Contractile response of normotensive rat aorta to serum from salt-loaded Sprague-Dawley rats

1993 ◽  
Vol 423-423 (1-2) ◽  
pp. 161-163 ◽  
Author(s):  
O. A. Sofola ◽  
P. C. M. Obiefuna ◽  
B. J. Adegunloye
Keyword(s):  
Contractile Response ◽  
Rat Aorta ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals Sexual dimorphism in prostanoid-potentiated vascular contraction: roles of endothelium and ovarian steroids

2002 ◽  
Vol 283 (5) ◽  
pp. H2062-H2073 ◽  
Author(s):  
Clifford T. Fulton ◽  
John N. Stallone
Keyword(s):  
Sexual Dimorphism ◽  
Vascular Reactivity ◽  
Contractile Response ◽  
Rat Aorta ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Similar Extent ◽  
Contractile Responses ◽  
Ovarian Steroids ◽  
Sprague Dawley Rats

The effects of constrictor prostanoid (CP) pathway inhibitors on vascular reactivity to vasopressin (VP) and phenylephrine (PE) were examined in thoracic aortas of male, female, and ovariectomized (OVX) female Sprague-Dawley rats. Maximal contractile response of control (Cont) aortas to VP was markedly higher in females (3,885 ± 332 mg/mg ring wt) than in males (810 ± 148 mg). Indomethacin (Indo; 10 μM) attenuated maximal response to VP in females (3,043 ± 277 mg) but not in males. SQ-29,548 (SQ; 1 μM) attenuated maximal response to VP in females (3,042 ± 290 mg) to a similar extent as Indo. Dazoxiben (Daz; 10 μM) alone had no effect, but Daz + SQ attenuated maximal contractile response to VP to a similar extent as SQ alone. Removal of the endothelium in female aortas attenuated contractile responses to VP in Cont aortas. OVX attenuated maximal contractile response to VP in Cont aortas (2,093 ± 329 mg) and abolished the attenuating effects of Indo. Indo, SQ, and Daz exerted identical effects on contractile responses of male, female, and OVX female aortas to PE. These findings establish the following in the rat aorta: 1) CP, probably thromboxane and/or endoperoxide, is responsible for ∼25–30% of contractile responses of females, but not males, to VP and PE; 2) CP production by the female aorta is primarily endothelial in origin; and 3) ovarian steroids modulate production and/or actions of CP in female aortas.

Sex Differences in the Response of Rat Heart Ventricle to Calcium

2004 ◽  
Vol 5 (4) ◽  
pp. 286-298 ◽  
Author(s):  
Dorie W. Schwertz ◽  
Jenny M. Beck ◽  
Jill M. Kowalski ◽  
James D. Ross
Keyword(s):  
Sex Differences ◽  
Papillary Muscle ◽  
Contractile Response ◽  
Ventricular Myocytes ◽  
Ventricular Myocardium ◽  
Contractile Proteins ◽  
Therapeutic Interventions ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Whole Heart

Calcium (Ca2+ ) is a key mediator of myocardial function. Calcium regulates contraction, and disruption of myocellular Ca2+ handling plays a role in cardiac pathologies such as arrhythmias and heart failure. This investigation examines sex differences in sensitivity of the contractile proteins to Ca2+ and myofibrillar Ca2+ delivery in the ventricular myocardium. Sensitivity of contractile proteins to Ca2+ was measured in weight-matched male and female Sprague-Dawley rats using the skinned ventricular papillary muscle fiber and Ca2+ -stimulated Mg2+ -dependent adenosine triphosphatase (ATPase) activity methodologies. Calcium delivery was examined by measuring the contractile response to a range of extracellular Ca2+ concentrations in isolated ventricular myocytes, papillary muscle, and the isolated perfused whole heart. Findings from studies in the whole heart suggest that at a fixed preload, the male left ventricle generates more pressure than a female ventricle over a range of extracellular Ca2+ concentrations. In contrast, results from myocyte and papillary muscle studies suggest that females require less extracellular Ca2+ to elicit a similar contractile response. Results obtained from the 2 methods used to determine sex differences in Ca2+ sensitivity were equivocal. Further studies are required to elucidate sex differences in myocardial Ca2+ handling and the reasons for disparate results in different heart muscle preparations. The results of these studies will lead to the design of sex-optimized therapeutic interventions for cardiac disease.

