Analysis of responses to angiotensin IV in the pulmonary vascular bed of the cat

Cheng, David Y.; DeWitt, Bracken J.; Dent, Edward L.; Nossaman, Bobby D.; Kadowitz, Philip J.

doi:10.1016/0014-2999(94)90324-7

Cited by 25 publications

(23 citation statements)

References 7 publications

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“…than All, although studies in the pulmonary vascular bed of cat and rat (Cheng et al, 1994;Nossaman et al, 1995) have indicated a smaller difference in potency between the two peptides. Thus, it seems that the variations of compared potency may occur either in the same tissue of different species or in different tissues of the same species.…”

Section: Aii Aiii and Aiv Induced Contractions In Endotheliwmdenudedmentioning

confidence: 99%

“…They naturally occur in substantial con-> had been concentrations in various species (Peach, 1977 (Pendleton et al, 1991;Robertson et al, 1992;Cheng et al, 1994;Nossaman et al, 1995). AIII proved only 3-4 times less potent than All on the basis of pD2 values.…”

Section: Aii Aiii and Aiv Induced Contractions In Endotheliwmdenudedmentioning

confidence: 99%

“…AIV is thought to be biologically inactive because of its inability to stimulate the aforementioned classic angiotensindependent processes (Fitzsimons, 1971;Tonnaer et al, 1982). However, recent investigations have shown the presence of a special binding site for AIV in a variety of tissues from many species (Hanesworth et al, 1993;Harding et al, 1994), and it has also been suggested that AIV may be implicated in the regulation of blood flow (Haberl et al, 1991;Cheng et al, 1994;Coleman et al, 1995). 1 Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

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Comparative effects of angiotensin II and its degradation products angiotensin III and angiotensin IV in rat aorta

Zhang

Pfaffendorf

et al. 1995

British J Pharmacology

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1 In the present study, the contractile effects of angiotensin III (AIII) and angiotensin IV (AIV) compared with those of angiotensin II (AII) were determined in rat aortic ring preparations. 2 All three peptides caused concentration-dependent contractions with similar maximal responses. AIII proved approximately 4 times less potent than AII, whereas AIV was about 1000 times less active than AIL.3 The selective AT,-receptor antagonist, losartan (10-300 nM) caused parallel rightward shifts of the concentration-response curves (CRC) for all three peptides. The Schild plot slopes for the effect of losartan on AIII curves were significantly lower than unity (P<0.05). The selective AT2-receptor antagonist, PD123177 did not influence the CRCs for AII and AIV. However, the AIII curves were moderately shifted leftward in the presence of PD123177 (0.1 and 1 JiM).4 Destruction of the endothelium or incubation with the NO-synthesis inhibitor N0-monomethyl-Larginine acetate (L-NMMA) (0.1 mM) significantly enhanced the contractile responses to all three peptides. 5Tachyphylaxis was investigated by constructing a second CRC for all three peptides, after an interval of 1 h. The presence of endothelium significantly enhanced the development of tachyphylaxis to all three peptides. However, in endothelium-denuded preparations, the E,,,,,, value of the second curve elicted by AII was about 50%, compared with the first one, whereas for AIII and AIV E,,,, values were as high as 90% and 100%, respectively. 6 Our results indicate that both AIII and AIV are less potent but similarly efficacious vasoconstrictor agents compared with AII. Their contractile effects are also mediated by AT,-receptors and probably modulated by endothelium. Tachyphylaxis induced by AIII and AIV proved weaker than that for AII. Tachyphylaxis appears to be enhanced by the presence of an intact endothelium.

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Section: Aii Aiii and Aiv Induced Contractions In Endotheliwmdenudedmentioning

confidence: 99%

Section: Aii Aiii and Aiv Induced Contractions In Endotheliwmdenudedmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Comparative effects of angiotensin II and its degradation products angiotensin III and angiotensin IV in rat aorta

Zhang

Pfaffendorf

et al. 1995

British J Pharmacology

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“…20 ANG III showed only 10 times less potency than ANG II in the cat pulmonary vascular bed. 22 In the rabbit penile CSM ANG III was approximately 10 times less potent than ANG II and was 1.5 times more potent than ANG I. 23 It has also been shown that the contractile responses to ANG II in the rabbit penile 4,23 and clitoral CSM 5,6 are related to the activation of AT1 receptor.…”

Section: Discussionmentioning

confidence: 99%

Comparison of effects of angiotensin peptides in the regulation of clitoral cavernosum smooth muscle tone

