scholarly journals Characterization of adrenergic and purinergic contractile responses in rat mesenteric arteries and veins

SURG Journal ◽  
2008 ◽  
Vol 2 (1) ◽  
pp. 30-38
Author(s):  
Rebekah Carter ◽  
Nathan Ludwig
Keyword(s):  
Purinergic Receptors ◽  
Pyridoxal Phosphate ◽  
Sympathetic Neurons ◽  
P2y Receptors ◽  
Mesenteric Arteries ◽  
Disulfonic Acid ◽  
Computer Assisted ◽  
Sprague Dawley ◽  
Contractile Responses ◽  
Arteries And Veins

Norepinephrine (NE) and adenosine 5’-triphosphate (ATP) are neurotransmitters released from sympathetic neurons that act to alter net vascular tone in the mesentery via activation of adrenergic (α1 and α2) and purinergic (P2X and P2Y) receptors. This study was designed to identify adrenergic and purinergic receptors in third order mesenteric arteries and veins in male Sprague-Dawley rats. Agonists and antagonists of adrenergic and purinergic receptors were exogenously applied to vessels and contractile responses were measured using computer assisted video microscopy. NE and ATP both caused contractions of mesenteric arteries and veins. The selective α1 antagonist prazosin attenuated NE-derived constriction of the vessels. The selective α1 agonist phenylephrine was a more efficacious constrictor of both mesenteric arteries and veins than the selective α2 agonist clonidine. The P2X/P2Y1 receptor antagonist pyridoxal-phosphate-6-azophenyl-2’,4-disulfonic acid (PPADS) caused a rightward shift in the ATP dose response curve in mesenteric arteries but not veins. These data indicate that the α1 adrenergic receptors are the primary adrenoreceptors mediating contraction to NE in mesenteric vessels. Additionally, these data suggest that the P2X/P2Y1 receptors mediate substantial contractile responses to ATP in mesenteric arteries but not veins.

scholarly journals Diminished mesenteric vaso- and venoconstriction and elevated plasma ANP and BNP with simulated microgravity

2008 ◽  
Vol 104 (5) ◽  
pp. 1273-1280 ◽  
Author(s):  
Bradley J. Behnke ◽  
David C. Zawieja ◽  
Anatoliy A. Gashev ◽  
Chester A. Ray ◽  
Michael D. Delp
Keyword(s):  
Simulated Microgravity ◽  
Plasma Concentrations ◽  
Bed Rest ◽  
Mesenteric Arteries ◽  
Sprague Dawley ◽  
Adrenergic Stimulation ◽  
Large Pressure ◽  
Arteries And Veins

Diminished constriction of arteries and veins following exposure to microgravity or bed rest is associated with a reduced ability to augment peripheral vascular resistance (PVR) and stroke volume during orthostasis. We tested the hypothesis that small mesenteric arteries and veins, which are not exposed to large pressure shifts during simulated microgravity via head-down tail suspension (HDT), will exhibit decrements in adrenergic constriction after HDT in rats. Small mesenteric arteries and veins from control (Con; n = 41) and HDT ( n = 35) male Sprague-Dawley rats were studied in vitro. Vasoactive responsiveness to norepinephrine (NE) in arteries (10−9 to 10−4 M) and veins (pressure-diameter responses from 2 to 12 cmH2O after incubation in 10−6 or 10−4 M NE) were evaluated. Plasma concentrations of atrial (ANP) and NH2-terminal prohormone brain (NT-proBNP) natriuretic peptides were also measured. In mesenteric arteries, sensitivity and maximal responsiveness to NE were reduced with HDT. In mesenteric veins there was a diminished venoconstriction to NE at any given pressure in HDT. Plasma concentrations of both ANP and NT-proBNP were increased with HDT, and maximal arterial and venous constrictor responses to NE after incubation with 10−7 M ANP or brain natriuretic peptide (BNP) were diminished. These data demonstrate that, in a vascular bed not subjected to large hydrodynamic differences with HDT, both small arteries and veins have a reduced responsiveness to adrenergic stimulation. Elevated levels of circulating ANP or NT-proBNP could adversely affect the ability of these vascular beds to constrict in vivo and conceivably could alter the intrinsic constrictor properties of these vessels with long-term exposure.

