Drinking and blood pressure during sodium depletion or ANG II infusion in chronic cholestatic rats

1999 ◽  
Vol 276 (1) ◽  
pp. R23-R31 ◽  
Author(s):  
Douglas A. Fitts ◽  
Jeannine R. Lane ◽  
Elizabeth M. Starbuck ◽  
Chi-Pei Li
Keyword(s):  
Blood Pressure ◽  
Saline Solution ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Drinking Response ◽  
Pressor Responses ◽  
The Common ◽  
Ad Libitum ◽  
Long Evans ◽  
Rapid Intake

After a chronic ligation of the common bile duct (BDL), Long-Evans rats are hypotensive and have elevated saline intake during both sodium-depleted and nondepleted conditions. We tested whether BDL rats have exaggerated hypotension during sodium depletion or an elevated dipsogenic response to angiotensin II (ANG II) that might help to explain the saline intake. After 4 wk of BDL, rats were hypotensive at baseline and developed exaggerated hypotension during acute furosemide-induced diuresis. Without saline to drink, BDL rats increased water intake during depletion equal to sham-ligated rats. However, with saline solution available at 22 h after sodium depletion, the BDL rats drank more water and saline than did sham-ligated rats. This rapid intake temporarily increased their mean arterial pressure to equal that of sham-ligated rats. Intravenous infusion of ANG II induced equal drinking responses despite reduced pressor responses in the BDL rats relative to sham-ligated rats during both ad libitum and sodium-depleted conditions. Thus BDL rats have exaggerated hypotension during diuresis, and their hypotension is corrected by drinking an exaggerated volume of saline, but they do not have an increased drinking response to ANG II.

Central effects of angiotensins I and II in conscious streptozotocin-treated rats

1990 ◽  
Vol 258 (5) ◽  
pp. R1147-R1156 ◽  
Author(s):  
K. C. Tomlinson ◽  
S. M. Gardiner ◽  
T. Bennett
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Brattleboro Rats ◽  
Ang Ii ◽  
Angiotensin I ◽  
Enhanced Sensitivity ◽  
Drinking Response ◽  
Pressor Responses ◽  
Long Evans ◽  
Residual Response

Responses to intracerebroventricular (icv) angiotensin II (ANG II) were measured in Long-Evans rats treated with the diabetogenic agent, streptozotocin (STZ), or saline 28 days earlier. STZ-treated Long-Evans rats showed normal pressor responses to ANG II in the absence of drinking water, but bradycardic responses were impaired although there was no reduction in baroreflex sensitivity. When allowed to drink, saline-treated, but not STZ-treated, rats showed an enhanced pressor response to icv ANG II and a tachycardia. Peripheral V1-receptor antagonism attenuated the pressor response to icv ANG II, leaving a residual response that was greater in saline-treated than in STZ-treated rats. STZ-treated rats had attenuated pressor and heart rate responses to icv angiotensin I (ANG I). Although some cardiovascular responses to icv ANG I and ANG II were reduced in STZ-treated rats, these animals showed enhanced sensitivity to the dipsogenic effects of the peptides. Vasopressin-deficient Brattleboro rats showed little pressor response to icv ANG II unless drinking was allowed, in which case the pressor response was less in STZ-treated than in saline-treated Brattleboro rats, although there was no difference in drinking response.

Interactions between ANP and ANG II in regulating blood pressure and sympathetic outflow

1991 ◽  
Vol 260 (6) ◽  
pp. R1145-R1151 ◽  
Author(s):  
M. K. Steele ◽  
D. G. Gardner ◽  
P. L. Xie ◽  
H. D. Schultz
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Contrast Injection ◽  
Synthesis Inhibitor ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Renal Sympathetic

In anesthetized rats with sinoaortic denervation, intracerebroventricular (icv) injection of atrial natriuretic peptide (ANP) resulted in decreased mean arterial blood pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) (depressor effects), whereas icv angiotensin II (ANG II) produced increases in these variables (pressor effects). The depressor effects of ANP were slower in onset and longer in duration than the pressor effects of ANG II. Intracerebroventricular injection of the ANG II-receptor blocker sarthran or the ANG II-synthesis inhibitor captopril resulted in a significant reduction in MAP; HR and RSNA were not affected. Both sarthran and captopril abolished the depressor responses to icv ANP. In contrast, injection of an anti-rat ANP antibody, which blocked the depressor effects of icv ANP, did not by itself modify MAP, HR, or RSNA, nor did the antibody affect the pressor responses to icv ANG II. These data suggest that, in this animal model, the depressor effects of icv ANP are mediated by the inhibition of brain ANG II-dependent neural activity. These results also demonstrate that, in this preparation, the endogenous ANG II system actively contributes to the maintenance of basal MAP, whereas the central ANP system, at least in regions accessible to the antirat ANP antibody, plays little role in this maintenance.