Sexual dimorphism in vasopressin-induced contraction of rat aorta

1991 ◽  
Vol 260 (2) ◽  
pp. H453-H458 ◽  
Author(s):  
J. N. Stallone ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Estrous Cycle ◽  
Vascular Reactivity ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Female Rats ◽  
Male Rats ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Tension Development ◽  
Sprague Dawley Rats

Previously, we reported that, in the rat, pressor responsiveness to vasopressin (VP) is higher in males than in females during most phases of the estrous cycle. To explore the role of the vasculature in this phenomenon, we examined vascular reactivity to VP in thoracic aortas of male rats and female rats during each phase of the estrous cycle. Aortic rings were prepared from age-matched male and female Sprague-Dawley rats and mounted for isometric tension recording. Maximal response of female aortas to VP (4,246 +/- 163 mg/mg ring dry wt) was more than twice (P less than 0.001) that of male aortas (1,877 +/- 215 mg/mg ring wt). Sensitivity of female aortas to VP was substantially higher (P less than 0.001) than that of male aortas (EC50: 10.9 +/- 0.7 vs. 19.0 +/- 1.6 nM, respectively). Maximal rate of tension development (dT/dtmax) during contraction with VP was nearly twofold higher (P less than 0.01) in female aortas (536 +/- 23 mg/min) than in male aortas (300 +/- 19 mg/min). Maximal response, sensitivity, and dT/dtmax of female aortas did not vary significantly during the estrous cycle. Maximal response of female aortas to phenylephrine (PE; 1,251 +/- 93 mg/mg ring wt) was half that (P less than 0.001) of male aortas (2,546 +/- 194 mg/mg ring wt); sensitivity to PE did not differ significantly (EC50: 0.33 +/- 0.02 vs. 0.38 +/- 0.06 microM, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Portal hypertension increases vasoconstrictor responsiveness of rat aorta

1999 ◽  
Vol 96 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Claire CONNOLLY ◽  
Teresa CAWLEY ◽  
P. Aiden MCCORMICK ◽  
James R. DOCHERTY
Keyword(s):  
Portal Hypertension ◽  
Wistar Rats ◽  
Rat Aorta ◽  
Maximum Response ◽  
Sprague Dawley ◽  
Portal Vein Stenosis ◽  
Sprague Dawley Rats ◽  
Significant Difference ◽  
Hepatic Portal

We have examined the effects of pre-hepatic portal hypertension on the responsiveness of aorta from Wistar and Sprague–Dawley rats. Rats were made portal hypertensive by creating a calibrated portal vein stenosis, or sham operated. In rat aorta, there was no significant difference between portal hypertensive and sham-operated animals in the contractile potency of KCl, noradrenaline or phenylephrine. In aortas from Wistar rats, the maximum response to KCl (0.71±0.12 ;g) and noradrenaline (1.00±0.17 ;g) but not phenylephrine (0.86±0.10 ;g) in portal hypertensive animals was significantly increased compared with that in sham-operated animals (0.45±0.04 ;g, 0.57±0.07 ;g, 0.71±0.05 ;g respectively). In aortas from Sprague–Dawley rats, the maximum response to KCl (1.21±0.21 ;g) and phenylephrine (1.54±0.30 ;g) but not noradrenaline (0.93±0.09 ;g) in portal hypertensive animals was significantly increased compared with that in sham-operated animals (0.59±0.09 ;g, 0.76±0.11 ;g, 1.04±0.10 ;g respectively). There was no difference between portal hypertensive and sham-operated Wistar rats in the affinity or maximum number of binding sites for [3H]prazosin to α1-adrenoceptors in cardiac ventricular membranes. It is concluded that portal hypertension tends to produce an increase rather than a decrease in the contractile response to vasoconstrictors in aorta from both Wistar and Sprague–Dawley rats. This suggests that the diminished responsiveness to vasoconstrictors reported in portal hypertensive rats in vivo is not due to a diminished responsiveness at the level of the vascular smooth muscle.