scholarly journals P2Y2 receptors mediate ATP-induced resensitization of TRPV1 expressed by kidney projecting sensory neurons

2010 ◽  
Vol 298 (6) ◽  
pp. R1634-R1641 ◽  
Author(s):  
Hui Wang ◽  
Donna H. Wang ◽  
James J. Galligan
Keyword(s):  
Sensory Neurons ◽  
Receptor Agonist ◽  
Pyridoxal Phosphate ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
P2y Receptors ◽  
Receptor Activation ◽  
Sensory Nerves ◽  
Disulfonic Acid ◽  
Transient Receptor Potential Vanilloid

The transient receptor potential vanilloid type 1 (TRPV1) channel is a ligand-gated cation channel expressed by sensory nerves. P2Y receptors are G protein-coupled receptors that are also expressed by TRPV1-positive sensory neurons. Therefore, we studied interactions between P2Y receptors and TRPV1 function on kidney projecting sensory neurons. Application of Fast Blue (FB) to nerves surrounding the renal artery retrogradely labeled neurons in dorsal root ganglia of rats. Whole cell recording was performed on FB-labeled neurons maintained in primary culture. Capsaicin was used to activate TRPV1. Four types of kidney projecting neurons were identified based on capsaicin responses: 1) desensitizing (35%), 2) nondesensitizing (29%), 3) silent (3%), and 4) insensitive (30%). Silent neurons responded to capsaicin only after ATP (100 μM) pretreatment. ATP reversed desensitization in desensitizing neurons. Insensitive neurons never responded to capsaicin. UTP, a P2Y purinoceptor 2 (P2Y2)/P2Y4 receptor agonist, reversed capsaicin-induced TRPV1 desensitization. 2-methyl-thio-ATP (2-Me-S-ATP), a P2Y1 receptor agonist, did not change desensitization. MRS 2179 and pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS), drugs that block P2Y1 receptors, did not block ATP-induced resensitization of TRPV1. Suramin, a P2Y2 receptor antagonist, blocked resensitization caused by UTP. Immunocytochemical studies showed that FB-labeled neurons coexpressed P2Y2 receptors and TRPV1. We conclude that P2Y2 receptor activation can maintain TRPV1 function perhaps during sustained episodes of activity of kidney projecting sensory neurons.

Connexins 37 and 40 transduce purinergic signals mediating renal autoregulation

2008 ◽  
Vol 294 (1) ◽  
pp. R1-R11 ◽  
Author(s):  
Tsuneo Takenaka ◽  
Tsutomu Inoue ◽  
Yoshihiko Kanno ◽  
Hirokazu Okada ◽  
Caryl E. Hill ◽  
...  
Keyword(s):  
Filtration Rate ◽  
Purinergic Receptors ◽  
Pyridoxal Phosphate ◽  
Renal Plasma Flow ◽  
Combined Treatment ◽  
Juxtaglomerular Apparatus ◽  
Disulfonic Acid ◽  
Renal Autoregulation ◽  
Mimetic Peptides ◽  
Wistar Kyoto

Our previous data indicated that various subtypes of connexin (Cx) were expressed in the juxtaglomerular apparatus. Experiments were performed to characterize the effects on renal autoregulation of specific mimetic peptides that inhibit these Cx subtypes in Wistar-Kyoto rats. Intrarenal infusion of Cx37,43GAP27 increased autoregulatory index of renal plasma flow (0.06 ± 0.05 to 0.47 ± 0.06, n = 6, P < 0.05) and glomerular filtration rate (GFR; 0.01 ± 0.07 to 0.49 ± 0.07, P < 0.05). The additional administration of 8-cyclopentyl- 1,3-dipropylxanthine (CPX) produced a further elevation of autoregulatory index of RPF (0.86 ± 0.07, P < 0.05) and GFR (0.88 ± 0.09, P < 0.05), compared with Cx37,43GAP27 alone. However, the addition of pyridoxal-phosphate-6-azophenyl-2,4-disulfonic acid (PPADS) to Cx37,43GAP27 did not. Combined treatment with CPX and PPADS markedly worsened autoregulatory index of RPF (0.04 ± 0.10 to 0.81 ± 0.06, n = 6 P < 0.01) and GFR (0.05 ± 0.08 to 0.79 ± 0.05, P < 0.01). Cx40GAP27 induced similar changes to Cx37,43GAP27. Renal autoregulation was preserved in the presence of Cx43GAP26. Our results indicate that the inhibition of gap junction impaired renal autoregulation. Furthermore, the present data provide evidence that both adenosine and purinergic receptors contribute to glomerular autoregulation. Finally, our findings suggest that gap junctions, at least in part, transduce purinergic signals mediating renal autoregulation.

