Tissue renin-angiotensin systems and reproduction

Vinson, Gavin P.; Sarıdoğan, Ertan; Puddefoot, J. R.; Djahanbakhch, O.

doi:10.1093/humrep/12.4.651

Cited by 76 publications

(71 citation statements)

References 16 publications

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“…All tissues were stained with the lectin Bandeirae simplicifolia (red) to visualise blood vessels within the pancreatic islets. Scale bar=50 μm effects [17][18][19][20][21][22][23][24]. The best known functions of angiotensin II, e.g.…”

Section: Discussionmentioning

confidence: 99%

“…3 Vascular density in native mouse pancreatic islets and in islet grafts 4 weeks after transplantation beneath the renal capsule of syngeneic C57BL/6 mice. Some of the transplanted animals were subjected to treatment with the angiotensin II type 1 receptor inhibitor losartan (30 mg·kg −1 ·day −1 ) dissolved in the drinking water throughout the 4-week post-transplantation period (days 0-28) or for the final 14 days (days [15][16][17][18][19][20][21][22][23][24][25][26][27][28]. Values are given for the endocrine tissue (closed bars), the connective tissue stroma (hatched bars) and the whole islet graft (empty bars).…”

Section: Graft Insulin Release and Insulin Contentsmentioning

confidence: 99%

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Angiotensin II type 1 receptor inhibition markedly improves the blood perfusion, oxygen tension and first phase of glucose-stimulated insulin secretion in revascularised syngeneic mouse islet grafts

et al. 2005

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Aims/hypothesis: We recently found evidence of an angiotensin-generating system in pancreatic islets. The present study investigated the effect of endogenously produced angiotensin II on microcirculation and function in transplanted islets. Materials and methods: Losartan, an angiotensin II type 1 receptor inhibitor, was administered either acute intravenously to mice with 4-week-old islet renal subcapsular transplants, or added to the drinking water for the final 14 days or throughout the 4-week post-transplantation period. The graft-bearing kidney was, in some cases, dissected out and perfused in vitro to evaluate the effect of angiotensin II and losartan on glucose-stimulated insulin release from the grafts. Results: Losartan treatment throughout the 4-week post-transplantation period had negative effects on islet revascularisation as well as on islet graft insulin release. However, administration of losartan, either intravenously or orally, after the formation of a new vascular network, improved islet graft blood perfusion. P O2 in the islet transplants was also effectively improved by the losartan treatment. Graft perfusion experiments showed a markedly better first phase of glucose-stimulated insulin release in transplanted islets when exposed to losartan. In contrast, acute administration of angiotensin II decreased islet graft blood flow, PO 2 and glucose-stimulated insulin release. Conclusions/interpretation: This study shows that inhibition of the islet reninangiotensin system may be a feasible strategy to increase the blood perfusion, PO 2 and function within islet grafts. Such treatment should not be initiated, however, before the islet vascular system has been formed.

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Section: Discussionmentioning

confidence: 99%

Section: Graft Insulin Release and Insulin Contentsmentioning

confidence: 99%

Angiotensin II type 1 receptor inhibition markedly improves the blood perfusion, oxygen tension and first phase of glucose-stimulated insulin secretion in revascularised syngeneic mouse islet grafts

et al. 2005

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“…Although the peptide angiotensin II (AII) is generally known for its roles in regulating cardiovascular and electrolyte homeostasis (Vinson et al 1997), AII is also found in seminal plasma at concentrations higher than in blood (O'Mahony et al 2000). This suggests that AII might be able to act on mammalian spermatozoa, in addition to other somatic cells and tissues.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of action of angiotensin II on mammalian sperm function