Park

Kim

et al. 2002

Int J Impot Res

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The isometric tension measurement and in vitro autoradiography were used in clitoral cavernosum smooth muscle (CSM). Angiotensin ANG III, ANG IV, ANG II and ANG I induced contractions in clitoral CSM strips. ANG III and ANG I-induced contraction was five times less active than ANG II, whereas ANG IV-induced contraction was 1181-fold less potent than ANG II. I-ANG II was displaced by unlabeled ANG peptides. This study suggests that the contractile responses to all four peptides of the ANG family are mediated via AT1 receptors but not AT2 receptors. Further, the rank order of potency of contraction was as follows, ANG II > ANG I > ANG III > ANG IV. It is also suggested that peptides of the ANG family have a cross-talk with the NO system and aminopeptidase is involved in the modulation of the tone of clitoral CSM by ANG III and ANG IV.

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“…57 Whilst these studies do lend support for a role of Ang IV in vasodilatation, others observed Ang IV mediated vasoconstriction, probably via the AT 1 receptor. [72][73][74][75][76] In addition to these vascular effects, Ang IV increased the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA in bovine aortic endothelial cells. 77 Ang IV also stimulated DNA synthesis in rat anterior pituitary cells 78 and stimulated DNA and RNA synthesis in cultures of rabbit fibroblasts.…”

Section: Ang IVmentioning

confidence: 99%

Bioactive angiotensin peptides

et al. 1998

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Angiotensin II is recognised as the principle active peptide of the renin-angiotensin system, exerting effects on fluid and electrolyte homeostasis, and cardiovascular control including neural and long term trophic effects. However, recent studies indicate that other angiotensin peptides such as angiotensin III, angiotensin II (1-7) and angiotensin IV, may have specific actions. Interestingly, recent work involving angiotensin IV demonstrates that this peptide binds to specific receptors and may be Keywords: angiotensin metabolites; angiotensin III; angiotensin II(1-7); angiotensin IV; globin Bioactive angiotensin peptidesThe renin-angiotensin system (RAS) was initially identified as a circulating humoral system with the effector peptide, angiotensin II (Ang II), generated by an enzymatic cascade. Angiotensinogen, which is synthesized in the liver, is cleaved by renin, a product of the juxtaglomerular cells of the kidney, to form Ang I, which in turn is cleaved by angiotensinconverting enzyme (ACE) to form Ang II. ACE is membrane bound and predominates on the endothelial cells of all vascular beds. Apart from the production of Ang II in plasma, Ang II, renin and ACE have all been described in tissues such as the brain, kidney, adrenal, vasculature, heart and ovaries. This suggests a separate and distinct RAS in these tissues and implies endocrine, paracrine and autocrine roles for Ang II. Actions of Ang IIAng II regulates blood pressure, fluid volume homeostasis and pituitary hormone release via AT 1 and AT 2 receptors located in the kidney, adrenal gland, and the cardiovascular and nervous systems. [2][3][4][5] In the kidney, for instance, Ang II acts on renal vessels, glomeruli, tubules and renomedullary interstitial cells, to alter renal blood flow, glomerular filtration rate and electrolyte reabsorption.6-9 Ang II also acts on the adrenal cortex to stimulate aldosterone secretion and hence renal sodium reabsorption. 10Ang II is a potent vasoconstrictor, acting directly on vascular smooth muscle and indirectly via facilitation of noradrenaline release from sympathetic terminals. 11,12 In the heart, Ang II exerts positive iono- tropic and chronotropic effects and facilitates sympathetic activity. 13Acting on the brain, Ang II induces fluid and salt ingestion, modulates neuroendocrine systems, including vasopressin and corticotropin releasing factor release, and interacts with the autonomic control of the cardiovascular system to influence blood pressure. 3,14,15 In many instances, these effects are complementary to those of the systemic peptide on peripheral target organs. Thus, systematic Ang II affects the brain through AT 1 receptors located in the circumventricular organs, regions with a deficient blood brain barrier. In addition, endogenous neurally derived Ang II appears to act at many central nervous system sites behind the blood brain barrier. [16][17][18] Most of the classical actions of Ang II are mediated via the AT 1 receptor whereas AT 2 receptor stimulation may cause opposing effects. This was o...

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Analysis of responses to angiotensin IV in the pulmonary vascular bed of the cat

Cited by 25 publications

References 7 publications

Comparative effects of angiotensin II and its degradation products angiotensin III and angiotensin IV in rat aorta

Comparative effects of angiotensin II and its degradation products angiotensin III and angiotensin IV in rat aorta

Comparison of effects of angiotensin peptides in the regulation of clitoral cavernosum smooth muscle tone

Bioactive angiotensin peptides

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