Inhibition of Cholinergic Contractions of Rat Ileum by Tropane-Type Alkaloids Present in Schizanthus hookeri

2013 ◽  
Vol 68 (5-6) ◽  
pp. 203-209 ◽  
Author(s):  
Miguel A. Morales ◽  
Frederick Ahumada ◽  
Erick Castillo ◽  
Rafael Burgos ◽  
Philippe Christen ◽  
...  
Keyword(s):  
Side Effects ◽  
Muscarinic Receptors ◽  
Contractile Response ◽  
Tropane Alkaloids ◽  
Sprague Dawley ◽  
Competitive Antagonist ◽  
Rat Ileum ◽  
Antagonistic Effects ◽  
Relative Lack ◽  
Sprague Dawley Rats

The relative lack of specifi city of atropine as a competitive antagonist of muscarinic receptors is a frequent cause of undesirable parasympathetic side effects. Consequently, new tropane alkaloids with potentially greater selectivity are usually seen with real interest. The cholinergic antagonistic effects of a purifi ed mixture of tropane alkaloids extracted from Schizanthus hookeri were evaluated in rat ileum. For this purpose, ileal segments were obtained from randomly selected male Sprague-Dawley rats, and the effect of 1 · 10−4, 1 · 10−3, and 1 · 10−2 mg/mL of the purifi ed mixture of alkaloids on the contractile response of the ileum induced with increasing doses of carbachol (5 · 10−8 − 8 · 10−4 M) was determined. The results were compared with those obtained in the presence of 3.46 · 10−7, 3.46 · 10−6, and 3.46 · 10−5 mg/mL atropine as an agonist. Tropane alkaloids extracted from Schizanthus hookeri competitively antagonized acetylcholine muscarinic receptors.

Role of endothelium in sexual dimorphism in vasopressin-induced contraction of rat aorta

1993 ◽  
Vol 265 (6) ◽  
pp. H2073-H2080 ◽  
Author(s):  
J. N. Stallone
Keyword(s):  
Contractile Response ◽  
Rat Aorta ◽  
Isometric Tension ◽  
No Synthase ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Phenylephrine Hydrochloride ◽  
Rat Thoracic Aorta ◽  
Increased Sensitivity

In rat thoracic aorta, contractile responses to arginine vasopressin (AVP) are twofold higher in females than in males. To determine the role of the endothelium in this phenomenon, the effects of endothelium removal and inhibition of nitric oxide (NO) synthase and cyclooxygenase were examined in thoracic aortas prepared from male and female Sprague-Dawley rats and mounted for isometric tension recording. Maximal contractile response to AVP was substantially higher in female (4,232 +/- 316 mg/mg ring dry wt) than in male aortas (1,365 +/- 239; P < 0.01). Removal of the endothelium markedly potentiated maximal response to AVP in male aortas (4,100 +/- 422 mg/mg ring wt; P < 0.01); endothelium removal increased sensitivity but not maximal response in female aortas. Inhibition of NO synthase with NG-monomethyl-L-arginine (L-NMMA, 250 microM) doubled maximal contraction to AVP in male aortas (3,175 +/- 193 mg/mg ring wt; P < 0.01); L-NMMA increased sensitivity but not maximal response in female aortas. Inhibition of cyclooxygenase with indomethacin (10 microM) did not alter maximal response to AVP in male aortas but significantly attenuated responses of female aortas (2,816 +/- 306 mg/mg ring wt; P < 0.01). In contrast, maximal contractile response to phenylephrine hydrochloride (PE) was 40% higher in males than in females (P < 0.01); L-NMMA increased both the sensitivity and maximal response to PE to a greater extent in female (3,061 +/- 121 vs. 4,971 +/- 135 mg/mg ring wt; P < 0.01) than in male aortas (4,317 +/- 227 vs. 4,899 +/- 104 mg/mg ring wt; P < 0.01). (ABSTRACT TRUNCATED AT 250 WORDS)

