Independent osmoregulatory control of central and systemic angiotensin II concentrations in dogs

1986 ◽  
Vol 250 (5) ◽  
pp. R918-R925 ◽  
Author(s):  
C. Simon-Oppermann ◽  
D. A. Gray ◽  
E. Simon
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Anterior Part ◽  
Conscious Dogs ◽  
Cerebral Ventricle ◽  
Ang Ii ◽  
Salt Loading ◽  
The Third ◽  
Rich Food ◽  
Conscious Animals

In 14 dogs angiotensin (ANG II)-like immunoreactivity was analyzed in simultaneously collected samples of cerebrospinal fluid (CSF) from the anterior part of the third cerebral ventricle and of plasma. Plasma and CSF ANG II were not different in euhydrated conscious dogs (29.3 +/- 2.7 and 30.8 +/- 2.8 pg X ml-1, means +/- SE). During anesthesia CSF ANG II was not significantly altered, but plasma ANG II was more than doubled in comparison with conscious animals. In conscious dogs 24 h of dehydration with sodium-rich food significantly increased ANG II concentration in the plasma (to 59.8 +/- 16.5 pg X ml-1) and CSF (to 71.8 +/- 20.1 pg X ml-1). Subsequent rehydration by drinking caused no consistent changes in plasma ANG II within 90 min but reduced CSF ANG II significantly. Salt loading by infusion of 5% saline in seven conscious dogs produced a small but consistent decrease in plasma ANG II by 20%, on average, whereas CSF ANG II rose in five animals. The directions of changes in concentration of central ANG II compared with plasma ANG II suggest that central endogenous ANG II may function as a central osmoregulatory mediator independent from systemic ANG II.

Vasopressin in blood and third ventricle CSF of dogs in chronic experiments

1983 ◽  
Vol 245 (4) ◽  
pp. R541-R548 ◽  
Author(s):  
C. Simon-Oppermann ◽  
D. Gray ◽  
E. Szczepanska-Sadowska ◽  
E. Simon
Keyword(s):  
Cerebrospinal Fluid ◽  
Arginine Vasopressin ◽  
Anterior Part ◽  
Third Ventricle ◽  
Conscious State ◽  
Conscious Dogs ◽  
Inhalation Anesthesia ◽  
Blood Samples ◽  
The Third ◽  
Device Implantation

A device for chronic implantation was developed that allowed sampling of cerebrospinal fluid (CSF) from the anterior part of the third cerebral ventricle (A3V) of dogs in repeated experiments for up to 4 mo. Osmolalities, electrolyte concentrations, and concentrations of arginine vasopressin (AVP) measured with a radioimmunoassay were determined in repeated experiments on the chronically prepared animals under conditions of normal hydration, both in the conscious state and during inhalation anesthesia. In conscious dogs, AVP concentrations in plasma and CSF were 3.3 +/- 0.4 and 21.8 +/- 2.5 pg X ml-1, respectively. During anesthesia without surgical interference, the AVP concentrations in plasma and CSF were increased twofold above the levels obtained in conscious dogs. During the time of observation (180 min) all measured parameters remained constant. The AVP concentrations in plasma and CSF samples collected during the surgical procedure of device implantation were about 10-fold higher than in the samples collected during the conscious state. Thus, in each experimental condition, AVP concentration in the CSF collected from the A3V was consistently higher than that in the simultaneously collected blood samples.

Abstract P301: Renal Expression of Collectrin (TMEM27) is Downregulated During Angiotensin II-induced Hypertension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sylvia Cechova ◽  
Pei-Lun Chu ◽  
Joseph Gigliotti ◽  
Thu H Le
Keyword(s):  
Angiotensin Ii ◽  
Catalytic Domain ◽  
Collecting Duct ◽  
Amino Acid Transporters ◽  
Ang Ii ◽  
Salt Loading ◽  
Transmembrane Glycoprotein ◽  
First Time ◽  
Renal Expression

Collectrin ( Tmem27 ) is transmembrane glycoprotein with homology to ACE-2, but lacks any catalytic domain. It plays a key role as a chaperone of amino acid transporters, and is abundantly expressed in the kidney in the proximal tubules and collecting duct. Deletion of collectrin in the mouse results in hypertension (HTN) at baseline and augmented salt-sensitivity that are associated with decreased renal nitric oxide and increased superoxide levels. During high salt diet, renal expression of collectrin is upregulated, suggesting an adaptive homeostatic response to salt loading. Here, we queried whether the expression of collectrin is regulated by angiotensin II (Ang II). Wild-type 129S6 mice were made hypertensive with Ang II osmotic minipump @ 600 ng/kg/min x 2 weeks, and were compared to age-matched untreated WT 129 mice. Shown in Fig. 1 , renal mRNA expression of collectrin is significantly reduced after 2 weeks of Ang II (Panel A). Immunostaining shows collectrin protein level is also significantly diminished to near undetectable level (Panel B). We show for the first time that Ang II regulates the expression of collectrin, suggesting that the action of Ang II on blood pressure may be mediated, in part, through the downregulation of collectrin. Further studies are needed to determine the effect of AT 1 and AT 2 receptor signaling on renal expression of collectrin during Ang II-HTN in vivo.

