Ovine maternal and fetal renal vasopressin receptor response to maternal dehydration

Kullama, Linda K.; Ross, Michael G.; Lam, Robert W.; Leake, Rosemary D.; Ervin, M. Gore; Fisher, Delbert A.

doi:10.1016/0002-9378(92)91766-4

Cited by 11 publications

(5 citation statements)

References 18 publications

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“…The blood samples were collected into iced tubes that contained lithium heparin and centrifuged immediately for AVP RIA. Plasma AVP concentrations were measured using SepPak C18 cartridge (Waters Associates, Milford, MA) extraction (19). Sensitivity of the AVP antiserum is 1.5 pg/tube with intra-assay and interassay coefficients of variation of 6 and 8%, respectively.…”

Section: Methodsmentioning

confidence: 99%

Vasopressin Mechanism–Mediated Pressor Responses Caused by Central Angiotensin II in the Ovine Fetus

et al. 2004

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AVP not only influences renal water excretion but also has profound cardiovascular effects in adults. Our recent studies have demonstrated that central angiotensin induced fetal pressor responses accompanied with AVP release. However, little is known of hormonal mechanisms in angiotensin-mediated fetal blood pressure (BP) changes. The present study determined AVP mechanisms in central angiotensin-mediated fetal pressor responses. The V1-receptor antagonist or V2-receptor antagonist was infused intravenously into the ovine fetus at 90% gestation. Angiotensin II (Ang II; 1.5 g/kg) was then injected intracerebroventricularly into the chronically instrumented fetus. Ang II produced a significant increase in fetal systolic, diastolic, and mean arterial pressure adjusted to amniotic pressure (A-MAP). The enhanced fetal A-MAP was associated with intense c-fos expression in the central putative cardiovascular area: the paraventricular nuclei (PVN). Double labeling demonstrated that a number of the AVP-containing neurons in the PVN were expressing c-fos in response to central Ang II. Consistent with the activation of AVP neurons in the PVN, fetal plasma AVP was markedly enhanced. Fetal i.v. V1-receptor antagonist or V2-receptor antagonist had no effect on either fetal or maternal baseline BP. However, intracerebroventricular Ang II-increased BP was partially inhibited, although not completely abolished, by the V1-receptor blockade. In contrast, fetal i.v. infusion of V2-receptor antagonist had no effect on the pressor responses induced by central Ang II. The results suggest that the central Ang II-mediated pressor responses at the last third of gestation is mediated partially by the AVP mechanism via V1 not V2 receptors. The nonapeptide AVP, also known as antidiuretic hormone, has multiple actions, including water reabsorption and vasoconstriction in the periphery. This peptide also plays a role in cardiovascular diseases, including hypertension and congestive heart failure (1). In adults, plasma AVP has been reported to be elevated in some forms of hypertension, and this elevation correlates best with the severity of hypertension (2). Recent findings have demonstrated that the development of cardiovascular regulatory mechanisms starts before birth and that the in utero development of cardiovascular regulation is critical for fetal cardiovascular homeostasis (3,4). Several peptides, including AVP and angiotensin II (Ang II), are essential in the control of cardiovascular functions. Central renin-angiotensin system (RAS) plays an important role in the regulation of arterial pressure and in the development of certain forms of clinical and experimental hypertension (3,5,6). Under certain conditions, the RAS and the AVP system operate as reciprocal mechanisms in the control of vascular resistance and arterial pressure in adults (7). For example, intracerebroventricular (i.c.v.) administration of Ang II causes a rise in blood pressure (BP) associated with AVP release (8 -10). The pressor response induced by the i.c.v. Ang II ...

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Section: Methodsmentioning

confidence: 99%

Vasopressin Mechanism–Mediated Pressor Responses Caused by Central Angiotensin II in the Ovine Fetus

et al. 2004

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“…Although fetal renal concentrating ability is limited, functional V 2 receptors are present in the fetal kidney by the beginning of the last third of gestation. 47 In addition, AVP-induced cyclic AMP production is not different from that in the adult. 48 Fetal infusions with a selective V 2 receptor agonist (deamino[D-Arg 8 ]vasopressin; dDAVP) appropriately increase early and late gestation fetal renal water reabsorption without affecting blood pressure or heart rate.…”