Effect of intravenous angiotensin II on Fos distribution and drinking behavior in rabbits

1997 ◽  
Vol 272 (5) ◽  
pp. R1515-R1524 ◽  
Author(s):  
E. Badoer ◽  
D. McKinlay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Intravenous Infusion ◽  
Drinking Behavior ◽  
Ventrolateral Medulla ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Solitary Tract ◽  
Cell Nuclei ◽  
Drinking Response

We investigated the effect of intravenous infusion of angiotensin II (ANG II, 40 ng.kg-1.min-1) on the distribution of Fos in the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), and the medulla of the conscious rabbit. ANG II elicited significant increases in the number of Fos-positive cell nuclei in the SFO and OVLT (15- and 10-fold, respectively). Raising blood pressure with phenylephrine did not elicit Fos in these nuclei. These nuclei are believed to be responsible for the dipsogenic actions of ANG II; however, ANG II was not dipsogenic. When blood pressure was held at preinfusion levels by the coadministration of sodium nitroprus-side and ANG II, the rabbits did not drink but Fos production in the lamina terminalis was elevated. In the medulla, ANG II did not significantly increase Fos production in the nucleus of the solitary tract (NTS) or ventrolateral medulla (VLM). However, with the coadministration of sodium nitroprusside, there were marked increases in the NTS and VLM. The results suggest that neurons in the SFO and OVLT are either not involved in the dipsogenic pathways or there is disruption further downstream in the central pathways that would normally mediate a drinking response to ANG II.

Effect of Sodium Depletion on the Steroidogenic and Pressor Actions of Angiotensin in the Rat

1979 ◽  
Vol 56 (4) ◽  
pp. 325-333 ◽  
Author(s):  
W. B. Campbell ◽  
J. M. Schmitz ◽  
H. D. Itskovitz
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Depletion ◽  
Angiotensin I ◽  
Arterial Blood ◽  
Serum Aldosterone ◽  
Pressor Responses ◽  
Angiotensin Iii

1. To investigate the relative roles of angiotensin II (AII) and des-Asp1-angiotensin II (angiotensin III) in the control of blood pressure and aldosterone release, the effects of seven angiotensin agonists on mean arterial blood pressure and serum aldosterone concentrations were compared in normal and sodium-depleted, conscious rats. 2. In normal rats, angiotensin I, α-Asp1-angiotensin II, β-Asp1-angiotensin II, and angiotensin II-amide were equipotent in elevating mean arterial blood pressure. Angiotensin III, des-Asp1-angiotensin I, and poly-O-acetylserine-angiotensin II were 25%, 25%, and 41% as potent as angiotensin II, respectively. After sodium depletion, pressor responses to these angiotensin peptides were reduced approximately 60–80% when compared with control responses. In contrast, pressor responses to noradrenaline were not significantly affected by sodium depletion. 3. Angiotensin II, β-Asp1-angiotensin II, angiotensin II-amide, and angiotensin III were equipotent in increasing serum aldosterone concentrations in normal animals. Angiotensin I was 59% and des-Asp1-angiotensin I only 5% as potent as angiotensin II in their abilities to release aldosterone. After sodium depletion, control serum aldosterone concentrations increased as did the slope of the dose—response curve for each angiotensin peptide. Angiotensin II was the most potent steroidogenic peptide in sodium-depleted rats with angiotensin III and β-Asp1-angiotensin II being 27%, angiotensin I 7%, angiotensin II-amide 3%, and des-Asp1-angiotensin I 1% as potent as angiotensin II in releasing aldosterone. Poly-O-acetylserine-angiotensin II has less steroidogenic effect than angiotensin II or III in both normal and sodium-depleted animals. 4. Infusions of the angiotensin II antagonist, Sar1-Ile8-angiotensin II, and the angiotensin III antagonist, Ile7-angiotensin III, enhanced aldosterone release in normal rats without altering blood pressure. After sodium depletion, Sar1-Ile8-angiotensin II decreased blood pressure without affecting aldosterone release whereas Ile7-angiotensin III diminished aldosterone release without altering blood pressure. 5. These data suggest that angiotensin II, independent of its conversion into angiotensin III, is an important regulator of steroidogenesis in the rat in normal sodium states. In sodium depletion, the octapeptide retains significant steroidogenic activity; however, the contribution of angiotensin III to its steroidogenic effects is increased.