Do P2X purinergic receptors regulate skeletal muscle blood flow during exercise?

2004 ◽  
Vol 286 (2) ◽  
pp. H633-H639 ◽  
Author(s):  
John B. Buckwalter ◽  
Jessica C. Taylor ◽  
Jason J. Hamann ◽  
Philip S. Clifford
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Femoral Artery ◽  
Purinergic Receptors ◽  
Pyridoxal Phosphate ◽  
Muscle Blood Flow ◽  
Sympathetic Nerves ◽  
P2x Receptor ◽  
Disulfonic Acid ◽  
Skeletal Muscle Blood Flow

Although there is evidence that sympathetic nerves release ATP as a neurotransmitter to produce vasoconstriction via P2X purinergic receptors, the role of these receptors in the regulation of blood flow to exercising skeletal muscle has yet to be determined. We hypothesized that there is tonic P2X receptor-mediated vasoconstriction in exercising skeletal muscle. To test this hypothesis, the effect of P2X receptor blockade on skeletal muscle blood flow was examined in six exercising mongrel dogs. P2X receptor antagonism was accomplished with pyridoxal-phosphate-6-azophenyl-2′4′-disulfonic acid (PPADs). Animals were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. PPADs (40 mg) was infused as a bolus into the femoral artery catheter during steady-state exercise at 6 miles/h. Intra-arterial infusion of PPADs increased iliac blood flow from 542 ± 55 to 677 ± 69 ml/min ( P < 0.05) and iliac vascular conductance from 5.17 ± 0.62 to 6.53 ± 0.80 ml·min–1·mmHg–1. The PPADs infusion did not affect blood flow in the contralateral iliac artery. These data support the hypothesis that P2X purinergic receptors produce vasoconstriction in exercising skeletal muscle.

Acidosis attenuates P2X purinergic vasoconstriction in skeletal muscle arteries

2005 ◽  
Vol 288 (1) ◽  
pp. H129-H132 ◽  
Author(s):  
Heidi A. Kluess ◽  
John B. Buckwalter ◽  
Jason J. Hamann ◽  
Philip S. Clifford
Keyword(s):  
Dose Response ◽  
Purinergic Receptors ◽  
Pyridoxal Phosphate ◽  
Sympathetic Nerves ◽  
Disulfonic Acid ◽  
Response Curves ◽  
Vasoconstrictor Response ◽  
Organ Tissue ◽  
Dose Response Curves ◽  
Krebs Henseleit Buffer

Vasoconstriction via α2-receptors is known to be sensitive to acidic pH, but little is known about the pH sensitivity of P2X receptors. ATP is a cotransmitter released with norepinephrine from the sympathetic nerves and causes vasoconstriction via P2X purinergic receptors on vascular smooth muscle. We hypothesized that reductions in pH would attenuate P2X-mediated vasoconstriction in iliofemoral artery rings. Twenty-five rats were killed, and the iliac and femoral arteries were dissected out and placed in modified Krebs-Henseleit buffer. The arteries were cut into 2-mm sections and mounted in an organ tissue bath. Tension (g) was measured during a potassium chloride and norepinephrine challenge (maximal tension). The arteries were then exposed to α,β-methylene ATP (10−7-10−3 M; n = 13) or phenylephrine (10−7-10−4 M; n = 6) with a tissue bath pH of 7.8, 7.4, and 7.0. Dose-response curves were fit with nonlinear regression analysis to calculate the EC50 and slope. The peak tension with α,β-methylene ATP was lower during pH 7.0 (1.37 ± 0.09 g) compared with pH 7.8 (1.90 ± 0.12 g). EC50 was highest with pH 7.4 (−5.38 ± 0.18 log M α,β-methylene ATP) and lowest with pH 7.0 (−4.9 ± 0.10 log M α,β-methylene ATP). The slopes of the dose-response curves were not different. Pyridoxal phosphate-6-azo(benzene-2,4-disulfonic acid) abolished contraction caused by the addition of α,β-methylene ATP ( n = 6). There was no effect of pH on phenylephrine dose-response curves. These data indicate that the vasoconstrictor response to α,β-methylene ATP is sensitive to pH and that lower pH attenuates the response of P2X purinergic receptors.

