonidine (an α2-adrenoceptor agonist) and cirazoline (a selective (α1-adrenoceptor agonist) were significantly greater in SHR than in SD or WKY, and the tissues were more sensitive to the agonists in SHR or SD than in WKY. Yohimbine (0.1 μM), a selective α2-adrenoceptor antagonist, shifted the dose–response curves for clonidine to the right. The effects of yohimbine were greater in SD than in WKY or SHR, but not different between WKY and SHR. Prazosin (0.05 μM), a selective α1-adrenoceptor antagonist, shifted the dose–response curves of cirazoline to the right, but the effects of prazosin were not different among these three strains of rats. Nifedipine (0.05 μM) completely blocked the response to clonidine in SD and WKY; however, in SHR, approximately one-third of the response to clonidine was resistant to nifedipine. Nifedipine, at 0.05 μM, only partially inhibited responses to cirazoline in SD, SHR, and WKY, and no differences were noted between the strains. Pertussis toxin pretreatment (50 μg/kg, 3 days before experiment) almost completely blocked the responses to clonidine, but only partially inhibited those to cirazoline. After pertussis toxin pretreatment, the responses (maximal effects and EC50s) to clonidine and cirazoline were not significantly different in arteries from the three strains of rats. A combination of pertussis toxin and nifedipine resulted in an additive inhibition of the responses induced by cirazoline. cholera toxin pretreatment (0.3 mg/kg, 3 days before experiment), however, had no effects on the contractile responses induced by either clonidine or cirazoline, or on the inhibitory effects of nifedipine in SHR, SD, and WKY. These results indicate that (i) the maximal responses to α1- and α2-adrenoceptor agonists are enhanced in rat tail artery rings from SHR; (ii) tissues from SH and SD rats are also more sensitive to cirazoline and clonidine than are tissues from WKY; (iii) responses to clonidine, but not cirazoline, in tissues from the SHR are less sensitive to nifedipine than tissues from SD and WKY; (iv) a G-protein sensitive to pertussis but not cholera toxin is involved in the regulation of both α1 and α2-adrenoceptor signal transduction processes in rat tail artery smooth muscle; and (v) pretreatment with pertussis toxin reduces the enhanced response levels of SHR tissues so that the maximal contractile responses to both α1- and α2-adrenoceptor agonists are equivalent in arteries from the three strains of rats.Key words: pertussis toxin, cholera toxin, α1-adrenoceptor, α2-adrenoceptor, rat tail artery ring.

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.

scholarly journals Pertussis toxin-sensitive Gi -proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

2000 ◽  
Vol 131 (7) ◽  
pp. 1337-1344 ◽  
Author(s):  
E Spitzbarth-Régrigny ◽  
M -A Petitcolin ◽  
J -L Bueb ◽  
E J Tschirhart ◽  
J Atkinson ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Pertussis Toxin ◽  
Calcium Sensitivity ◽  
Rat Tail Artery ◽  
Tail Artery ◽  
Rat Tail ◽  
Gi Proteins

Postsynaptic α-adrenoceptor characterization and Ca2+ channel antagonist and activator actions in rat tail arteries from normotensive and hypertensive animals

1986 ◽  
Vol 64 (7) ◽  
pp. 909-921 ◽  
Author(s):  
C. M. Su ◽  
V. C. Swamy ◽  
D. J. Triggle
Keyword(s):  
Rank Order ◽  
Rat Tail Artery ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tail Artery ◽  
Mechanical Responses ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Wistar Kyoto ◽  
Rat Tail

Postsynaptic α-adrenoceptors in the rat tail artery have been examined by determining the pA2 values for antagonists against several α-adrenoceptor agonists. In this tissue the α-adrenoceptor agonists all produce concentration-dependent mechanical responses with the following rank order of potency: clonidine > norepinephrine > phenylephrine > UK 14304 > B-HT 920. Antagonism by prazosin and yohimbine of phenylephrine, norepinephrine, and clonidine responses does not reveal the anticipated discrimination between α1- and α2-adrenoceptors. Thus, pA2 values for prazosin (9.1–9.5), yohimbine (7.2–7.4), and corynanthine (7.0–7.1) and idazoxan (7.6) do not show large differences between these receptor agonists and suggests the predominance of α1-adrenoceptor mediated contractile responses in this preparation. Significant differences between antagonist activities (pA2 values) in Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) artery preparations have not been observed. The sensitivity sequence of α-adrenoceptor agonist-induced responses to nifedipine and D 600 is B-HT 920 > clonidine > phenylephrine > norepinephrine. Dependence of agonist response upon extracellular Ca2+ parallels the sensitivity to Ca2+ channel antagonists. Sensitivity to D 600 of phenylephrine responses increased with decreasing concentration of phenylephrine or with receptor blockade by phenoxybenzamine: sensitivity of responses to B-HT 920 was not affected by these procedures. Tail artery strips from WKY and SHR do not exhibit major differences in sensitivity to D 600 or to Ca2+ depletion. Bay k 8644, a Ca2+ channel activator, produces concentration-dependent mechanical responses in the tail artery in the presence of modestly elevated K+ concentrations (10–15 mM): these actions of elevated K+ can be mimicked by both α1- and α2-adrenoceptor agonists including methoxamine, St 587, UK 14304, and clonidine. These studies do not provide clear evidence for the existence of discrete postsynaptic α1- and α2-adrenoceptor populations in rat tail artery as indicated by pA2 values or Ca2+ dependence of response.

