Increased Angiotensin-(1–7) in Hypophysial-Portal Plasma of Conscious Sheep

Lawrence, Anne C.; Clark, Iain J.; Campbell, Duncan J.

doi:10.1159/000126103

Cited by 31 publications

(21 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…data] and it is possible that this activity on the external membrane surface of these cells is responsible for our observations that levels of some peptides are lower in portal blood. Further support for this proposition comes from the work of Lawrence et al [52], which showed the degradation of angiotensin i_io to angiotensin 1-7 by passage through the hypophysial portal vessels.…”

Section: Discussionmentioning

confidence: 94%

Many Peptides that Are Present in the External Zone of the Median Eminence Are Not Secreted into the Hypophysial Portal Blood of Sheep

et al. 1993

View full text Add to dashboard Cite

Apart from the well recognized factors that are produced by the hypothalamus and secreted into hypophysial portal blood to regulate pituitary function, there is a range of neuropeptides that are present in the median eminence and could be secreted to serve a modulatory function. In this study we have collected hypophysial portal blood and jugular venous blood from sheep in an attempt to identify which of these putative modulatory peptides might be secreted from the median eminence. We have measured neuropeptide Y(NPY), substance P (SP), galanin (GAL), neurokinin A (NKA), peptide histidine isoleucine (PHI), vasoactive intestinal peptide (VIP), neurotensin (NT) and cholecystokinin (CCK). We also examined the sheep median eminence using immunohistochemistry for NPY, SP and GAL and determined degradation profiles of NPY, SP, GAL and NKA in portal and jugular plasma. In no instance did we find that levels of the above peptides were consistently higher in portal blood than in peripheral blood. In some cases levels of peptide were lower in portal plasma e.g. for NPY (6/10 sheep). In one experimental series SP levels in portal plasma were significantly (p < 0.05) lower than levels in jugular plasma but this was not found in another experimental series. Galanin levels were significantly (p < 0.01) lower in portal plasma compared to levels in jugular plasma. We conducted in vitro studies to determine whether or not the above peptides are selectively degraded in portal blood but were unable to show any differences between the rates of degradation in portal and jugular plasma. Immunohistochemistry revealed projections into the external zone of the median eminence for NPY, GAL and SP. This study shows that none of the above peptides are secreted into the hypophysial portal blood of sheep. For some peptides e.g. GAL, enzymes from the endothelial cells of the portal vessels may enhance degradation. Projections into the external zone of the median eminence of neuronal systems containing these peptides may serve to modulate the secretion of the well recognized release and inhibiting factors by acting on the neurosecretory terminals.

show abstract

Section: Discussionmentioning

confidence: 94%

Many Peptides that Are Present in the External Zone of the Median Eminence Are Not Secreted into the Hypophysial Portal Blood of Sheep

et al. 1993

View full text Add to dashboard Cite

show abstract

“…Furthermore, treatment with various ACE inhibitors augment peptide levels substantially (5-to 25-fold) in the circulation. [23][24][25][26][27] These data generate a new perspective on the factors that regulate the opposing actions of Ang II and Ang-(1-7) on blood pressure and cell growth. 1 To establish the mechanisms contributing to the removal of Ang-(1-7) from the circulation and ascertain whether clearance is altered in hypertensive animals, we determined the MCR Ang-(1-7) in Sprague-Dawley (SD), SHR, and TG ϩ rats given long-term treatment with an ACE inhibitor or in combination with concurrent therapy with a selective AT 1 receptor blocker.…”

Section: S Ubstantial Evidence Now Exists That Angiotensin-(1-7)mentioning

confidence: 94%

Converting Enzyme Determines Plasma Clearance of Angiotensin-(1–7)