Mededovic¹,

Fraser²

2005

Reproduction

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Angiotensin II (AII) stimulates capacitation and fertilizing ability in mammalian spermatozoa, with the binding of AII to its receptors resulting in stimulation of cAMP production in both uncapacitated and capacitated cells. This study investigated possible mechanisms whereby AII affects cAMP availability. The first question was whether extracellular Ca 21 is required for responses in mouse spermatozoa and, using chlortetracycline fluorescence analysis, it was clear that cells responded to AII only when the medium contained CaCl 2 , with both 90 mM and 1.80 mM supporting a significant acceleration of capacitation. Consistent with those results, AII significantly stimulated cAMP production in both CaCl 2 -containing media tested, the response being greater in that containing 1.80 mM. Several different agents that might affect the signalling pathway stimulated by AII were then evaluated in uncapacitated suspensions. Chlortetracycline analysis revealed that pertussis toxin abolished responses to AII, suggesting the involvement of an inhibitory Ga subunit; dideoxyadenosine, a specific membrane-associated adenylyl cyclase (mAC) P-site inhibitor, also blocked responses, suggesting involvement of an mAC. cAMP determinations confirmed that both reagents also abolished AII's stimulation of cAMP. In contrast, nifedipine, a Ca 21 channel blocker, did not inhibit AII's effects on spermatozoa. Finally, in capacitated suspensions, both pertussis toxin and dideoxyadenosine were again shown to block AII's stimulation of cAMP. These results suggest that responses to AII involve an inhibitory G protein and an mAC, but it is likely that AII -receptor coupling does not stimulate directly mAC but rather does so in an indirect manner, perhaps by altering the intracellular Ca 21 concentration.Reproduction (2005) 129 211-218

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“…Although the responses to FPP and calcitonin appear to involve G protein-mediated regulation of AC activity, the precise mechanism by which AII is able to stimulate cAMP production remains unclear. The AT1 receptor for AII belongs to the G protein-coupled receptor family (Vinson et al 1997). In somatic cells, AT1 receptors are usually linked to Ga q -containing G proteins; consequently, AII stimulation is often linked with phospholipase C activation, resulting in increased generation of diacylglycerol and inositol trisphosphate, activation of protein kinase C (PKC) and elevated intracellular Ca 2þ concentration (Sayeski et al 1998).…”

Section: Discussionmentioning

confidence: 99%

“…Angiotensin II (AII) is an octapeptide (Asp-Arg-Val-TyrIle-His-Pro-Phe) widely known for its roles in regulating cardiovascular and electrolyte homeostasis (see review by Vinson et al 1997). However, AII is also found in seminal plasma at concentrations higher than in blood plasma (O'Mahony et al 2000) and there is evidence that AII receptors of subtype 1 (AT1) are present on mammalian spermatozoa (Vinson et al 1995, Gur et al 1998, Wennemuth et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II stimulates cAMP production and protein tyrosine phosphorylation in mouse spermatozoa

Mededovic

Fraser

2004

Reproduction

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Angiotensin II (AII), found in seminal plasma, has been shown to stimulate capacitation in uncapacitated mammalian spermatozoa. The present study investigated the location of AII receptors on spermatozoa and AII's mechanism of action. AT1 type receptors for AII are present on the acrosomal cap region and along the whole of the flagellum of both mouse and human spermatozoa. Because combinations of low concentrations of AII and either calcitonin or fertilization-promoting peptide (FPP), both known to regulate the adenylyl cyclase (AC)/cAMP signal transduction pathway, elicited a significant response, this study investigated the hypothesis that these peptides act on the same pathway. AII was shown to significantly stimulate cAMP production in both uncapacitated and capacitated mouse spermatozoa and this was associated with increases in protein tyrosine phosphorylation. Using an anti-phosphotyrosine antibody to visualize the location of tyrosine phosphoproteins within individual cells, AII significantly stimulated phosphorylation within 20 min in both the head, especially in the acrosomal cap region, and the flagellum, especially in the principal piece, of uncapacitated mouse spermatozoa; combined AII 1 FPP was stimulatory within 5 min. In addition, Western blotting revealed that AII stimulation increased phosphorylation in a number of tyrosine phosphoproteins in both uncapacitated and capacitated mouse spermatozoa, with some being altered only in the latter category of cells. These results support the hypothesis that AII stimulates AC/cAMP in mammalian spermatozoa.

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Tissue renin-angiotensin systems and reproduction

Cited by 76 publications

References 16 publications

Angiotensin II type 1 receptor inhibition markedly improves the blood perfusion, oxygen tension and first phase of glucose-stimulated insulin secretion in revascularised syngeneic mouse islet grafts

Angiotensin II type 1 receptor inhibition markedly improves the blood perfusion, oxygen tension and first phase of glucose-stimulated insulin secretion in revascularised syngeneic mouse islet grafts

Mechanisms of action of angiotensin II on mammalian sperm function

Angiotensin II stimulates cAMP production and protein tyrosine phosphorylation in mouse spermatozoa

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