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Caudal Artery (caudal + artery)

Distribution by Scientific Domains

Medical Sciences	62%
Life Sciences	37%

Selected Abstracts

The ,-adrenoceptor antagonist, zolertine, inhibits ,1D- and ,1A-adrenoceptor-mediated vasoconstriction in vitro

AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 3 2000
M. Ibarra
1 The antagonist effect of zolertine (4-phenyl-1-[2-(5-tetrazolyl)ethyl]piperazine trihydrochloride), on vascular contraction elicited by noradrenaline in aorta, carotid (,1D-adrenoceptors), mesenteric (,1A/D-adrenoceptors) and caudal arteries (,1A-adrenoceptors) from Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats and rabbit aorta (,1B-adrenoceptors), was investigated in endothelium-denuded arterial rings. 2 The selective ,1D-adrenoceptor agonist, noradrenaline, elicited concentration-dependent contractions in all arterial rings from both species. Noradrenaline selectivity was: carotid=aorta>>.Gt;mesenteric=rabbit aorta>caudal arteries. 3 The contractile responses induced by noradrenaline were competitively antagonized by zolertine in rat carotid and aorta arteries, yielding pA2 values of WKY, 7.48±0.18; SHR, 7.43±0.13 and WKY, 7.57±0.24; SHR, 7.40±0.08, respectively. Zolertine was a non-competitive antagonist in some blood vessels as Schild plot slopes were lower than unity. The pKb estimates for zolertine were WKY, 6.98±0.16; SHR, 6.81±0.18 in the mesenteric artery, WKY, 5.73±0.11; SHR, 5.87±0.25 in the caudal artery and 6.65±0.09 in rabbit aorta. 4 Competition binding experiments using the ,1-adrenoceptor antagonist [3H]prazosin showed a zolertine pKi of 6.81±0.02 in rat liver (,1B-adrenoceptors) and 6.35±0.04 in rabbit liver (,1A-adrenoceptors) membranes. 5 Zolertine showed higher affinity for ,1D-adrenoceptors compared to ,1A-adrenoceptors, while it had an intermediate affinity for ,1B-adrenoceptors. The ability of the ,1-adrenoceptor antagonist zolertine to block ,1D-adrenoceptor-mediated constriction in different vessels of WKY and SHR rats may explain its antihypertensive efficacy despite its low order of potency. [source]

DYSFUNCTION OF PURINERGIC REGULATION OF SYMPATHETIC NEUROTRANSMISSION IN SHR/NDMCR-CP (SHR-CP) RAT

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2004
Naoko Tanaka
SUMMARY 1.,The effect of 2-chloroadenosine (2CA), a P1 receptor agonist and ,,,-methylene ATP (,,mATP), a P2 receptor agonist, on the overflow of endogenous noradrenaline (NE) and the contractile response were examined in the electrically field-stimulated (EFS) (1 Hz) caudal artery obtained from Wistar-Kyoto (WKY) and SHR/NDmcr-cp (SHR-cp) rats. 2.,Both 2CA and ,,mATP reduced the EFS-evoked release of NE from the arteries of WKY. Also, 2CA significantly reduced the EFS-evoked contractile response in WKY, while it had no effect at all in SHR-cp. ,,mATP significantly reduced the EFS-evoked contractile response in both WKY and SHR-cp. Both 2CA and ,,mATP did not affect the contractile response induced by NE at 1 µmol/L. 3.,These results indicate that in the caudal arteries of SHR-cp, the P2 agonist but not the P1 agonist is functional in the prejunctional inhibitory regulation of adrenergic neurotransmission. This P1 dysfunction may play a role in the sympathetic hyperinnervation in metabolic syndrome. [source]

,-Adrenergic and neuropeptide Y Y1 receptor control of collateral circuit conductance: influence of exercise training

THE JOURNAL OF PHYSIOLOGY, Issue 24 2008
Jessica C. Taylor
This study evaluated the role of ,-adrenergic receptor- and neuropeptide Y (NPY) Y1 receptor-mediated vasoconstriction in the collateral circuit of the hind limb. Animals were evaluated either the same day (Acute) or 3 weeks following occlusion of the femoral artery; the 3-week animals were in turn limited to cage activity (Sed) or given daily exercise (Trained). Collateral-dependent blood flows (BFs) were measured during exercise with microspheres before and after ,-receptor inhibition (phentolamine) and then NPY Y1 receptor inhibition (BIBP 3226) at the same running speed. Blood pressures (BPs) were measured above (caudal artery) and below (distal femoral artery) the collateral circuit. Arterial BPs were reduced by ,-inhibition (50,60 mmHg) to ,75 mmHg, but not further by NPY Y1 receptor inhibition. Effective experimental sympatholysis was verified by 50,100% increases (P < 0.001) in conductance of active muscles not affected by femoral occlusion with receptor inhibition. In the absence of receptor inhibition, vascular conductance of the collateral circuit was minimal in the Acute group (0.13 ± 0.02), increased over time in the Sed group (0.41 ± 0.03; P < 0.001), and increased further in the Trained group (0.53 ± 0.03; P < 0.02). Combined receptor inhibition increased collateral circuit conductances (P < 0.005), most in the Acute group (116 ± 37%; P < 0.02), as compared to the Sed (41 ± 6.6%; P < 0.001) and Trained (31 ± 5.6%; P < 0.001) groups. Thus, while the sympathetic influence of the collateral circuit remained in the Sed and Trained animals, it became less influential with time post-occlusion. Collateral conductances were collectively greater (P < 0.01) in the Trained as compared to Sed group, irrespective of the presence or absence of receptor inhibition. Conductances of the active ischaemic calf muscle, with combined receptor inhibition, were suboptimal in the Acute group, but increased in Sed and Trained animals to exceptionally high values (e.g. red fibre section of the gastrocnemius: ,7 ml min,1 (100 g),1 mmHg,1). Thus, occlusion of the femoral artery promulgated vascular adaptations, even in vessels that are not part of the collateral circuit. The presence of active sympathetic control of the collateral circuit, even with exercise training, raises the potential for reductions in collateral BF below that possible by the structure of the collateral circuit. However, even with release of this sympathetic vasoconstriction, conductance of the collateral circuit was significantly greater with exercise training, probably due to the network of structurally larger collateral vessels. [source]