Ovariectomy eliminates sex differences in rat tail artery response to adrenergic nerve stimulation

1997 ◽  
Vol 272 (4) ◽  
pp. H1819-H1825 ◽  
Author(s):  
Z. Li ◽  
D. N. Krause ◽  
S. Doolen ◽  
S. P. Duckles
Keyword(s):  
Nerve Stimulation ◽  
Gonadal Hormones ◽  
Adrenergic Nerve ◽  
Rat Tail Artery ◽  
Vascular Response ◽  
Contractile Responses ◽  
Tail Artery ◽  
Resting Tension ◽  
Low Concentrations ◽  
Rat Tail

The influence of gonadal hormones on vasoconstrictor responses to adrenergic nerve stimulation was investigated by comparing tail arteries from intact and gonadectomized male and female Fisher 344 rats. Arterial ring segments from females were significantly less responsive to transmural nerve stimulation (1-8 Hz) than arteries from age-matched males. Significant male-female differences persisted after correcting the contractile responses for sex-related differences in arterial mass, optimal resting tension, and maximal contractile force. Arteries were taken from cycling, intact females in either proestrus, estrus, metestrus, or diestrus, but no significant differences were found among the four stages for vasoconstrictor responses to either adrenergic nerve stimulation or exogenous norepinephrine. These data suggest adrenergic function in the artery is not affected by hormonal variations during the estrous cycle. After bilateral ovariectomy, however, contractile responses of female arteries to adrenergic nerve stimulation were increased to levels similar to those observed in male arteries. Orchidectomy of males, in contrast, had no effect on neural-evoked contraction. Low concentrations of norepinephrine also produced greater contractile responses in male compared with female arteries; however, this sex-related difference was eliminated by orchidectomy but not ovariectomy. Taken together, the results indicate that circulating gonadal hormones contribute to gender differences observed in rat tail artery. Vasoconstrictor responses to exogenous norepinephrine appear to be enhanced by testicular hormones. In contrast, vasoconstriction induced by adrenergic nerve stimulation appears to be influenced by chronic exposure to circulating ovarian hormones, resulting in a smaller vascular response in female arteries.

Effects of varying impulse number on cotransmitter contributions to sympathetic vasoconstriction in rat tail artery

2003 ◽  
Vol 284 (6) ◽  
pp. H2007-H2014 ◽  
Author(s):  
Eamonn Bradley ◽  
Andrea Law ◽  
David Bell ◽  
Christopher D. Johnson
Keyword(s):  
Receptor Antagonist ◽  
Purinergic Receptor ◽  
Rat Tail Artery ◽  
Vascular Responses ◽  
Tail Artery ◽  
Vascular Rings ◽  
Adrenoceptor Antagonist ◽  
Agonist Action ◽  
Sympathetic Vasoconstriction ◽  
Rat Tail

We examined the contributions of the cotransmitters norepinephrine (NE), ATP, and neuropeptide Y (NPY) to sympathetically evoked vasoconstriction in the rat tail artery in isolated vascular rings by using 1–100 stimulation impulses at 20 Hz. Phentolamine (2 μM), the α-adrenoceptor antagonist, markedly reduced responses to all stimuli, although responses to lower impulse numbers were reduced less than responses to longer trains. The purinergic receptor antagonist suramin (100 μM) reduced all responses, but to a much greater extent with few impulse trains. Responses were further reduced or abolished by addition of the second antagonist. Any remaining responses were abolished by the NPY-Y1 receptor antagonist BIBP-3226 (75 nM). NPY had a direct agonist action and potentiated sympathetically mediated responses. NPY (75 nM) potentiated responses and BIBP-3226 decreased responses to 2- and 20-impulse trains. Both affected responses from 2 impulses to >20 impulses, but there was no preferential effect on purinergic contributions to responses because neurally released NPY potentiated both “pure” NE and ATP responses equally. We conclude that all three cotransmitters contribute significantly to vascular responses and their contribution varies markedly with impulse numbers. There is considerable synergy between cotransmitters, especially with lower impulse numbers where NPY contributions are greater than expected.

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