Section: Arginine Vasopressinmentioning

confidence: 94%

Fetal Endocrine Maturation and Perinatal Renal Function

Ervin¹

1993

Semin Reprod Med

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“…Plasma AVP concentrations were measured using Sep-Pak C18 cartridge (Waters Associates, Milford, MA) extraction. Samples for AVP extraction were acidified with 1 N HCl and extracted using a modification of the method (14). Acidified plasma samples were added slowly to the columns, and the columns were washed with 0.1% trifluoroacetic acid (TFA).…”

Section: Methodsmentioning

confidence: 99%

“…Although there are a number of studies that have demonstrated the importance of ANG mechanisms in the regulation of AVP in adults, very little is known about the relationship between peripheral ANG and central AVP systems in the fetus. Addressing this question is important not only to prenatal life but also to postnatal health.Previous fetal studies have demonstrated that an active RAS is present in the fetus before birth, and ANG II has been ascribed important functions in the fetus (11,13,14). Its major function appears to be maintenance of fetal arterial pressure under conditions of fetal stress, including acute hemorrhage or hypoxia (13).…”

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Intravenous angiotensin induces brain c-fosexpression and vasopressin release in the near-term ovine fetus

Shi

Morrissey

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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2003.-The effect of intravenous angiotensin II (ANG II) on fetal brain c-fos expression and arginine vasopressin (AVP) release was studied in the near-term ovine fetus. Fetuses with chronically implanted catheters received an intravenous infusion of ANG II or saline. Fetal plasma AVP concentrations were significantly increased after the peripheral administration of ANG II, with peak levels (3-fold) at 30 min after the intravenous infusion. There was no change in fetal plasma osmolality, sodium, and hematocrit levels between the control and experimental groups or between the periods before and after the infusion of ANG II. Intravenous ANG II administration induced Fos immunoreactivity (Fos-IR) in the circumventricular organs and the median preoptic nucleus of the fetal brain. Fos-IR was also demonstrated in the fetal supraoptic nuclei (SON). Double labeling demonstrated that the AVP-containing neurons in the SON were expressing c-fos in response to intravenous ANG II. These results indicate that the peripheral ANG II in the fetus may play a significant role in stimulating the central hypothalamic-neurohypophysial system during late gestation. It supports the hypothesis that circulating ANG II may act at the fetal AVP neurons in the hypothalamus in body fluid balance via the circumventricular organs, which are situated outside the blood-brain barrier, and the central neural pathway between these two brain structures has been relatively established in utero, at least at near-term. angiotensin II; fetal brain development; arginine vasopressin NUMEROUS EARLIER STUDIES have shown that the central renin-angiotensin system (RAS) is as important as peripheral RAS in the control of body fluid and cardiovascular homeostasis. In adults, there is significant information regarding the effects of central and peripheral angiotensin (ANG) (8, 21). Administration of either ANG II or its precursors into the brain or the peripheral bloodstream produces a pressor response, induces drinking behavior, and causes release of adrenocorticotropic hormone and arginine vasopressin (AVP) (1,8,25). A link between peripheral administration of ANG II and AVP release in adult animals has been well established (9). The effect of intravenous ANG II on the hypothalamic-neurohypophysial system has been suggested via circumventricular organs (CVOs), which lack blood-brain barriers (BBB) (28). Furthermore, blockade of the ANG receptors can suppress AVP release into the circulation (3). Although there are a number of studies that have demonstrated the importance of ANG mechanisms in the regulation of AVP in adults, very little is known about the relationship between peripheral ANG and central AVP systems in the fetus. Addressing this question is important not only to prenatal life but also to postnatal health.Previous fetal studies have demonstrated that an active RAS is present in the fetus before birth, and ANG II has been ascribed important functions in the fetus (11,13,14). Its major function appears to be maintenance of fetal arterial pressure und...

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Ovine maternal and fetal renal vasopressin receptor response to maternal dehydration

Cited by 11 publications

References 18 publications

Vasopressin Mechanism–Mediated Pressor Responses Caused by Central Angiotensin II in the Ovine Fetus

Vasopressin Mechanism–Mediated Pressor Responses Caused by Central Angiotensin II in the Ovine Fetus

Fetal Endocrine Maturation and Perinatal Renal Function

Intravenous angiotensin induces brain c-fosexpression and vasopressin release in the near-term ovine fetus

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