Angiotensin and Na appetite of sheep

1986 ◽  
Vol 251 (4) ◽  
pp. R690-R699 ◽  
Author(s):  
R. S. Weisinger ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
A. F. Muller ◽  
E. Tarjan
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Ang Ii ◽  
Nacl Solution ◽  
Parotid Saliva ◽  
Continuous Access ◽  
Access To Water

The effect of both intravenous (iv; 24 micrograms/h) and intracerebroventricular (ivt; 3.8 micrograms/h) infusion over 1-2 days of angiotensin II (ANG II) on Na intake of both Na-replete and -deplete sheep (i.e., 22 h loss of parotid saliva) was observed. In Na-replete sheep with continuous access to water and 2-h daily access to 0.5 M NaCl solution, both iv and ivt ANG II caused an increase in Na intake. The increase in Na intake caused by iv or ivt ANG II was preceded by a Na deficit due to increased urinary Na excretion. The increase in Na intake was eliminated by the continuous return of urine. In Na-deplete sheep with continuous access to water and 2-h daily access to 0.6 M NaHCO3 solution, iv ANG II caused no change in Na loss but a small increase in Na intake during the 1st day of infusion. The ivt ANG II caused no change in Na loss or in Na intake. The iv ANG II caused a small and inconsistent increase in water intake in Na-replete sheep but did not cause any change in water intake of Na-deplete sheep. The ivt ANG II caused a large increase in water intake in both Na-replete and -deplete sheep. In both Na-replete and -deplete sheep, iv ANG II did not alter cerebrospinal fluid or plasma [Na] or osmolality but decreased plasma [K]. The ivt ANG II decreased both cerebrospinal fluid and plasma [Na] and osmolality. The results of the present experiments are consistent with the proposition that the ANG II-induced Na appetite in sheep is largely due to an ANG II-induced Na loss preceding the development of appetite.

scholarly journals Brain Prostaglandin D2 Increases Neurogenic Pressor Activity and Mean Arterial Pressure in Angiotensin II-Salt Hypertensive Rats

Hypertension ◽  
2019 ◽  
Vol 74 (6) ◽  
pp. 1499-1506 ◽  
Author(s):  
Ninitha Asirvatham-Jeyaraj ◽  
A. Daniel Jones ◽  
Robert Burnett ◽  
Gregory D. Fink
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Developmental Stage ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Salt Hypertension ◽  
Pressor Activity

This study tested whether brain L-PGDS (lipocalin-type prostaglandin [PG] D synthase), through prostanoid signaling, might increase neurogenic pressor activity and thereby cause hypertension. Sprague Dawley rats on high-salt diet received either vehicle or Ang II (angiotensin II) infusion. On day 4, the developmental stage of hypertension, brains from different sets of control and Ang II–treated rats were collected for measuring L-PGDS expression, PGD2 levels, and DP1R (type 1 PGD2 receptor) expression. In a different set of 14-day Ang II-salt–treated rats, mini-osmotic pumps were used to infuse either a nonselective COX (cyclooxygenase) inhibitor ketorolac, L-PGDS inhibitor AT56, or DP1R inhibitor BWA868C to test the role of brain COX-PGD2-DP1R signaling in Ang II-salt hypertension. The acute depressor response to ganglion blockade with hexamethonium was used to quantify neurogenic pressor activity. During the developmental stage of Ang II-salt hypertension, L-PGDS expression was higher in cerebrospinal fluid, and PGD2 levels were increased in the choroid plexus, cerebrospinal fluid, and the cardioregulatory brain region rostral ventrolateral medulla. DP1R expression was decreased in rostral ventrolateral medulla. Both brain COX inhibition with ketorolac and L-PGDS inhibition with AT56 lowered mean arterial pressure by altering neurogenic pressor activity compared with vehicle controls. Blockade of DP1R with BWA868C, however, increased the magnitude of Ang II-salt hypertension and significantly increased neurogenic pressor activity. In summary, we establish that the development of Ang II-salt hypertension requires increased COX- and L-PGDS–derived PGD2 production in the brain, making L-PGDS a possible target for treating neurogenic hypertension.

