Vasopressin Receptors in Human Seminal Vesicles: Identification, Pharmacologic Characterization, and Comparison with the Vasopressin Receptors Present in the Human Kidney

Maggi, Mario; Baldi, Elisabetta; Genazzani, Alessandro D.; Giannini, Stefano; Natali, Alessandro; Costantini, A.; Rodbard, David; Serio, Mario

doi:10.1002/j.1939-4640.1989.tb00126.x

Cited by 8 publications

(4 citation statements)

References 33 publications

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“…The K¿ for binding (2.5 nM) is comparable with that reported in other tissues (Jard, Lombard, Marie & Devilliers, 1987;Maggi, Baldi, Genazzani et al 1989) and is close to the EC5o value reported for secretion of insulin from normal mouse islets (Gao et al 1990). Although the value is higher than plasma levels of vasopressin (Schrier, Berl & Anderson, 1979), the existence of high concentrations of vasopressin in the pancreas (Amico, Finn & Haldar, 1988) suggests a possible local action of the hormone.…”

Section: Discussionsupporting

confidence: 86%

Stimulation of insulin release by vasopressin in the clonal β-cell line, HIT-T15: the role of protein kinase C

Hughes

Carpinelli²,

Niki³

et al. 1992

Journal of Molecular Endocrinology

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We have studied the effects of vasopressin and tetradecanoyl phorbol acetate (TPA) on cytosolic free Ca2+ ([Ca2+]i) and insulin release in HIT-T15 beta-cells. Saturable binding of [3H] [Arg8]-vasopressin to HIT cell microsomes indicated a single class of receptors with a dissociation constant (Kd) of 2.5 nM and a total number of binding sites (Bmax) equal to 120 fmol/mg protein. [Arg8]-vasopressin (0.1-100 nM) elicited dose-dependent insulin release from HIT cells by up to 25-fold. This increase was dependent on the presence of extracellular glucose and was blocked by omission of extracellular Ca2+ or addition of verapamil. The stimulation was biphasic; a rapid but short-lived large increase in release was followed by a smaller sustained rise. Vasopressin also evoked a marked, concentration-dependent increase in [Ca2+]i which was also biphasic; an initial spike was followed by a sustained elevation. This increase also required glucose and was blocked by the absence of extracellular Ca2+ or the addition of verapamil. Pretreatment of the cells with TPA overnight to deplete protein kinase C activity did not affect the [Ca2+]i or insulin responses to vasopressin. However, short-term exposure to TPA markedly reduced glucose-induced steady-state [Ca2+]i, despite potentiating glucose-stimulated insulin release sevenfold, and blocked the [Ca2+]i increase induced by vasopressin. These inhibitory effects of TPA were absent in protein kinase C-depleted cells and were prevented by staurosporine. TPA had no significant effect on vasopressin-induced insulin release. Vasopressin did not modify the activity of ATP-sensitive K+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 86%

Stimulation of insulin release by vasopressin in the clonal β-cell line, HIT-T15: the role of protein kinase C

Hughes

Carpinelli²,

Niki³

et al. 1992

Journal of Molecular Endocrinology

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“…be considerable higher in many other species including human (47,48). Interestingly, maximum increases in intracellular cAMP levels induced by the V2R agonist dDAVP were reduced by about 50% in IMCD tubule suspensions prepared from kidneys of V2R +/-mice (Figure 5), providing a molecular correlate for the XNDI phenotype observed with the V2R +/-mutant mice.…”

Section: Figurementioning

confidence: 90%

Generation and phenotype of mice harboring a nonsense mutation in the V2 vasopressin receptor gene

et al. 2000

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The V2 vasopressin receptor (V2R) plays a key role in the maintenance of a normal body water balance. To generate an in vivo model that allows the physiological and molecular analysis of the role of V2Rs in kidney function, we have created mouse lines that lack functional V2Rs by using targeted mutagenesis in mouse embryonic stem cells. Specifically, we introduced a nonsense mutation known to cause X-linked nephrogenic diabetes insipidus (XNDI) in humans (Glu242stop) into the mouse genome. V2R-deficient hemizygous male pups showed a decrease in basal urine osmolalities and were unable to concentrate their urine. These pups also exhibited an enlargement of renal pelvic space, failed to thrive, and died within the first week after birth due to hypernatremic dehydration. Interestingly, female mice heterozygous for the V2R mutation showed normal growth but displayed an XNDI-like phenotype, characterized by reduced urine concentrating ability of the kidney, polyuria, and polydipsia. Western blot analysis and immunoelectron microscopic studies showed that the loss of functional V2Rs had no significant effect on the basal expression levels of aquaporin-2 and the bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1). The V2R mutant mice described here should serve as highly useful tools for the development of novel therapeutic strategies for the treatment of XNDI.

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“…The major peripheral biological effects of AVP are antidiuretic and vasopressor activity ( 1), whereas AVP may also be involved in sexual arousal ( 4). In humans, receptors for AVP have been described on platelets ( 5), in kidney and seminal vesicles ( 6). Furthermore, AVP neurones of the SON were shown to be activated in ageing, also in Alzheimer’s disease ( 7).…”

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confidence: 99%

Activity of Vasopressinergic Neurones of the Human Supraoptic Nucleus os Age‐ and Sex‐Dependent

Ishunina

Salehi

Hofman

et al. 1999

J Neuroendocrinology

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In the human hypothalamus, arginine-vasopressin (AVP) is produced for a major part by the neurones of the supraoptic nucleus (SON). Since plasma AVP levels in men were reported to be higher than those of women and we did not find a sex difference in the neurone number, a higher vasopressinergic neurone activity was supposed to be present in the SON of men. Therefore we studied the size of the Golgi-apparatus (GA), which has been demonstrated previously to be a sensitive parameter for protein synthetic ability of neurones, in 15 men and 17 women ranging in age from 29 to 94 years. A polyclonal antibody against immunoaffinity purified MG-160, a sialoglycoprotein of the medial cisternae of the GA was applied on paraffin-embedded sections containing the dorsolateral SON (dl-SON) from which 90-95% of neurones are vasopressinergic. SON areas that contain oxytocin (OT) cells were excluded on the basis of adjacent sections stained with a monoclonal antibody against OT. By means of an image analysis system the size of the GA and the cellular profile area were determined in dl-SON neurones with a nucleolus. Our results showed indeed an age-dependent sex difference in the size of the GA that appeared to be twice as large in young men (< or = 50 years old) than in young women of the same age. The size of the GA increased with age in women but not in men. In addition, the mean cell profile area, another measure for neuronal activity, was significantly larger in young men than in young women and was in old women larger than in young women. In conclusion, these data show the presence of a sex-dependent age-difference in the activity of vasopressinergic neurones in dl-SON which may relate to differences in AVP and sex hormone levels and kidney AVP receptors.

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Vasopressin Receptors in Human Seminal Vesicles: Identification, Pharmacologic Characterization, and Comparison with the Vasopressin Receptors Present in the Human Kidney

Cited by 8 publications

References 33 publications

Stimulation of insulin release by vasopressin in the clonal β-cell line, HIT-T15: the role of protein kinase C

Stimulation of insulin release by vasopressin in the clonal β-cell line, HIT-T15: the role of protein kinase C

Generation and phenotype of mice harboring a nonsense mutation in the V2 vasopressin receptor gene

Activity of Vasopressinergic Neurones of the Human Supraoptic Nucleus os Age‐ and Sex‐Dependent

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