et al. 1998

View full text Add to dashboard Cite

Abstract-We determined the mechanism accounting for the removal and metabolism of angiotensin-(1-7) [Ang-(1-7)] in 21 anesthetized spontaneously hypertensive (SHR), 18 age-matched normotensive Sprague-Dawley (SD), and 36 mRen-2 transgenic (TG ϩ ) rats. Animals of all 3 strains were provided with tap water or tap water containing losartan, lisinopril, or a combination of lisinopril and losartan for 2 weeks. On the day of the experiment, Ang-(1-7) was infused for a period of 15 minutes at a rate of 278 nmol ⅐ kg Ϫ1 ⅐ min Ϫ1. After this time, samples of arterial blood were collected rapidly at regular intervals for the assay of plasma Ang-(1-7) levels by radioimmunoassay. Infusion of Ang-(1-7) had a minimal effect on vehicle-treated SD rats but elicited a biphasic pressor/depressor response in vehicle-treated SHR and TG ϩ rats. In lisinopril-treated rats, Ang-(1-7) infusion increased blood pressure, whereas losartan treatment abolished the pressor component of the response without altering the secondary fall in arterial pressure. Combined treatment with lisinopril and losartan abolished the cardiovascular response to Ang-(1-7) in all 3 strains. In vehicle-treated SD, SHR and TG ϩ the half-life (t 1/2 ) of Ang-(1-7) averaged 10Ϯ1, 10Ϯ1, and 9Ϯ1 seconds, respectively. Lisinopril alone or in combination with losartan produced a statistically significant rise in the half-life of Ang-(1-7) in all 3 strains of rats. Plasma clearance of Ang-(1-7) was significantly greater in the untreated SD rats compared with either the SHR or TG ϩ rat. Lisinopril treatment was associated with reduced clearance of Ang-(1-7) in all 3 strains. Concurrent experiments in pulmonary membranes from SD and SHR showed a statistically significant inhibition of 125 I-Ang-(1-7) metabolism in the presence of lisinopril. These studies showed for the first time that the very short half-life of Ang-(1-7) in the circulation is primarily accounted for peptide metabolism by ACE. These findings suggest a novel role of ACE in the regulation of the production and metabolism of the two primary active hormones of the renin angiotensin system. (Hypertension. 1998;32:496-502.)

show abstract

“…It is thought that the active peptides angiotensin II, III, or IV may have roles within the brain in functions as diverse as the regulation of cardiovascular and fluid homeostasis (2,3,11,19,35,40,41,46), reproduction (15), thermoregulation (28), memory (49), cognition, emotional responses to stress and anxiety, cerebral blood flow regulation, and brain developmental processes (39). However, some studies have questioned whether angiotensin is a neuropeptide because of its very low abundance in brain (23) and have proposed that an alternative endogenous ligand may act on angiotensin receptors in the brain (6).…”

mentioning

confidence: 99%

Osmoregulatory fluid intake but not hypovolemic thirst is intact in mice lacking angiotensin

Walker

Alexiou

Allen

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

View full text Add to dashboard Cite

Water intakes in response to hypertonic, hypovolemic, and dehydrational stimuli were investigated in mice lacking angiotensin II as a result of deletion of the angiotensinogen gene (AgtϪ/Ϫ mice), and in C57BL6 wild-type (WT) mice. Baseline daily water intake in AgtϪ/Ϫ mice was approximately threefold that of WT mice because of a renal developmental disorder of the urinary concentrating mechanisms in AgtϪ/Ϫ mice. Intraperitoneal injection of hypertonic saline (0.4 and 0.8 mol/l NaCl) caused a similar dose-dependent increase in water intake in both AgtϪ/Ϫ and WT mice during the hour following injection. As well, AgtϪ/Ϫ mice drank appropriate volumes of water following water deprivation for 7 h. However, AgtϪ/Ϫ mice did not increase water or 0.3 mol/l NaCl intake in the 8 h following administration of a hypovolemic stimulus (30% polyethylene glycol sc), whereas WT mice increased intakes of both solutions during this time. Osmoregulatory regions of the brain [hypothalamic paraventricular and supraoptic nuclei, median preoptic nucleus, organum vasculosum of the lamina terminalis (OVLT), and subfornical organ] showed an increased number of neurons exhibiting Fos-immunoreactivity in response to intraperitoneal hypertonic NaCl in both AgtϪ/Ϫ mice and WT mice. Polyethylene glycol treatment increased Fos-immunoreactivity in the subfornical organ, OVLT, and supraoptic nuclei in WT mice but only increased Fos-immunoreactivity in the supraoptic nucleus in AgtϪ/Ϫ mice. These data show that brain angiotensin is not essential for the adequate functioning of neural pathways mediating osmoregulatory thirst. However, angiotensin II of either peripheral or central origin is probably necessary for thirst and salt appetite that results from hypovolemia.

show abstract

Increased Angiotensin-(1–7) in Hypophysial-Portal Plasma of Conscious Sheep

Cited by 31 publications

References 37 publications

Many Peptides that Are Present in the External Zone of the Median Eminence Are Not Secreted into the Hypophysial Portal Blood of Sheep

Many Peptides that Are Present in the External Zone of the Median Eminence Are Not Secreted into the Hypophysial Portal Blood of Sheep

Converting Enzyme Determines Plasma Clearance of Angiotensin-(1–7)

Osmoregulatory fluid intake but not hypovolemic thirst is intact in mice lacking angiotensin

Contact Info

Product

Resources

About