Central angiotensin II-induced pressor responses and neural activity in utero and hypothalamic angiotensin receptors in preterm ovine fetus

2004 ◽  
Vol 286 (4) ◽  
pp. H1507-H1514 ◽  
Author(s):  
Zhice Xu ◽  
Lijun Shi ◽  
Jiaming Yao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
In Utero ◽  
Angiotensin Receptors ◽  
Ang Ii ◽  
Central Administration ◽  
Pressor Responses ◽  
Ovine Fetus ◽  
Fos Expression ◽  
Sympathetic Pathway

The central renin-angiotensin system is important in the control of blood pressure in the adult. However, few data exist about the in utero development of central angiotensin-mediated pressor responses. Our recent studies have shown that the application of ANG II into the fetal brain can increase blood pressure at near term. The present study determined fetal blood pressure and heart rate in response to a central application of ANG II in the chronically prepared preterm ovine fetus, determined the action sites marked by c-Fos expression in the fetal central pathways after intracerebroventricular injection of ANG II in utero, and determined angiotensin subtype 1 receptors in the fetal hypothalamus. Central injection of ANG II significantly increased fetal mean arterial pressure (MAP). Adjusted fetal MAP against amniotic pressure was also increased by ANG II. Fetal heart rate was subsequently decreased after the central administration of ANG II and/or the increase of blood pressure. ANG II induced c-Fos expression in the central putative cardiovascular area, the paraventricular nuclei in the brain sympathetic pathway. Application of ANG II also caused intense Fos immunoreactivity in the tractus solitarius nuclei in the hindbrain. In addition, intense angiotensin subtype 1 receptors were expressed in the hypothalamus at preterm. These data demonstrate that central ANG II-related pressor centers start to function as early as at preterm and suggest that the central angiotensin-related sympathetic pathway is likely intact in the control of blood pressure in utero.

Effect of paraventricular nucleus lesions on drinking and pressor responses to ANG II

1988 ◽  
Vol 255 (6) ◽  
pp. R882-R887 ◽  
Author(s):  
M. B. Gutman ◽  
D. L. Jones ◽  
J. Ciriello
Keyword(s):  
Angiotensin Ii ◽  
Paraventricular Nucleus ◽  
Phosphate Buffer ◽  
Pressor Response ◽  
Neural Circuitry ◽  
Ang Ii ◽  
Drinking Response ◽  
Pressor Responses ◽  
Vehicle Injection ◽  
Bilateral Lesions

Experiments were done to investigate the contribution of cells of the paraventricular nucleus of the hypothalamus (PVH) to the drinking and pressor responses elicited by microinjection of angiotensin II (ANG II) into the subfornical organ (SFO) in the awake unrestrained rat. Microinjection of ANG II (5 eta g in 0.2 microliter) elicited drinking (7.1 +/- 0.7 ml in 15 min, n = 18) and pressor (19 +/- 1 mmHg, n = 17) responses. Bilateral lesions of the PVH by the administration of kainic acid (KA; 0.2 microgram in 0.2 microliter of phosphate buffer) resulted in the abolition of the drinking response (before, 7.8 +/- 1.8 ml in 15 min; after, 0 ml in 15 min, n = 6) and significant (P less than 0.05) attenuation of the pressor response (before, 15 +/- 1 mmHg; after, 5 +/- 2 mmHg, n = 5). Administration of 0.2 microliter of the phosphate buffer vehicle bilaterally into the PVH and KA into regions adjacent to the PVH had no significant effect on the drinking or pressor responses. KA injections into the PVH resulted in the loss of 70-80% of parvocellular cells in the posterodorsal component of the PVH compared with animals with KA injections into adjacent non-PVH tissue (n = 7) or vehicle injection into the PVH (n = 5). These results suggest that parvocellular cells of the PVH are an important component of the neural circuitry that mediates the drinking and pressor response to ANG II acting at the SFO.

Blood pressure in streptozotocin-treated Brattleboro and Long-Evans rats

1990 ◽  
Vol 258 (4) ◽  
pp. R852-R859 ◽  
Author(s):  
K. C. Tomlinson ◽  
S. M. Gardiner ◽  
T. Bennett
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Insulin Treatment ◽  
Renin Angiotensin System ◽  
Brattleboro Rats ◽  
Ang Ii ◽  
Angiotensin System ◽  
Resting Blood Pressure ◽  
Long Evans

The diabetogenic agent streptozotocin (STZ) was injected intraperitoneally in Long-Evans and arginine vasopressin (AVP)-deficient Brattleboro rats. Twenty-eight days later both strains had a bradycardia and systolic hypotension; STZ-treated Brattleboro rats also had diastolic hypotension. The vasopressin (V1-receptor) antagonist, d(CH2)5[Tyr(Et)]DAVP, had no effect on resting blood pressure (BP) or heart rate (HR) in either strain of rat, indicating the relative maintenance of diastolic BP in STZ-treated Long-Evans rats was not dependent on acute vascular actions of AVP. Captopril caused a modest hypotension in all groups of rats, indicating that BP was not differentially dependent on the renin-angiotensin system in the different groups. In the presence of captopril and the ganglion blocker, pentolinium tartrate, the AVP-mediated recovery in BP was impaired in STZ-treated Long-Evans rats. During administration of d(CH2)5[Tyr(Et)]DAVP and pentolinium, the angiotensin II (ANG II)-mediated BP recovery was smaller in both groups of STZ-treated rats, indicating that this abnormality was not likely to be caused by inhibition of renin release by AVP. The abnormalities in ANG II- and AVP-mediated recovery were prevented by insulin treatment.