,-Adrenergic inhibition increases collateral circuit conductance in rats following acute occlusion of the femoral artery

THE JOURNAL OF PHYSIOLOGY, Issue 6 2008
Jessica C. Taylor
This study evaluated whether ,-adrenergic activation contributes to collateral circuit vascular resistance in the hindlimb following acute unilateral occlusion of the femoral artery in rats. Blood pressures (BPs) were measured above (caudal artery) and below (distal femoral artery) the collateral circuit. Arterial BPs were reduced (15,35 mmHg) with individual (prazosin, rauwolscine) or combined (phentolamine) ,-receptor inhibition. Blood flows (BFs) were measured using microspheres before and after , inhibition during the same treadmill speed. ,1 inhibition increased blood flow by ,40% to active muscles that were not affected by femoral occlusion, whereas collateral-dependent BFs to the calf muscles were reduced by 29 ± 8.4% (P < 0.05), due to a decrease in muscle conductance with no change in collateral circuit conductance. ,2 inhibition decreased both collateral circuit (39 ± 6.0%; P < 0.05) and calf muscle conductance (36 ± 7.3%; P < 0.05), probably due to residual ,1 activation, since renal BF was markedly reduced with rauwolscine. Most importantly, inhibiting ,2 receptors in the presence of ,1 inhibition increased (43 ± 12%; P < 0.05) collateral circuit conductance. Similarly, non-selective , inhibition with phentolamine increased collateral conductance (242 ± 59%; P < 0.05). We interpret these findings to indicate that both ,1 - and ,2 -receptor activation can influence collateral circuit resistance in vivo during the high flow demands caused by exercise. Furthermore, we observed a reduced maximal conductances of active muscles that were ischaemic. Our findings imply that in the presence of excessive sympathetic activation, which can occur in the condition of intermittent claudication during exertion, an exaggerated vasoconstriction of the existing collateral circuit and active muscle will occur. [source]

Macroscopic Features of the Arterial Supply to the Reproductive System of the Male Ostrich (Struthio camelus)

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 4 2007
M. Z. J. Elias
Summary The macroscopic features of the arterial supply to the reproductive system of the male ostrich was studied in 16 pre-pubertal and eight sexually mature and active birds. The left and right cranial renal arteries arise from the aorta, between the cranial divisions of the kidneys. These vessels supply the cranial divisions of the kidneys, the testes, the epididymides and the cranial segments of the ducti deferentia. Accessory testicular arteries which arise directly from the aorta are present in 45.8% of the specimens. They supply the testes and cranial parts of the ducti deferentia. They are variable in number and origin, and four variants are identified. A cranial ureterodeferential branch originates from the cranial renal artery, supplies the cranial portion of the ductus deferens and ureter, and runs caudally to anastomose with the middle renal artery. The sciatic artery arises laterally from the aorta, just caudal to the acetabulum, and gives rise, ventrally, to a common trunk, the common renal artery, which divides into the middle and caudal renal arteries. The middle renal artery gives rise to the middle ureterodeferential branch which supplies the middle part of the ductus deferens and ureter. A few centimetres caudal to the kidney, the aorta terminates in three branches, namely, the left and right internal iliac arteries and the median caudal artery. The internal iliac artery divides into the lateral caudal artery and the pudendal artery; the latter gives off caudal ureterodeferential branches that supply the caudal segments of the ductus deferens and ureter. In addition, the pudendal artery gives off vessels that supply the cloaca, some of which continue to the base of the phallus, where they form an arterial network. In conclusion, the pattern of the blood supply to the reproductive organs of the male ostrich is, in general, similar to that of the domestic fowl and pigeon, although there are a few highlighted distinctive features. [source]

The Influence of Cannulation Technique on Blood Flow to the Brain in Rats Undergoing Cardiopulmonary Bypass: A Cautionary "Tail"

ARTIFICIAL ORGANS, Issue 6 2010
Terence Gourlay
Abstract Recently, there has been an increase in the use of rat models of cardiopulmonary bypass (CPB) for research purposes. Much of this work has focused on cerebral injury associated with CPB. Many of these studies employ a peripheral cannulation approach, often utilizing the caudal artery and internal or external jugular vein. The aim of the present study was to establish whether there is any alteration in blood flow to the brain associated with the use of different cannulation routes. Twenty-four adult male Sprague Dawley rats were allocated to one of three study groups: Group 1,caudal artery return, Group 2,open-chest aortic return, and Group 3,nonbypass control group. Colored microspheres were injected into all animals at four time points (postinduction, initiation of bypass, midbypass, and end bypass). After the termination of each experiment, the brains were excised, the tissue was digested, the microspheres were harvested, and the global blood flow to the brain was assessed using the reference flow method. There was a significant reduction in blood flow to the brain between both bypass groups and the control group. Additionally, cerebral blood flow was significantly lower in the caudal return group than in the aortic return group. There is a significant drop in blood flow to the brain associated with the initiation and continuation of CPB when compared to non-CPB controls. These results also confirm a considerable cerebral hypoperfusion associated with the peripheral cannulation technique, and suggest that peripheral bypass may exaggerate the influence CPB has on cerebral injury. This technique must therefore be employed with caution. [source]