Connexin mimetic peptides fail to inhibit vascular conducted calcium responses in renal arterioles

2008 ◽  
Vol 295 (3) ◽  
pp. R840-R847 ◽  
Author(s):  
Charlotte Mehlin Sorensen ◽  
Max Salomonsson ◽  
Thomas Hartig Braunstein ◽  
Morten Schak Nielsen ◽  
Niels-Henrik Holstein-Rathlou
Keyword(s):  
Electrical Current ◽  
Vascular Wall ◽  
Rat Aorta ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Microcirculatory Blood Flow ◽  
Sprague Dawley Rats ◽  
Resistance Vessels ◽  
Mimetic Peptides ◽  
Preglomerular Arterioles

Vascular conducted responses are believed to play a central role in controlling the microcirculatory blood flow. The responses most likely spread through gap junctions in the vascular wall. At present, four different connexins (Cx) have been detected in the renal vasculature, but their role in transmission of conducted vasoconstrictor signals in the preglomerular arterioles is unknown. Connexin mimetic peptides were previously reported to target and inhibit specific connexins. We, therefore, investigated whether conducted vasoconstriction in isolated renal arterioles could be blocked by the use of mimetic peptides directed against one or more connexins. Preglomerular resistance vessels were microdissected from kidneys of Sprague-Dawley rats and loaded with fura 2. The vessels were stimulated locally by applying electrical current through a micropipette, and the conducted calcium response was measured 500 μm from the site of stimulation. Application of connexin mimetic peptides directed against Cx40, 37/43, 45, or a cocktail with equimolar amounts of each, did not inhibit the propagated response, whereas the nonselective gap junction uncoupler carbenoxolone completely abolished the propagated response. However, the connexin mimetic peptides were able to reduce dye coupling between rat aorta endothelial cells shown to express primarily Cx40. In conclusion, we did not observe any attenuating effects on conducted calcium responses in isolated rat interlobular arteries when exposed to connexin mimetic peptides directed against Cx40, 37/43, or 45. Further studies are needed to determine whether conducted vasoconstriction is mediated via previously undescribed pathways.

Effect of high-salt diet on NO release and superoxide production in rat aorta

2004 ◽  
Vol 286 (2) ◽  
pp. H575-H583 ◽  
Author(s):  
Jiaxuan Zhu ◽  
Takefumi Mori ◽  
Tianjian Huang ◽  
Julian H. Lombard
Keyword(s):  
Rat Aorta ◽  
High Salt ◽  
Superoxide Production ◽  
Fluorescence Signal ◽  
Sprague Dawley ◽  
High Salt Diet ◽  
Salt Diet ◽  
Sprague Dawley Rats ◽  
Low Salt ◽  
No Release

Sprague-Dawley rats were fed either a high-salt (HS) diet (4.0% NaCl) or a low-salt (LS) diet (0.4% NaCl) for 3 days. Nitric oxide (NO) and superoxide production were assessed in the thoracic aorta by evaluating the fluorescence signal intensity from 4,5-diaminofluorescein (DAF-2DA) and dihydroethidine, respectively. Methacholine caused increased NO release in the aortas from rats on a LS but not HS diet. The SOD mimetic tempol restored methacholine-induced NO release in aortas from rats on a HS diet. Methacholine also caused superoxide production in the aortas of rats on a HS diet but not in the aortas of rats on a LS diet. Tempol and NG-monomethyl-l-arginine eliminated methacholine-induced superoxide production in the aortas of rats on a HS diet. Aortic rings from rats on the HS diet showed impaired methacholine-induced relaxation, which was improved by tempol. Tempol alone caused a NO-dependent relaxation of norepinephrine-precontracted aortas that was significantly greater in the aortas of rats on the HS diet than in vessels from rats on the LS diet. These data suggest that a HS diet impairs endothelium-dependent relaxation via reduced NO levels and increased superoxide production.

scholarly journals Polyphenolic Composition and Hypotensive Effects of Parastrephia quadrangularis (Meyen) Cabrera in Rat