scholarly journals Role of the Na+/H+ exchanger 3 in angiotensin II-induced hypertension

2015 ◽  
Vol 47 (10) ◽  
pp. 479-487 ◽  
Author(s):  
Xiao C. Li ◽  
Gary E. Shull ◽  
Elisa Miguel-Qin ◽  
Jia L. Zhuo
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Glycogen Synthase ◽  
Proximal Tubules ◽  
Dependent Manner ◽  
Ang Ii ◽  
Lower Systolic Blood Pressure ◽  
Salt Wasting ◽  
Pressor Responses ◽  
Induced Hypertension

The renal mechanisms responsible for angiotensin II (ANG II)-induced hypertension remain incompletely understood. The present study tested the hypothesis that the Na+/H+ exchanger 3 (NHE3) is required for ANG II-induced hypertension in mice. Five groups of wild-type ( Nhe3 +/+) and Nhe3 −/− mice were treated with vehicle or high pressor doses of ANG II (1.5 mg/kg/day ip, via minipump for 2 wk, or 10 pmol/min iv for 30 min). Under basal conditions, Nhe3 −/− mice had significantly lower systolic blood pressure (SBP) and mean intra-arterial pressure (MAP) ( P < 0.01), 24 h urine ( P < 0.05), urinary Na+ ( P < 0.01) and urinary K+ excretion ( P < 0.01). In response to ANG II, SBP and MAP markedly increased in Nhe3 +/+ mice in a time-dependent manner, as expected ( P < 0.01). However, these acute and chronic pressor responses to ANG II were significantly attenuated in Nhe3 −/− mice ( P < 0.01). Losartan blocked ANG II-induced hypertension in Nhe3 +/+ mice but induced marked mortality in Nhe3 −/− mice. The attenuated pressor responses to ANG II in Nhe3 −/− mice were associated with marked compensatory humoral and renal responses to genetic loss of intestinal and renal NHE3. These include elevated basal plasma ANG II and aldosterone and kidney ANG II levels, salt wasting from the intestines, increased renal AQP1, Na+/HCO3−, and Na+/K+-ATPase expression, and increased PKCα, mitogen-activated protein kinases ERK1/2, and glycogen synthase kinase 3αβ signaling proteins in the proximal tubules ( P < 0.01). We concluded that NHE3 in proximal tubules of the kidney, along with NHE3 in intestines, is required for maintaining basal blood pressure as well as the full development of ANG II-induced hypertension.

Role of AVP in pressor responses during activation of central TxA2/PGH2receptors

1997 ◽  
Vol 273 (4) ◽  
pp. H1927-H1932 ◽  
Author(s):  
Christopher S. Wilcox ◽  
Hubin Gao ◽  
Joseph G. Verbalis ◽  
William J. Welch
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Receptor Agonist ◽  
Pressor Response ◽  
Brattleboro Rats ◽  
Pressor Responses ◽  
Long Evans ◽  
Plasma Arginine ◽  
Prostaglandin H

Administration of thromboxane A2/prostaglandin H2(TxA2/PGH2)-receptor agonist U-46619 (2.86 nmol/kg iv) to conscious rats increased mean arterial pressure (MAP) by 17 ± 2 mmHg ( n = 6; P < 0.001) and plasma arginine vasopressin (AVP) by 3.5 ± 1.1 IU/ml ( n = 6; P < 0.001). Ifetroban (TxA2/PGH2antagonist; intracerebroventricularly) prevented both responses. Intracerebroventricular U-46619 increased MAP in Long-Evans rats ( n = 6) more than in AVP-deficient Brattleboro rats. AVP V1-receptor antagonist d(CH2)5Tyr(Me)AVP (3 μg/kg iv) blocked 67 ± 5% and 69 ± 7% of pressor response to intravenous AVP and intracerebroventricular U-46619, respectively. AVP (10 ng/kg iv) increased AVP by 4.7 ± 0.5 pg/ml, comparable to the increase of 3.5 ± 1.2 pg/ml with intracerebroventricular U-46619 (2.86 nmol/kg), but the rise in MAP was only one-half as great (+8 ± 3 mmHg for AVP vs. +17 ± 2 mmHg for U-46619; P < 0.05). In conclusion, U-46619 raises blood pressure and releases AVP by activating brain receptors. AVP explains approximately one-half of the pressor response.

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