Modulation of K+ and Ca2+ currents in cultured neurons by an angiotensin II type 1a receptor peptide

1997 ◽  
Vol 273 (3) ◽  
pp. C1040-C1048 ◽  
Author(s):  
M. Zhu ◽  
R. R. Neubig ◽  
S. M. Wade ◽  
P. Posner ◽  
C. H. Gelband ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
G Protein ◽  
At1 Receptor ◽  
Delayed Rectifier ◽  
Cultured Neurons ◽  
Ang Ii ◽  
Cytoplasmic Loop ◽  
At1 Receptors ◽  
The Third ◽  
Intracellular Changes

Angiotensin II (ANG II) inhibits delayed rectifier K+ current (IK) and stimulates total Ca2+ current (ICa) in neurons cocultured from newborn rat hypothalamus and brain stem, effects mediated via ANG II type 1 (AT1) receptors. Here, we identify potential G protein activator regions of the AT1 receptor responsible for initiating the intracellular changes that lead to alterations in these currents. Intracellular application into cultured neurons of a peptide corresponding to the third cytoplasmic loop of the AT1 receptor (AT1a/i3) mimicked the actions of ANG II on IK and ICa, whereas application of a peptide corresponding to the second cytoplasmic loop (AT1a/i2) did not alter these currents. This modulation of IK and ICa by AT1a/i3 involves intracellular messengers (G alpha q, protein kinase C, and intracellular Ca2+) that are identical to those involved in the modulation of IK and ICa following ANG II activation of AT1 receptors. These data provide functional evidence for a role of the third cytoplasmic loop of the AT1 receptor in G protein coupling and subsequent modulation of ion channel effectors.

Dehydration and arginine vasotocin and angiotensin II in CSF and plasma of pekin ducks

1987 ◽  
Vol 253 (2) ◽  
pp. R285-R291 ◽  
Author(s):  
D. A. Gray ◽  
E. Simon
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Anas Platyrhynchos ◽  
Salt Water ◽  
The State ◽  
Arginine Vasotocin ◽  
Plasma Samples ◽  
Ang Ii ◽  
Independent Control ◽  
Pekin Ducks

Osmolalities and, by radioimmunoassay, the contents of arginine vasotocin (AVT) and angiotensin II (ANG II) in simultaneously collected cisternal cerebrospinal fluid (CSF) and plasma samples were determined in chronically prepared conscious Pekin ducks (Anas platyrhynchos) adapted to either freshwater (FW ducks) or salt water (2% saline, SW ducks) for drinking. In FW ducks the AVT in CSF was approximately 10-fold higher than in plasma; ANG II concentration in CSF was about two-thirds of that in plasma. In SW ducks concentrations of AVT were increased approximately threefold and of ANG II fourfold in both CSF and plasma. Dehydration in FW ducks (24-48 h) increased AVT and ANG II in both CSF and plasma, the relative rise being greater in plasma. Within 150 min after rehydration plasma AVT fell at unchanged CSF AVT, whereas CSF ANG II fell at unchanged plasma ANG II. Hydration of SW ducks with freshwater had similar effects. The results indicate separate avenues of release of central and systemic AVT and ANG II and support the idea of an independent control of central ANG II as a mediator in osmoregulation, with CSF AVT reflecting the state of osmoregulatory activity of the hypothalamopituitary vasotocinergic system.

Effect of renal denervation on the suppression of renin secretion by vasopressin in conscious dogs

1984 ◽  
Vol 247 (6) ◽  
pp. F881-F887 ◽  
Author(s):  
L. C. Gregory ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Reflex Response ◽  
Renal Nerves ◽  
Ang Ii ◽  
Before And After

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracerebroventricular losartan inhibits postprandial drinking in sheep

1997 ◽  
Vol 272 (4) ◽  
pp. R1055-R1059 ◽  
Author(s):  
M. Mathai ◽  
M. D. Evered ◽  
M. J. McKinley
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Food Intake ◽  
Water Intake ◽  
Fluid Balance ◽  
Intravenous Infusion ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
Drinking Response ◽  
Dependent Mechanism

We investigated the contribution of brain angiotensinergic mechanisms to postprandial drinking in sheep. Sheep in fluid balance were given 0.8 kg chaff for 30 min, and water intake was measured for the next hour. Intracerebroventricular infusion of the AT1 type angiotensin II (ANG II) receptor blocker losartan (1 mg/h) reduced postprandial drinking by approximately 70% (n = 7, P < 0.01) but did not affect food intake. The same losartan dose given intravenously had little or no effect on prandial drinking. Feeding increased Na+ concentrations in plasma and cerebrospinal fluid (CSF; n = 5, P < 0.05). Intracerebroventricular losartan (1 mg/h) inhibited the drinking responses to intracarotid infusion of ANG II (0.8 microg/min for 30 min, n = 4, P < 0.01) and to intracerebroventricular infusion of 0.5 M NaCl (1 ml/h for 1 h, n = 5, P < 0.05) but had no effect on drinking responses to intravenous infusion of 4 M NaCl (1.3 ml/min for 30 min). These findings indicate that a brain ANG II-dependent mechanism is involved in postprandial drinking in sheep. They suggest also that the mechanism by which increasing CSF Na+ causes thirst involves brain ANG II and is different from the mechanism subserving the drinking response to changes in blood Na+.

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