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 591 ◽  
Author(s):  
Fredi Cifuentes ◽  
Javier Palacios ◽  
Chukwuemeka Nwokocha ◽  
Jorge Bórquez ◽  
Mario Simirgiotis ◽  
...  
Keyword(s):  
Cardiac Contractility ◽  
Folk Medicine ◽  
Negative Inotropic Effect ◽  
Cytosolic Calcium ◽  
Rat Aorta ◽  
Sprague Dawley ◽  
The Andes ◽  
Polyphenolic Composition ◽  
Sprague Dawley Rats ◽  
Blood Pressures

Parastrephia quadrangularis (Pq), commonly called “Tola”, is widely used in folk medicine in the Andes, including for altitude sickness. In this study, polyphenolic composition was determined, and hypotensive effects were measured; the ethnopharmacological use as hypotensive was related to the presence of phenolic compounds. For this purpose, male Sprague-Dawley rats (6 to 8 weeks of age, 160 to 190 g) were fed Pq extract (10 to 40 mg/kg) for 10 days through gavage. Blood pressures and heart rate were significantly (p < 0.01) reduced in normotensive rats receiving Pq extract (40 mg/kg body weight). Pq extract induced a negative inotropic effect, and endothelium-dependent vasodilation mediated by nitric oxide (NO). Furthermore, preincubation with Pq extract significantly decreased the cytosolic calcium on vascular smooth muscle cells A7r5 in response to L-phenylephrine (PE). Seven metabolites were isolated from the Pq extract, but three flavonoids (10−4 M) showed similar vasodilation to the extract in intact rat aorta as follows: 5,3′,4′-trihydroxy-7-methoxyflavanone (2); 3,5,4′-trihydroxy-7,8,3′-trimethoxyflavone (6); and 5,4′-dihydroxy-3,7,8,3′-tetramethoxyflavone (7). The Pq extract and compounds 2 and 7 significantly (p < 0.05) reduced the contraction to Bay K8644 (10 nM, an agonist of CaV1.2 channels). Administration of Pq decreased cardiac contractility and increased endothelium-dependent and -independent vasodilation.

Role of intracellular alkalinization in inhibition of acetylcholine-induced relaxation by FMLP in rat aorta

1996 ◽  
Vol 271 (6) ◽  
pp. H2405-H2410
Author(s):  
K. Ando ◽  
T. Fujita
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Inhibitory Effect ◽  
Rat Aorta ◽  
Vascular Endothelial ◽  
Sprague Dawley ◽  
Thromboxane A2 Receptor ◽  
Protein Kinase C Inhibitors ◽  
Sprague Dawley Rats ◽  
Intracellular Alkalinization

N-formylmethionyl-leucyl-phenylalanine (FMLP), a chemotactic tripeptide, is known to cause intracellular alkalinization. Moreover, there is a specific receptor for FMLP in vascular endothelial cells but not in vascular smooth muscle cells. Because we have already reported that intracellular alkalinization inhibits acetylcholine (ACh)-induced relaxation, we examined whether FMLP alters the vasodilation of endothelial cells through intracellular alkalinization. FMLP reduced ACh-induced relaxation in aortic rings from Sprague-Dawley rats but did not affect nitroglycerin-induced relaxation. N-t-butoxycarbonyl-phenylalanyl -D-leucyl-phenylalanyl-D-leucyl-phenylalanine, a specific formyl receptor antagonist, reversed the impairment of ACh-induced relaxation, as did the protein kinase C inhibitors sphingosine and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7). The sodium/proton antiport inhibitor amiloride and the proton ionophore nigericin normalized the attenuated ACh-induced relaxation. FMLP-induced impairment was normalized by the phospholipase A2 inhibitor quinacrine, the cyclooxygenase inhibitor indomethacin, and the antagonists of the prostaglandin H2 and/or thromboxane A2 receptor, ONO-3708 and S-1452, respectively. Superoxide dismutase inhibited the effect of FMLP. In conclusion, FMLP attenuated ACh-induced relaxation, possibly through intracellular alkalinization. Increased production of vasoconstrictor prostaglandin(s) and superoxide may contribute to the inhibitory effect of FMLP-induced alkalinization on ACh-induced relaxation.

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