scholarly journals Mechanism of the Enhanced Vasoconstrictor Responses to Endothelin-1 in Canine Cerebral Arteries

1991 ◽  
Vol 11 (3) ◽  
pp. 371-379 ◽  
Author(s):  
Chiharu Tanoi ◽  
Yoshio Suzuki ◽  
Masato Shibuya ◽  
Kenichiro Sugita ◽  
Kaoru Masuzawa ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Resting State ◽  
Mesenteric Artery ◽  
Cerebral Arteries ◽  
Mesenteric Arteries ◽  
Free Solution ◽  
Contractile Responses ◽  
Endothelin 1 ◽  
Voltage Dependent ◽  
Small Contraction

Vasoconstrictor effects of endothelin-1 (ET) were investigated in endothelium-denuded strips of cerebral (basilar and posterior cerebral) and mesenteric arteries of the dog. ET produced a concentration-dependent contraction in these arteries. Contractile responses to lower concentrations (below 3 × 10−10 M) of ET were significantly greater in the cerebral arteries than in the mesenteric artery. Inhibition by nifedipine of the contractile responses to ET was greater in the basilar artery than in the mesenteric artery. After the inhibition by 10−7 M nifedipine, the remaining responses to ET were similar in the two arteries. Cerebral arteries, but not the mesenteric artery, relaxed significantly from the resting level when placed in a Ca2+ -free solution containing 0.1 m M EGTA (0-Ca solution). Readdition of Ca2+ to the cerebral arteries placed in the 0-Ca solution caused a biphasic contraction that was sensitive to nifedipine. When 10−9 M ET was introduced before the Ca2+-induced contraction, this peptide produced only a very small contraction, but enhanced the Ca2+-induced contraction. The extent of the enhancement induced by ET was much greater in the cerebral arteries than in the mesenteric artery. These results indicate that the enhanced responses to ET in the cerebral arteries were dependent to a large extent on Ca2+ influx through voltage-dependent Ca2+ channels (VDCs). It is likely that the VDCs in these arteries are more activated in the resting state than those in the mesenteric artery.

Decreased vascular contractile and inositol phosphate responses in portal hypertensive rats

1995 ◽  
Vol 73 (3) ◽  
pp. 378-382 ◽  
Author(s):  
Yi-Tsau Huang ◽  
Chuang-Ye Hong ◽  
Pi-Chin Yu ◽  
Ming-Fang Lee ◽  
May C. M. Yang ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Contractile Response ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Venous Pressure ◽  
Portal Vein Ligation ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Contractile Responses ◽  
Tail Artery

The purpose of this study was to investigate the vascular contractile and inositol phosphate responses in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague–Dawley rats. Sham-operated rats served as controls. Pressures, vasoconstrictor responses, and inositol phosphate responses were determined at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower, in PVL rats. Dose-dependent contractile responses were observed for both norepinephrine (1 × 10−8 – 3 × 10−6 M) and vasopressin (3 × 10−10 – 3 × 10−8 M) in the tail artery of both groups. The contractile response to norepinephrine was significantly decreased in PVL rats compared with controls at all doses. The contractile response to vasopressin was significantly decreased in PVL rats at higher doses. After myo-[3H]inositol incorporation in tail artery, the levels of 3H-labelled phosphatidylinositols (cpm/mg) were similar between the two groups. Norepinephrine (10−7 – 10−5 M) and vasopressin (10−10 – 10−8 M) dose dependently stimulated the 3H-labelled inositol phosphate production in the tail artery of both PVL and sham-operated rats. However, the response was significantly lower in PVL rats. The results suggested that the attenuation of vascular contractile responses in portal hypertension was reflected in the phosphoinositide messenger system.Key words: portal hypertension, inositol phosphates, phosphoinositide, tail artery, contractile response.

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